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BIOMARKER:

EZH2 overexpression

i
Other names: EZH2, ENX-1, EZH1, KMT6, KMT6A, Enhancer of zeste 2 polycomb repressive complex 2 subunit
Entrez ID:
Related biomarkers:
17d
BMP2 inhibits cell proliferation by downregulating EZH2 in gastric cancer. (PubMed, Cell Cycle)
Altogether, in this study, we demonstrate that BMP2 serves as a tumor suppressor in gastric cancer cells by downregulating EZH2 and H3K27me3 through the non-SMAD BMP pathway, suggesting that BMP2 might be a new therapeutic target for gastric cancer treatment. Abbreviations: BMP: bone morphogenetic protein; TGF-β: transforming growth factor-beta; EZH2: enhancer of zeste homolog 2; H3K27me3: trimethylation histone H3 lysine 27; HRECs: human retinal endothelial cells; PcG: polycomb group; PRC: polycomb repressive complexes.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • CDK4 (Cyclin-dependent kinase 4) • CDK6 (Cyclin-dependent kinase 6) • TGFB1 (Transforming Growth Factor Beta 1) • CDK2 (Cyclin-dependent kinase 2) • CDKN1A (Cyclin-dependent kinase inhibitor 1A)
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EZH2 overexpression
25d
EZH2 promotes the progression of osteosarcoma through the activation of the AKT/GSK3β pathway. (PubMed, Clin Exp Pharmacol Physiol)
MK-2206 erased EZH2 up-regulation-induced promotion of OS cell growth. It is demonstrated that EZH2 promotes the progression of OS via inducing the activation of the AKT/GSK3β pathway, offering a therapeutic direction for OS treatment.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
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EZH2 overexpression
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MK-2206
27d
CRABP2 accelerates epithelial mesenchymal transition in serous ovarian cancer cells by promoting TRIM16 methylation via upregulating EZH2 expression. (PubMed, Environ Toxicol)
The SKOV3 cells were incubated with si-EZH2 alone or combined with si-TRIM16, and we found that si-TRIM16 reversed the effect of si-EZH2. In vivo studies showed that knockdown of CRABP2 inhibited tumor volume and weight, suppressed the expression of EZH2 and EMT related proteins vimentin and snail, and increased the expression of TRIM16 and E-cadherin.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • CDH1 (Cadherin 1) • DNMT1 (DNA methyltransferase 1) • VIM (Vimentin)
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CDH1 expression • EZH2 overexpression • VIM expression • DNMT1 overexpression
2ms
Ultrasound microbubble-mediated delivery of ANLN silencing-repressed EZH2 expression alleviates cervical cancer progression. (PubMed, Tissue Cell)
The modulatory role of UTMD-siANLN on EMT- and apoptosis-related markers was reversed by EZH2 overexpression. UTMD can improve the efficiency of siANLN transfection into CC cells to induce suppression of CC cell malignant phenotypes, which may become a new target of gene therapy for CC.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • ANLN (Anillin Actin Binding Protein)
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EZH2 overexpression
2ms
A nucleus-targeting peptide antagonist towards EZH2 displays therapeutic efficacy for lung cancer. (PubMed, Int J Pharm)
The observed anti-tumor activity of EIP103 and M-EIP103 demonstrated a promising therapy to improve clinical treatment of lung cancers as well as other EZH2-overexpressing malignant cancers. This study also illustrates the feasibility of developing targeted delivery of therapeutic peptides to nucleus for cancer therapy.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
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EZH2 overexpression
2ms
The correlation of EZH2 expression with the progression and prognosis of hepatocellular carcinoma. (PubMed, BMC Immunol)
EZH2 plays an essential role in the immune microenvironment and is a potential prognostic marker and immunotherapy target for hepatocellular carcinoma.
Journal • IO biomarker
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
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EZH2 overexpression
2ms
High Expression of EZH2 Mediated by ncRNAs Correlates with Poor Prognosis and Tumor Immune Infiltration of Hepatocellular Carcinoma. (PubMed, Genes (Basel))
SNHG6 or MALAT1/hsa-miR-101-3p/EZH2 axis were identified as potential regulatory pathways in the progression of HCC.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • MALAT1 (Metastasis associated lung adenocarcinoma transcript 1)
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EZH2 overexpression
2ms
Lycopene enhances the sensitivity of castration-resistant prostate cancer to enzalutamide through the AKT/EZH2/ androgen receptor signaling pathway. (PubMed, Biochem Biophys Res Commun)
Of note, a combination of lycopene and enzalutamide significantly inhibited the proliferation and invasion of CRPC cells in vitro, as well as tumor growth and bone metastasis in vivo. These results suggest that the enhanced antitumor effects of enzalutamide by lycopene may be related to the reduction of AR protein levels through lycopene-mediated inhibition of AKT/EZH2 pathway, which may provide a new approach to improve the efficacy of enzalutamide in CRPC.
Journal
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AR (Androgen receptor) • EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
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AR expression • EZH2 overexpression
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enzalutamide capsule
2ms
Effects of long-chain noncoding RNA Linc00673 overexpression on proliferation and apoptosis of gastric cancer cell line MGC-803 (PubMed, Zhongguo Ying Yong Sheng Li Xue Za Zhi)
Western blot showed that Linc00673 overexpression not only promoted the expressions of the key molecule pAkt in PI3K / Akt signaling pathway and its downstream target NF-κ B and Bcl-2 protein, but also up regulated the expressions of tumor related factors β-catenin and EZH2 proteins. Overexpression of Linc00673 may promote proliferation and inhibit apoptosis of MGC-803 cells through PI3K/Akt signaling pathway.
Preclinical • Journal • IO biomarker
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BCL2 (B-cell CLL/lymphoma 2) • EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • CDK1 (Cyclin-dependent kinase 1)
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EZH2 overexpression
3ms
Targeting EZH2 for cancer therapy: From current progress to novel strategies. (PubMed, Eur J Med Chem)
The internal relationship between EZH2 and various diseases will be expounded. The development status of specific inhibitors for EZH2, and the latest progress of new strategies such as drug combination, dual-target inhibitors, targeted protein degradation technology and protein-protein interactions (PPI) inhibitors will be emphatically summarized and analyzed.
Review • Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
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EZH2 overexpression
3ms
USP7 inhibits TIMP2 by up-regulating the expression of EZH2 to activate the NF-κB/PD-L1 axis to promote the development of cervical cancer. (PubMed, Cell Signal)
The study discovered the function and mechanism of USP7 and highlighted its oncogenic role in cervical cancer development. Our results indicated that targeting USP7 could be a therapeutic strategy the treatment of cervical cancer.
Journal • PD(L)-1 Biomarker • IO biomarker
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • TIMP2 (TIMP Metallopeptidase Inhibitor 2)
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PD-L1 expression • EZH2 overexpression
3ms
Prognostic value of EZH2 expression for immunotherapy-based schemes in advanced soft-tissue sarcoma: A translational research from Spanish Group of Research on Sarcoma (GEIS). (ASCO 2022)
IMMUNOSARC (NCT03277924) is a phase Ib/II trial [from Spanish (GEIS) and Italian (ISG) sarcoma groups], that tested the combination of nivolumab (anti-PD-1 inhibitor) plus sunitinib (anti-angiogenic agent) in advanced sarcomas. Low expression of EZH2 was associated with better outcome in advanced STS patients treated with immunotherapy-based schemes. These results might support the rationale for the combination of EZH2 inhibitors with immune-modulating agents for future studies.
PD(L)-1 Biomarker • IO biomarker
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
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EZH2 overexpression
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HTG EdgeSeq Oncology Biomarker Panel (OBP)
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Opdivo (nivolumab) • Sutent (sunitinib)
4ms
Inhibition of EZH2 Action has Contrasting Effects on Ovarian Cancer Stem Cell Populations (SRI 2022)
We demonstrated in vitro and in vivo that cisplatin and PARP inhibitors (PARPi) enrich for ovarian cancer stem cells (CSCs). Therefore, our objective was to assess how disruption of EZH2 action and/or reduction of EZH2 affects CSC populations alone or in combination with PARPi or carboplatin treatment. We treated OvCa cell lines (A2780, OVCAR4, displaying relatively high levels of EZH2) with vehicle(s), single agent EZH2 inhibitor GSK-126, carboplatin, the PARPi (olaparib), and combinations of GSK-126 with carboplatin or olaparib... Together, these data suggest EZH2 disruption of H3K27 trimethylation status negatively impacts the levels of ALDH active cells, but promotes an increase in PROM1 and subsequently CD133 positive cells. However, the combination of GSK-126 with carboplatin or PARPi was sufficient to negate the increase in CD133 positive populations suggesting the combination strategy could reduce CSC populations that contribute to recurrence.
Clinical • Late-breaking abstract • PARP Biomarker
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • CD133 • CASP3 (Caspase 3) • ALDH1A1 (Aldehyde Dehydrogenase 1 Family Member A1) • PROM1 (Prominin 1)
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CD133 positive • EZH2 overexpression
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Lynparza (olaparib) • cisplatin • carboplatin • GSK2816126
4ms
EZH2 Mediates Proliferation, Migration, and Invasion Promoted by Estradiol in Human Glioblastoma Cells. (PubMed, Front Endocrinol (Lausanne))
Even in the GBM cluster with high expression of ERs and those of their target genes, the expression of PCR2 target genes did not change. Overall, our data suggest that in GBM cells, pro-oncogenic actions of E2 are mediated by EZH2, without changes in EZH2 expression and by mechanisms that appear to be unrelated to the transcriptional activity of ERs.
Journal
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ER (Estrogen receptor) • EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
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EZH2 overexpression • ER expression
4ms
circSYPL1 Promotes the Proliferation and Metastasis of Hepatocellular Carcinoma via the Upregulation of EZH2 Expression by Competing with hsa-miR-506-3p. (PubMed, J Oncol)
Furthermore, circSYPL1 overexpression could upregulate EZH2 expression, while miR-506-3p mimics or EZH2 shRNAs could reverse the circSYPL1-induced malignancy of HCC cells. On a mechanistic level, circSYPL1 can interact with miR-506-3p in a competitive manner to upregulate EZH2, hence increasing the aggressiveness of tumors.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • MIR506 (MicroRNA 506)
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EZH2 overexpression
5ms
Identification and Targeting of the Developmental Blockade in Extranodal Natural Killer/T-cell Lymphoma. (PubMed, Blood Cancer Discov)
To investigate therapeutic targeting, we treated novel patient-derived xenograft (PDX) models of ENKTL with the DNA hypomethylating agent, 5-azacytidine...Disrupting this epigenetic blockade in novel PDX models led to ENKTL differentiation and improved survival. This article is highlighted in the In This Issue feature, p. 85.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
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EZH2 overexpression
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azacitidine
5ms
Clinical Value of EZH2 in Hepatocellular Carcinoma and Its Potential for Target Therapy. (PubMed, Medicina (Kaunas))
In conclusion, the overexpression of EZH2 was an independent biomarker for poor outcomes of HCC. However, more in vivo studies are required to identify the downstream target genes in HCC to improve our understanding of the biological role of EZH2 in HCC.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • AFP (Alpha-fetoprotein) • STAT3 (Signal Transducer And Activator Of Transcription 3)
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STAT3 expression • EZH2 overexpression
6ms
Evaluation of an EZH2 inhibitor in patient-derived orthotopic xenograft models of pediatric brain tumors alone and in combination with chemo- and radiation therapies. (PubMed, Lab Invest)
Therapeutic efficacy was evaluated in 4 models (1 GBM, 2 medulloblastomas and 1 ATRT) via systematically administered tazemetostat (250 and 400 mg/kg, gavaged, twice daily) alone and in combination with cisplatin (5 mg/kg, i.p., twice) and/or radiation (2 Gy/day × 5 days). Analysis of in vivo drug resistance detected predominance of EZH2-negative cells in the remnant PDOX tumors accompanied by decreased H3K27me2 and H3K27me3 expressions. These data supported the use of tazemetostat in a subset of pediatric brain tumors and suggests that EZH2-negative tumor cells may have caused therapy resistance and should be prioritized for the search of new therapeutic targets.
Preclinical • Journal • Combination therapy
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
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EZH2 overexpression
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cisplatin • Tazverik (tazemetostat)
6ms
MicroRNA-506-3p inhibits ovarian cancer metastasis by down-regulating the expression of EZH2. (PubMed, J Cancer)
The orthotopic OvCa mouse models and clinical cases also confirmed the negative correlation between miR-506-3p and EZH2 in OvCa MiR-506-3p can suppress cell migration and invasion by targeting EZH2 in OvCa. Our study provides evidence supporting miR-506-3p-based therapy in OvCa.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • MIR506 (MicroRNA 506)
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EZH2 overexpression
7ms
Elevated lncRNA-UCA1 upregulates EZH2 to promote inflammatory response in sepsis-induced pneumonia via inhibiting HOXA1. (PubMed, Carcinogenesis)
UCA1 targeted EZH2 that interacted with HOXA1. UCA1 overexpression upregulates EZH2 to repress HOXA1 expression, thus aggravating the progression of sepsis-induced pneumonia, which could be alleviated by EZH2 inhibition.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
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EZH2 overexpression
8ms
The molecular mechanisms and therapeutic potential of EZH2 in breast cancer. (PubMed, Life Sci)
In this review, we discuss biological aspects of the EZH2 molecule with a focus on its newly identified action mechanisms. We also highlight how EZH2 plays an essential role in breast cancer initiation, progression, metastasis, and invasion, which emerged as a worthy target for treating breast cancer in different approaches.
Review • Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
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EZH2 overexpression
8ms
EZH2 Expression and Response to Neoadjuvant Endocrine Therapy in Estrogen Receptor Positive Invasive Breast Cancer (USCAP 2022)
In our pilot study EZH2 protein expression levels were significantly associated with response to NET in pts with high risk (Ki67>30%) ER+ IBC ; high EZH2 expression (>130) in IDC in pretherapy core biopsies was associated with resistance to NET in these pts. During the Covid-19 Pandemic , or in other situations where surgery might be deferred, our results suggest that EZH2 might useful to predict tumor response to NET in high risk (Ki67>30%) ER+ IBC.
Clinical
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ER (Estrogen receptor) • EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
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ER positive • EZH2 overexpression
9ms
TPH1 and 5-HT Receptor Overexpression Leading to Gemcitabine-Resistance Requires Non-Canonical Permissive Action of EZH2 in Pancreatic Ductal Adenocarcinoma. (PubMed, Cancers (Basel))
EZH2 KD or GSK-126 (an EZH2 inhibitor) inhibited activities of these signaling pathways which altered nuclear level of NF-kB, Sp1, and p-STAT3, accompanied by downregulation of TPH1 and 5-HT. Furthermore, the inhibitor of EZH2, TPH1, or 5-HT effectively regressed pancreatic tumor growth in a xenografted mouse tumor model. Overall, the results revealed that long-term exposure to 5-HT upregulated EZH2, and the noncanonical action of EZH2 allowed the expression of TPH1-5-HT axis leading to gemcitabine resistance and CSC population in PDAC.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
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EZH2 overexpression
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gemcitabine • GSK2816126
9ms
Targeting EZH2 Promotes Chemosensitivity of BCL-2 Inhibitor through PIK3IP1-PI3K/AKT Axis in Acute Myeloid Leukemia (ASH 2021)
Venetoclax (Ven, ABT-199), a BCL-2 selective inhibitor has anti-tumor activity in AML but its overall response rate of monotherapy was unsatisfied owing to the clinical resistance to the inhibitor...Our results also reveal a novel mechanism that accounts for the synergistic effect of the two drugs and the fact that DZNeP may increase the chemosensitivity of BCL-2 inhibitor through PIK3IP1-PI3K/AKT axis in AML. Our findings suggest the potential combined therapy of Ven+DZNeP for AML.
PARP Biomarker • IO biomarker
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • PIK3CB (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) • CASP3 (Caspase 3) • CASP9 (Caspase 9) • PIK3C2B (Phosphatidylinositol-4-Phosphate 3-Kinase Catalytic Subunit Type 2 Beta)
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EZH2 overexpression
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Venclexta (venetoclax)
9ms
NEK2 Inhibition Enhances the Efficacy of PD-1/PD-L1 Blockade in Multiple Myeloma (ASH 2021)
Conclusion Our study showed that expression of CD274/PD-L1 is suppressed in primary HRMM and that CD274/PD-L1 expression is negatively regulated by NEK2 via EZH2-mediated methylation. Inhibition of NEK2 sensitizes myeloma cells to PD-1/PD-L1 blockade, showing either a synergistic or an additive effect in MM cell cytotoxicity.
Clinical • PD(L)-1 Biomarker • IO biomarker
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • IFNG (Interferon, gamma) • SDC1 (Syndecan 1) • NEK2 (NIMA Related Kinase 2)
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PD-L1 expression • EZH2 overexpression
9ms
Diverse Drug Combinations with an Eed Inhibitor Confer Context-Specific Benefit across Multiple Tumor Types (ASH 2021)
Combination activity is also observed with the EED inhibitor in combination with the BTK inhibitor, acalabrutinib, in DLBCL, although this appears to be context dependent...In SCLC, the EED inhibitor increased expression of SLFN11, a biomarker that has been linked to clinical response to a PARP inhibitor / temozolomide combination (Pietanza et al., 2018). Therefore, we evaluated the EED inhibitor in combination with the PARP inhibitor, olaparib, in an aggressive SCLC xenograft model and observed reduced tumor growth in the combination arm but not in monotherapy arms. In ovarian cancer, ARID1A mutations are proposed to sensitize to EZH2 and ATR inhibitors (Bitler et al., 2015, Williamson et al., 2016) which prompted evaluation of the EED inhibitor with the ATR inhibitor, AZD6738...Interestingly, we find that EEDi has significant anti-tumor activity alone, as compared with either control or CTLA4 antibody treatment alone. Together, these data show that while our EEDi has strong single-agent activity in vitro and in vivo, combining the EEDi together with inhibitors of select oncogenic pathways may bring deeper therapeutic response in a context dependent manner.
PARP Biomarker • IO biomarker
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ARID1A (AT-rich interaction domain 1A) • SLFN11 (Schlafen Family Member 11)
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ARID1A mutation • EZH2 mutation • EZH2 overexpression
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Lynparza (olaparib) • temozolomide • Calquence (acalabrutinib) • ceralasertib (AZD6738)
9ms
An EZH2 Gene Expression Signature Is Predictive of Differential Efficacy of Chemotherapy Irrespective of EZH2 Mutation Status in Patients with Follicular Lymphoma Treated within the Gallium Trial (ASH 2021)
Background : Chemotherapy combined with anti-CD20 antibodies is the current standard treatment for patients with symptomatic advanced stage follicular lymphoma (FL). Of the 129 genes from the original EZH2 GEP signature, 96 (74%) were evaluable in our transcriptome data. We used the unsupervised k-means algorithm to identify 2 GEP clusters, EZH2_mut and EZH2_WT, comprising 67 patients each ( Fig A ). Patients in the EZH2_mut cluster had significantly longer PFS with CHOP/CVP-based regimens (HR = 4.99, P = 0.002), while the EZH2 GEP signature was not predictive in patients receiving Bendamustine-based treatment ( Fig B ).
Clinical
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • GNA13 (G Protein Subunit Alpha 13) • BCL7A (BAF Chromatin Remodeling Complex Subunit BCL7A) • SOCS1 (Suppressor Of Cytokine Signaling 1) • TNFRSF14 (TNF Receptor Superfamily Member 14) • TNFRSF18 (TNF Receptor Superfamily Member 18)
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EZH2 mutation • EZH2 overexpression
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Rituxan (rituximab) • Gazyva (obinutuzumab) • bendamustine
10ms
JAM2 inhibits breast cancer invasion and migration by inhibiting the EMT process and potentially affects the immune microenvironment by increasing CXCL9/CXCL10 (SABCS 2021)
Through the combination of RNA-seq sequencing and machine learning algorithms, we predicted the chemotherapeutic drugs that might be sensitized after JAM2 overexpression and verified that JAM2 overexpression could sensitize breast cancer cells to Doxorubicin, and we found in the follow-up experiments that JAM2 overexpression could increase BAX and inhibit BCL-2 thereby leading to apoptosis of breast cancer cells. JAM2 was found to be significantly downregulated in breast cancer tissues by our study, and the area under the curve (AUC) associated with JAM2 expression in Para-cancerous tissue and breast cancer tissues was analyzed by two algorithms, logistic regression and random forest algorithm, respectively, which calculated an AUC of 0.929 and 0.887 for the TCGA cohort, indicating that JAM2 has good clinical diagnostic value. Pearson's correlation analysis revealed that the expression of JAM2 and DNMT1 (r = -0.12, P < 0.01), DNMT3B (r = -0.14, P < 0.01) and EHMT2 (r = -0.19, P < 0.01) DNA methyltransferase expression showed a significant negative correlation, and after specific inhibition of DNA methyltransferase with 5-azacytidine, there was a significant increase in JAM2 mRNA levels in the JAM2-treated group compared with the control group, suggesting that the low expression of JAM2 in breast cancer is partly regulated by DNA methylation. By analyzing the database, we found that the expression of JAM2 was significantly lower in distant recurrent tumors than in primary focal tumors.
IO biomarker
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BCL2 (B-cell CLL/lymphoma 2) • CDH1 (Cadherin 1) • CXCL10 (Chemokine (C-X-C motif) ligand 10) • CXCL9 (Chemokine (C-X-C motif) ligand 9) • DNMT1 (DNA methyltransferase 1) • VIM (Vimentin) • DNMT3B (DNA Methyltransferase 3 Beta)
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BAX expression • EZH2 overexpression • VIM expression
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doxorubicin hydrochloride • azacitidine
10ms
[VIRTUAL] EFFECTS OF EZH2 INHIBITION ON TUMOR AND TUMOR MICROENVIRONMENT IN HEPATOCELLULAR CARCINOMA (AASLD 2021)
H22 cells, a BALB/c background HCC cell line, were treated with EZH2 inhibitor UNC1999 in culture... Our results of allogenic mouse model revealed that EZH2 inhibition is associated with attenuation of tumor immunity caused by a decrease in TILs and an increase in MDSCs. These findings implicate that partnering agents which is able to reverse these alterations may be important in the treatment of HCC with EZH2 inhibitor .
CD8 (cluster of differentiation 8) • EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • CD4 (CD4 Molecule)
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EZH2 overexpression
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UNC1999
10ms
EZH2-mediated SLC7A11 upregulation via miR-125b-5p represses ferroptosis of TSCC. (PubMed, Oral Dis)
EZH2 inhibits erastin-induced ferroptosis in TSCC cells via miR-125b-5p/SLC7A11 axis.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • SLC7A11 (Solute Carrier Family 7 Member 11)
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EZH2 overexpression
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erastin
10ms
Lonicerin targets EZH2 to alleviate ulcerative colitis by autophagy-mediated NLRP3 inflammasome inactivation. (PubMed, Acta Pharm Sin B)
More importantly, in vivo studies verify that lonicerin dose-dependently disrupts the NLRP3-ASC-pro-caspase-1 complex assembly and alleviates colitis, which is compromised by administration of EZH2 overexpression plasmid. Thus, these findings together put forth the stage for further considering lonicerin as an anti-inflammatory epigenetic agent and suggesting EZH2/ATG5/NLRP3 axis may serve as a novel strategy to prevent ulcerative colitis as well as other inflammatory diseases.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • ATG5 (Autophagy Related 5)
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EZH2 mutation • EZH2 overexpression
11ms
TGF-β-MTA1-SMAD7-SMAD3-SOX4-EZH2 Signaling Axis Promotes Viability, Migration, Invasion and EMT of Hepatocellular Carcinoma Cells. (PubMed, Cancer Manag Res)
The present study provides a theoretical basis for TGF-β-MTA1-SMAD7-SMAD3-SOX4-EZH2 signaling cascade in viability, migration, invasion, and EMT of HCC cells. Inhibiting these signals may represent a therapeutic pathway for the treatment of metastatic HCC.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • CDH1 (Cadherin 1) • TGFB1 (Transforming Growth Factor Beta 1) • VIM (Vimentin) • YBX1 (Y-Box Binding Protein 1) • SMAD7 (SMAD Family Member 7) • SMAD3 (SMAD Family Member 3) • SOX4 (SRY-Box Transcription Factor 4)
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CDH1 expression • EZH2 overexpression • VIM expression
11ms
LncRNA HOXA-AS2 Promotes Oral Squamous Cell Proliferation, Migration, and Invasion via Upregulating EZH2 as an Oncogene. (PubMed, Technol Cancer Res Treat)
In summary, the findings suggested that HOXA-AS2 may inhibit cell proliferation, invasion, and migration, induce cell cycle arrest in the G0/G1 phase, and increase cell apoptosis by targeting EZH2. The research indicated that HOXA-AS2/EZH2 axis may play a key role in the development of OSCC.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
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EZH2 overexpression • EZH2 deletion • EZH2 positive
11ms
Upregulation of the ErbB family by EZH2 in hepatocellular carcinoma confers resistance to FGFR inhibitor. (PubMed, J Cancer Res Clin Oncol)
The upregulation of the ErbB family by EZH2 appears to contribute to infigratinib resistance. The combination of infigratinib and varlitinib showed a potent antitumour effect and did not result in additional toxicity, warranting further clinical investigation.
Journal
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HER-2 (Human epidermal growth factor receptor 2) • ERBB3 (V-erb-b2 avian erythroblastic leukemia viral oncogene homolog 3) • EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
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EZH2 overexpression
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Truseltiq (infigratinib) • varlitinib (ASLAN001)
11ms
The Synergistic Anti-Tumor Activity of EZH2 Inhibitor SHR2554 and HDAC Inhibitor Chidamide through ORC1 Reduction of DNA Replication Process in Diffuse Large B Cell Lymphoma. (PubMed, Cancers (Basel))
SHR2554, a potent, highly selective small molecule inhibitor of EZH2, inhibited EZH2-mutant DLBCL more significantly in vitro and in vivo. The combination of HDAC inhibitor HBI8000 with EZH2 inhibitor SHR2554 exhibited dramatic anti-tumor activity in both mutant and wild-type DLBCL, which may become a potential therapeutic modality for the treatment of DLBCL patients.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
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EZH2 mutation • EZH2 overexpression
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Epidaza (chidamide) • SHR2554
12ms
EZH2/EHMT2 Histone Methyltransferases Inhibit the Transcription of DLX5 and Promote the Transformation of Myelodysplastic Syndrome to Acute Myeloid Leukemia. (PubMed, Front Cell Dev Biol)
Levels of H3K27me3/H3K9me2 were decreased by EZH2/EHMT2 inhibitor (EPZ-6438/BIX-01294), and changes of DLX5 expression and cell proliferation were observed...Enhanced DLX5 repressed SKM-1 cell proliferation. In conclusion, EZH2/EHMT2 catalyzed H3K27me3/H3K9me2 to inhibit the transcription of DLX5, thus promoting the transformation from MDS to AML.
Journal • Epigenetic controller
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
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EZH2 overexpression
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Tazverik (tazemetostat)
1year
A proteogenomic portrait of lung squamous cell carcinoma. (PubMed, Cell)
Finally, triangulation between LSCC, LUAD, and HNSCC identified both unique and common therapeutic vulnerabilities. These observations and proteogenomics data resources may guide research into the biology and treatment of LSCC.
Journal
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FGFR1 (Fibroblast growth factor receptor 1) • CDKN2A (Cyclin-dependent kinase inhibitor 2A) • RB1 (RB Transcriptional Corepressor 1) • BIRC5 (Baculoviral IAP repeat containing 5) • SOX2 • TP63 (Tumor protein 63)
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FGFR1 amplification • CDKN2A mutation • EZH2 overexpression • SOX2 overexpression
1year
[VIRTUAL] ARID1A and EZH2 expression by Immunohistochemistry Staining of Carcinoma in Situ Specimens in Patients Treated With Bacillus Calmette-Guerin Immunotherapy (AUA 2021)
Low ARID1A expression may be associated with lower response to BCG. Optimized ARID1A IHC staining, in vitro, and in vivo studies are ongoing to better understand the functional role of ARID1A loss and its clinical implications.
Clinical • IO biomarker
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ARID1A (AT-rich interaction domain 1A) • EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
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ARID1A mutation • EZH2 overexpression
1year
EZH2 Exacerbates Breast Cancer by Methylating and Activating STAT3 Directly. (PubMed, J Cancer)
Eventually, disturbed STAT3 methylation by EZH2 in animal model showed decreased breast cancer growth. These data confirm that EZH2 exacerbates breast cancer by methylating STAT3 directly, and thus providing a promising therapeutic target for breast cancer.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • STAT3 (Signal Transducer And Activator Of Transcription 3)
|
STAT3 mutation • STAT3 expression • EZH2 overexpression
1year
Diagnostic Utility of BAP1, EZH2 and Survivin in Differentiating Pleural Epithelioid Mesothelioma and Reactive Mesothelial Hyperplasia: Immunohistochemical Study. (PubMed, Pathol Oncol Res)
Adding EZH2, Survivin and BAP1 to the diagnostic IHC panel for differentiating pleural EM and RMH could enhance diagnostic sensitivity. Moreover, Survivin is a potentially promising marker in this context, especially when combined with EZH2.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • BAP1 (BRCA1 Associated Protein 1) • BIRC5 (Baculoviral IAP repeat containing 5)
|
BIRC5 expression • EZH2 overexpression
1year
MiR-137 inhibits the proliferation, invasion and migration of glioma via targeting to regulate EZH2. (PubMed, Genes Genomics)
Our study found that miR-137 could suppress the proliferation, invasion and migration of glioma cells through regulating the expression of EZH2. So far, we have found a novel regulatory pair that influences glioma progression, providing a basis for further development of new therapeutic strategies.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
|
EZH2 overexpression
1year
CircPRDM2 Contributes to Doxorubicin Resistance of Osteosarcoma by Elevating EZH2 via Sponging miR-760. (PubMed, Cancer Manag Res)
Also, circPRDM2 silencing improved DXR sensitivity in vivo. Our study demonstrated the role of circPRDM2/miR-760/EZH2 axis in enhancing DXR resistance.
Journal
|
EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • MIR760 (MicroRNA 760)
|
EZH2 overexpression
|
doxorubicin hydrochloride
1year
Myristoylation-mediated phase separation of EZH2 compartmentalizes STAT3 to promote lung cancer growth. (PubMed, Cancer Lett)
Thus, targeting EZH2 myristoylation may have significant therapeutic efficacy in the treatment of lung cancer. Altogether, these observations not only extend the list of myristoylated proteins, but also indicate that hydrophobic lipidation may serve as a novel incentive to induce or maintain LLPS.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • STAT3 (Signal Transducer And Activator Of Transcription 3)
|
EZH2 overexpression
1year
HMGA1 induces EZH2 overexpression in human B-cell lymphomas. (PubMed, Am J Cancer Res)
Consistently, silencing of HMGA1 expression results in the downregulation of the EZH2 levels leading to a decreased proliferation and migration rate of human lymphoma cell lines. Therefore, these data identify HMGA1 as an EZH2 activator, suggesting a novel molecular mechanism contributing to EZH2 overexpression in human malignancies and a synergism of these proteins in cancer progression.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • HMGA1 (High Mobility Group AT-Hook 1) • HMGA2 (High mobility group AT-hook 2)
|
EZH2 overexpression • HMGA1 overexpression
1year
lncRNA TUG1 inhibits the cancer stem cell‑like properties of temozolomide‑resistant glioma cells by interacting with EZH2. (PubMed, Mol Med Rep)
Of note, overexpression of TUG1 inhibited the tumorigenicity of A172/TMZ cells by downregulating EZH2 expression in vivo. Collectively, the present study demonstrated that TUG1 served an essential regulatory role in TMZ resistance of gliomas.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
|
EZH2 overexpression
|
temozolomide
over1year
BLM interaction with EZH2 regulates MDM2 expression and is a poor prognostic biomarker for prostate cancer. (PubMed, Am J Cancer Res)
Our results demonstrated that the expression of P53 is affected by the binding of BLM and EZH2 to the MDM2 promoter region. This finding indicated that EZH2 regulates the expression of MDM2 at the transcriptional level by interacting with BLM.
Journal
|
TP53 (Tumor protein P53) • EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • MDM2 (E3 ubiquitin protein ligase)
|
TP53 expression • EZH2 overexpression
over1year
EZH2 inhibition activates a dsRNA-STING-interferon stress axis that potentiates response to PD-1 checkpoint blockade in prostate cancer. (PubMed, Nat Cancer)
Our study identifies EZH2 as a potent inhibitor of antitumor immunity and responsiveness to CPI. These data suggest EZH2 inhibition as a therapeutic direction to enhance prostate cancer response to PD-1 CPI.
Journal • Checkpoint inhibition
|
PD-L1 (Programmed death ligand 1) • CD8 (cluster of differentiation 8) • EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • PD-1 (Programmed cell death 1) • STING (stimulator of interferon response cGAMP interactor 1)
|
EZH2 overexpression
over1year
EZH2-Mediated microRNA-375 Upregulation Promotes Progression of Breast Cancer via the Inhibition of FOXO1 and the p53 Signaling Pathway. (PubMed, Front Genet)
This study showed that miR-375 is an important oncogene in BC. EZH2 is an upstream regulator of miR-375 through mediating the methylation of STAT3, while FOXO1 is a downstream target mRNA of miR-375 that activates the p53 signaling pathway to suppress BC development.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • STAT3 (Signal Transducer And Activator Of Transcription 3) • FOXO1 (Forkhead box O1) • MIR375 (MicroRNA 375)
|
EZH2 overexpression
over1year
Bcl-2-negative IGH-BCL2 translocation-negative follicular lymphoma of the thyroid differs genetically and epigenetically from Bcl-2-positive IGH-BCL2 translocation-positive follicular lymphoma. (PubMed, Histopathology)
Different genetic and epigenetic abnormalities might be involved in the oncogenesis of Bcl-2 /IGH-BCL2 tFLs from Bcl-2 /IGH-BCL2 tFLs and other FLs.
Journal • IO biomarker
|
BCL2 (B-cell CLL/lymphoma 2) • ARID1A (AT-rich interaction domain 1A) • KMT2D (Lysine Methyltransferase 2D) • TET2 (Tet Methylcytosine Dioxygenase 2) • KMT2C (Lysine Methyltransferase 2C) • CREBBP (CREB binding protein) • EP300 (E1A binding protein p300) • MLL2 (Myeloid/lymphoid or mixed-lineage leukemia 2) • BAX (BCL2-associated X protein)
|
KMT2D mutation • TET2 mutation • BCL2 expression • BCL2 positive • EZH2 overexpression • BCL2 translocation
over1year
Finding an easy way to harmonize: a review of advances in clinical research and combination strategies of EZH2 inhibitors. (PubMed, Clin Epigenetics)
Therefore, elucidating the underlying mechanisms of the individual constituents of the combination therapies is fundamental for their clinical application. In this review, we have summarized notable clinical trials and preclinical studies using EZH2i, their progress, and combinations of EZH2i with different therapeutic modalities, aiming to provide new insights for tumor treatment.
Clinical • Review • Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
|
EZH2 overexpression
over1year
LncRNA PART1 promotes cell proliferation and inhibits apoptosis of oral squamous cell carcinoma by blocking EZH2 degradation. (PubMed, J Biochem)
The in vivo experiment revealed that PART1 knockdown inhibited tumor growth of OSCC cells in nude mice. This study indicated that PART1 exerts a carcinogenic role in OSCC by enhancing the stability of EZH2 protein.
Journal
|
EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • FUS (FUS RNA Binding Protein)
|
EZH2 overexpression
over1year
EZH2-miRNA Positive Feedback Promotes Tumor Growth in Ovarian Cancer. (PubMed, Front Oncol)
We confirmed that a feedback loop exists between EZH2 and miRNA that maintained EZH2 overexpression, thus promoting ovarian cancer proliferation in vivo and in vitro. We further explored that EZH2 inhibited miRNA expression through PRC2, as determined by CHIP (chromatin immunoprecipitation), and EZH2 decreased the expression of p21, p53, and RUNX3. These results suggest that EZH2 inhibits the expression of Et-miRNAs (EZH2-targeting miRNAs) through the H3K27me3 pathway, thus forming an EZH2-miRNA positive feedback loop that maintains the high expression of EZH2 and promotes the malignant proliferation of cancer cells by regulating the expression of cell proliferation-related proteins.
Journal
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TP53 (Tumor protein P53) • EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • RUNX3 (RUNX Family Transcription Factor 3) • CDKN1A (Cyclin-dependent kinase inhibitor 1A)
|
TP53 expression • EZH2 overexpression • EZH2 positive
over1year
Histone Methyltransferase EZH2: A Potential Therapeutic Target for Kidney Diseases. (PubMed, Front Physiol)
The pharmacological and/or genetic inhibition of EZH2 can alleviate AKI, renal fibrosis, and LN, but potentiate podocyte injury in animal models, suggesting that the functional role of EZH2 varies with renal cell type and disease model. In this article, we summarize the role of EZH2 in the pathology of renal injury and relevant mechanisms and highlight EZH2 as a potential therapeutic target for kidney diseases.
Review • Journal
|
EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
|
EZH2 mutation • EZH2 overexpression
over1year
Overexpression of EZH2/NSD2 Histone Methyltransferase Axis Predicts Poor Prognosis and Accelerates Tumor Progression in Triple-Negative Breast Cancer. (PubMed, Front Oncol)
Bioinformatic analysis further revealed the function and pathway enrichments of co-expressed genes and interactive genes of EZH2/NSD2 axis, suggesting that EZH2/NSD2 axis was associated with cell division, mitotic nuclear division and transition of mitotic cell cycle in TNBC. Taken together, EZH2/NSD2 axis may act as a predictive marker for poor prognosis and accelerate the progression of TNBC.
Journal
|
EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • SETD2 (SET Domain Containing 2, Histone Lysine Methyltransferase)
|
EZH2 overexpression
over1year
Overexpression of SERPINA3 promotes tumor invasion and migration, epithelial-mesenchymal-transition in triple-negative breast cancer cells. (PubMed, Breast Cancer)
SERPINA3 can regulate the migration, invasion and EMT of TNBC cells and increased expression of SERPINA3 confers resistance to cisplatin in TNBC cells. We discern it is required for the regulation of BC progression and is a critical target for the clinical treatment of BC.
Journal
|
AGT (Angiotensinogen)
|
EZH2 overexpression
|
cisplatin
over1year
Clinical and Biological Features of Neuroendocrine Prostate Cancer. (PubMed, Curr Oncol Rep)
These biologic insights have provided a framework for the study of this subgroup of advanced prostate cancers and have started to provide rationale for the development of biomarker-driven therapeutic strategies. Further study of the dynamic process that leads to NEPC is required for the development of effective strategies to identify and treat patients developing lineage plasticity as a mechanism of treatment resistance.
Clinical • Review • Journal
|
TP53 (Tumor protein P53) • RB1 (RB Transcriptional Corepressor 1) • EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • FOLH1 (Folate hydrolase 1) • SOX2
|
EZH2 overexpression
over1year
Downregulation of circ-TRPS1 suppressed prostatic cancer prognoses by regulating miR-124-3p/EZH2 axis-mediated stemness. (PubMed, Am J Cancer Res)
In summary, data demonstrated that circ-TRPS1 suppressed PCa progression through functioning similar to a miR-124-3p sponge to enhance EZH2 expression and cancer stem-like cell differentiation. Thus, circ-TRPS1 might be a candidate target for PCa treatment.
Journal
|
EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
|
EZH2 overexpression
over1year
Analysis of 24 cases of epithelioid glioblastoma: Experience from a tertiary centre of North India. (PubMed, Ann Diagn Pathol)
eGB is a distinct variant of glioblastoma which has predilection towards younger age group. It shows high percentage of BRAF V600E mutation and a subset of it shows longer survival. Cases with presence of tumor infiltrating lymphocytes are associated with better outcome.
Clinical • Journal
|
BRAF (B-raf proto-oncogene) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • ATRX (ATRX Chromatin Remodeler) • SMARCB1 • VIM (Vimentin) • GFAP (Glial Fibrillary Acidic Protein)
|
BRAF V600E • BRAF V600 • EZH2 mutation • EZH2 overexpression • TILs
over1year
Long noncoding RNA ATB promotes ovarian cancer tumorigenesis by mediating histone H3 lysine 27 trimethylation through binding to EZH2. (PubMed, J Cell Mol Med)
These data revealed the oncogenic of lnc-ATB and provided a novel biomarker for OC diagnosis. Furthermore, these findings indicated the mechanism of lnc-ATB functioning in the progression of OC, which provided a new target for OC therapy.
Journal
|
EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • CDH1 (Cadherin 1)
|
EZH2 overexpression • EZH2 positive
over1year
FOXF2 aggravates the progression of non-small cell lung cancer through targeting lncRNA H19 to downregulate PTEN. (PubMed, Eur Rev Med Pharmacol Sci)
FOXF2 was upregulated in NSCLC. It accelerated the proliferative and migratory abilities of the NSCLC cells by targeting H19 to downregulate PTEN, thus aggravating the progression of NSCLC.
Journal
|
PTEN (Phosphatase and tensin homolog) • EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • H19 (H19 Imprinted Maternally Expressed Transcript)
|
EZH2 overexpression • EZH2 positive • H19 overexpression
over1year
LncRNA ANCR promotes glioma cells invasion, migration, proliferation and inhibits apoptosis via interacting with EZH2 and repressing PTEN expression. (PubMed, Cancer Gene Ther)
EZH2 interacted with ANCR in glioma cells. In conclusion, we have found that restrained ANCR could repress invasion, migration, and proliferation, as well as promote apoptosis of glioma cells through interacting with EZH2 and regulating the expression of PTEN, offering an effective therapeutic target for patients with glioma.
Journal
|
PTEN (Phosphatase and tensin homolog) • EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
|
PTEN expression • EZH2 overexpression • EZH2 positive
over1year
Tazemetostat for advanced epithelioid sarcoma: current status and future perspectives. (PubMed, Future Oncol)
Tazemetostat though represents a new treatment option for ES patients, although clinical/molecular predictors of response are still to be identified. The combination of tazemetostat with other drugs like doxorubicin and immunotherapeutic agents is currently under investigation in ES patients.
Journal
|
EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • SMARCB1
|
EZH2 mutation • EZH2 overexpression
|
doxorubicin hydrochloride • Tazverik (tazemetostat)
over1year
LINC00565 promotes the progression of colorectal cancer by upregulating EZH2. (PubMed, Oncol Lett)
Validation was performed by overexpressing EZH2, which abolished the role of silenced LINC00565 in regulating proliferative and migratory abilities in CRC. Therefore, the upregulation of LINC00565 in CRC tissues was found to stimulate the aggravation of CRC by upregulating EZH2.
Journal
|
EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
|
EZH2 overexpression • EZH2 positive
over1year
Downregulation of histone-lysine N-methyltransferase EZH2 inhibits cell viability and enhances chemosensitivity in lung cancer cells. (PubMed, Oncol Lett)
Overall, the results of the present study demonstrated that high EZH2 expression was associated with poor prognosis, accompanied with a potential impairment of migration and viability in lung cancer cells. These findings suggest that EZH2 may act as a candidate molecular target for gene therapy, and treatment with EZH2 inhibitor may be used to increase chemosensitivity to CDDP agents in lung cancer.
Journal
|
EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • KMT2C (Lysine Methyltransferase 2C)
|
EZH2 overexpression
|
cisplatin
over1year
miR-101 suppresses colon cancer cell migration through regulation of EZH2. (PubMed, Rev Esp Enferm Dig)
Our study suggests that miR-101 functions as a tumor suppressor in CRC, and miR-101 may be a potential therapeutic target for CRC treatment.
Journal
|
EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
|
EZH2 overexpression
over1year
LncRNA SNHG6 Inhibits Apoptosis by Regulating EZH2 Expression via the Sponging of MiR-101-3p in Esophageal Squamous-Cell Carcinoma. (PubMed, Onco Targets Ther)
In this study, we found that upregulation of the lncRNA SNHG6 inhibited apoptosis via miR-101-3p/EZH2 axis in ESCC. These findings may contribute to the diagnosis and treatment of ESCC.
Journal
|
BCL2 (B-cell CLL/lymphoma 2) • EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • MCL1 (Myeloid cell leukemia 1) • CASP3 (Caspase 3)
|
MCL1 expression • EZH2 overexpression
over1year
Long Non-Coding RNA SNHG1 Regulates the Wnt/β-Catenin and PI3K/AKT/mTOR Signaling Pathways via EZH2 to Affect the Proliferation, Apoptosis, and Autophagy of Prostate Cancer Cell. (PubMed, Front Oncol)
This study reveals that lncRNA-SNHG1 regulates Wnt/β-catenin and PI3K/AKT/mTOR signaling pathways via EZH2 gene to affect proliferation, apoptosis and autophagy of PCa cells. This experiment provides ideas and experimental basis for the improvement and treatment of PCa.
Journal
|
EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
|
EZH2 overexpression • EZH2 positive
over1year
EZH2 facilitates BMI1-dependent hepatocarcinogenesis through epigenetically silencing microRNA-200c. (PubMed, Oncogenesis)
Finally, combination treatment of EZH2 and BMI1 inhibitors further inhibited the viability of HCC cells compared with the cells treated with EZH2 or BMI1 inhibitor alone. Our findings demonstrated that alteration of EZH2 gene copy number status induced BMI1-mediated hepatocarcinogenesis via epigenetically silencing miR-200c, providing novel therapeutic targets for HCC treatment.
Journal
|
EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • BMI1 (BMI1 proto-oncogene, polycomb ring finger) • MIR200C (MicroRNA 200c)
|
EZH2 overexpression • EZH2 positive • miR-200-c expression
almost2years
[VIRTUAL] Super-Enhancer-Driven TOX2 Mediates Oncogenesis in Natural Killer⁄T Cell Lymphoma (ASH 2020)
New drugs, including anti-PD1 antibody pembrolizumab, have been explored...Among them, we demonstrated that TOX2 is a novel tumor driver, which promotes NKTL cell growth and enhances ability of colony formation, as well as protects cell viability under adverse condition. This study not only provides novel insight into the NKTL pathology, but also offer novel, potential therapeutic targets, such as TOX2 for the treatment of NKTL patients.
PD(L)-1 Biomarker • IO biomarker
|
EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • IL2 (Interleukin 2) • TBX21 (T-Box Transcription Factor 21) • GATA3 (GATA binding protein 3)
|
EZH2 overexpression
|
Keytruda (pembrolizumab)
almost2years
Inhibition of microRNA let-7b expression by KDM2B promotes cancer progression by targeting EZH2 in ovarian cancer. (PubMed, Cancer Sci)
In conclusion, in ovarian cancer, let-7b expression is epigenetically suppressed by high expression of KDM2B. The loss of let-7b upregulates the expression of EZH2, which promotes ovarian cancer growth in vitro and in vivo.
Journal
|
EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
|
EZH2 overexpression
almost2years
Structural assembly of Polycomb group protein and Insight of EZH2 in cancer progression: A review. (PubMed, J Cancer Res Ther)
In this review, we summarized various studies reported till date, elucidating the structure of PRC2 complex, various mechanisms involved with this, and highlighting the role of EZH2 in breast cancer and prostate cancer progression. An increased understanding of the mechanisms that underlie the pathogenesis of wide spectrum of cancers is therefore needed to develop novel therapeutic approaches for this disease and to improve the quality of life in patients.
Review • Journal
|
EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • BMI1 (BMI1 proto-oncogene, polycomb ring finger)
|
EZH2 mutation • EZH2 overexpression
almost2years
Journal
|
EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit)
|
EZH2 overexpression
almost2years
EZH2 overexpression dampens tumor-suppressive signals via an EGR1 silencer to drive breast tumorigenesis. (PubMed, Oncogene)
Deletion of the EGR1 silencer resulted in reduced cell growth, invasion, tumorigenicity of breast cancer cells, and extensive changes in gene expression, such as upregulation of GADD45, DDIT3, and RND1; and downregulation of genes encoding cholesterol biosynthesis pathway enzymes. We hypothesize that EZH2/PRC2 acts as a "brake" for EGR1 expression by targeting the EGR1 silencer, and EZH2 overexpression dampens tumor-suppressive signals mediated by EGR1 to drive breast tumorigenesis.
Journal
|
EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • GADD45A (Growth arrest and DNA-damage-inducible, alpha) • EGR1 (Early Growth Response 1)
|
EZH2 overexpression
almost2years
STAT3-Induced Upregulation of lncRNA CASC9 Promotes the Progression of Bladder Cancer by Interacting with EZH2 and Affecting the Expression of PTEN. (PubMed, Onco Targets Ther)
More significantly, CASC9 silencing-mediated inhibition of BC progression was partly reversed by EZH2 overexpression or PTEN inhibition. Upregulation of CASC9 induced by STAT3 promoted the progression of BC by interacting with EZH2 and affecting the expression of PTEN, representing a novel regulatory mechanism for BC progression.
Journal
|
PTEN (Phosphatase and tensin homolog) • EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • STAT3 (Signal Transducer And Activator Of Transcription 3)
|
PTEN expression • EZH2 overexpression • EZH2 positive
almost2years
Journal
|
EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • STAT3 (Signal Transducer And Activator Of Transcription 3) • HOTAIR (HOX Transcript Antisense RNA)
|
EZH2 overexpression • HOTAIR overexpression