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GENE:

MYBL2 (MYB Proto-Oncogene Like 2)

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Other names: MYBL2, MYB Proto-Oncogene Like 2, V-Myb Avian Myeloblastosis Viral Oncogene Homolog-Like 2, Myb-Related Protein B, Myb-Like Protein 2, BMYB, V-Myb Myeloblastosis Viral Oncogene Homolog-Like 2, B-MYB, B-Myb
11d
SUMOylation of UBE2C facilitates hepatocellular carcinoma proliferation and invasion via the MAPK pathway. (PubMed, Transl Cancer Res)
Rescue experiments were performed with the MAPK inhibitor trametinib...We reveal a novel oncogenic axis in which MYBL2 and SUMOylation cooperatively increase UBE2C expression and stability, promoting HCC progression via MAPK pathway activation. Targeting the MYBL2/UBE2C/MAPK axis represents a potential therapeutic strategy for treating HCC.
Journal
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PLCG2 (Phospholipase C Gamma 2) • MYBL2 (MYB Proto-Oncogene Like 2) • PRKCB (Protein Kinase C Beta) • UBE2C (Ubiquitin Conjugating Enzyme E2 C) • UBE2I (Ubiquitin Conjugating Enzyme E2 I)
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Mekinist (trametinib)
12d
Exploratory transcriptomics and in vivo analyses of suramin in tongue squamous cell carcinoma. (PubMed, Biomed Rep)
Effect size estimates were relatively large for both the group effect (partial η2=0.20) and the time x group interaction (partial η2=0.24), suggesting that the study may have been underpowered to detect this difference statistically. In conclusion, the present exploratory study suggests that suramin exerts a dual antitumor effect on tongue squamous cell carcinoma by suppressing proliferative transcriptional programs, and modulating extracellular and stress response pathways, providing a basis for future studies to further elucidate its therapeutic relevance.
Preclinical • Journal
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AURKA (Aurora kinase A) • FOXM1 (Forkhead Box M1) • CDC20 (Cell Division Cycle 20) • MYBL2 (MYB Proto-Oncogene Like 2) • TNFSF10 (TNF Superfamily Member 10) • TXNIP (Thioredoxin Interacting Protein) • CCNB1 (Cyclin B1) • TIMP3 (TIMP Metallopeptidase Inhibitor 3)
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Germanin (suramin)
16d
SPP1+ Macrophage-POSTN+ Fibroblast-Endothelial Triad Dictates Immunotherapy Response in Bladder Cancer. (PubMed, FASEB J)
Our study reveals a triad cellular structure mediated by SPP1+ TAMs, POSTN+ CAFs, and endothelial cells that contribute to immunotherapy resistance in BCa. Targeting this structure, particularly through SPP1 blockade, represents a promising strategy to augment the efficacy of immune checkpoint inhibitors.
Journal • PD(L)-1 Biomarker • IO biomarker
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SPP1 (Secreted Phosphoprotein 1) • MYBL2 (MYB Proto-Oncogene Like 2) • POSTN (Periostin)
19d
Extrachromosomal DNA drives molecular and clinical heterogeneity in hepatocellular carcinoma: a multi-omics analysis and prognostic model development. (PubMed, Hum Genomics)
Our study characterizes the molecular and clinical distinctions between ecDNA-negative and ecDNA-positive HCC and establishes a clinically applicable gene signature for patient prognosis. These findings advance our understanding of ecDNA-driven tumor heterogeneity and provide potential strategies for personalized HCC management.
Journal
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TP53 (Tumor protein P53) • BMP6 (Bone Morphogenetic Protein 6) • MYBL2 (MYB Proto-Oncogene Like 2) • DNASE1L3 (Deoxyribonuclease 1 Like 3)
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TP53 mutation
24d
Exploring the mechanism and therapeutic potential of BUB1 in regulating esophageal cancer progression based on 5-FU target prediction. (PubMed, Discov Oncol)
This study revealed the important role of BUB1, one of the potential targets of 5-FU, in the development of esophageal cancer. Through bioinformatics analysis and experimental validation, we found that the high expression of BUB1 in esophageal cancer tissues was closely related to the biological properties of the tumor. the regulation of cell cycle by BUB1 and its role in the invasion and migration ability of the cells marked its potential as a new target for the treatment of esophageal cancer.
Journal
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CCNA2 (Cyclin A2) • CDK1 (Cyclin-dependent kinase 1) • MYBL2 (MYB Proto-Oncogene Like 2) • BUB1 (BUB1 Mitotic Checkpoint Serine/Threonine Kinase)
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5-fluorouracil
27d
Alterations in the transcriptional profile of genes in tumors as a prerequisite for personalization of treatment in breast cancer patients (PubMed, Arkh Patol)
Comparative mRNA expression analysis confirms that a short preoperative course of aromatase inhibitors induces a more potent and uniform molecular response, characterized by profound suppression of proliferation and complete inhibition of estrogen-dependent signaling. Tamoxifen therapy is also effective but results in less pronounced suppression of key targets and, crucially, may be accompanied by early activation of the MYC oncogene, a potential marker for resistance development.
Journal • PD(L)-1 Biomarker • IO biomarker
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EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • PD-L1 (Programmed death ligand 1) • ER (Estrogen receptor) • PGR (Progesterone receptor) • PTEN (Phosphatase and tensin homolog) • BCL2 (B-cell CLL/lymphoma 2) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • CCND1 (Cyclin D1) • CCNE1 (Cyclin E1) • FGFR4 (Fibroblast growth factor receptor 4) • BIRC5 (Baculoviral IAP repeat containing 5) • TYMS (Thymidylate Synthetase) • AURKA (Aurora kinase A) • FOXA1 (Forkhead Box A1) • PPP2R2A (Protein Phosphatase 2, Regulatory Subunit B, Alpha) • PTTG1 (PTTG1 Regulator Of Sister Chromatid Separation, Securin) • BAG1 (BAG Cochaperone 1) • EMSY (EMSY Transcriptional Repressor BRCA2 Interacting) • GATA3 (GATA binding protein 3) • KRT5 (Keratin 5) • MMP11 (Matrix Metallopeptidase 11) • MYBL2 (MYB Proto-Oncogene Like 2) • SFRP1 (Secreted frizzled related protein 1) • TMEM45B (Transmembrane Protein 45B) • ANLN (Anillin Actin Binding Protein) • CCNB1 (Cyclin B1) • SCGB2A2 (Secretoglobin Family 2A Member 2) • ZNF703 (Zinc Finger Protein 703)
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HER-2 negative • HER-2 expression
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tamoxifen • letrozole • anastrozole
1m
Regulation of INSM1 Gene Expression and Neuroendocrine Differentiation in High-Risk Neuroblastoma. (PubMed, Biology (Basel))
INSM1 overexpression in SH-SY-5Y cells upregulated neuroendocrine and thyroid hormone-related genes (CHGA, CHGB, DDC, NCAM1, DIO3, TH), while suppressing genes involved in cell cycle (RRM, CDC25A), methionine metabolism (AHCY, MAT2A), transcriptional regulation (MYBL2, EZH2), and oncogenic signaling (ALK, LINC011667). These findings suggest that INSM1 promotes NB aggressiveness by sustaining a neuroendocrine progenitor-like phenotype through metabolic-epigenetic coupling.
Journal
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ALK (Anaplastic lymphoma kinase) • MYCN (MYCN Proto-Oncogene BHLH Transcription Factor) • NCAM1 (Neural cell adhesion molecule 1) • MYBL2 (MYB Proto-Oncogene Like 2) • CDC25A (Cell Division Cycle 25A) • CHGA (Chromogranin A) • GNRP (Ras-Specific Guanine Nucleotide-Releasing Factor 1) • INSM1 (INSM Transcriptional Repressor 1) • MAT2A (Methionine Adenosyltransferase 2A)
2ms
Upregulation of MYBL2 ameliorates senescence of nucleus pulposus cells in degenerative intervertebral discs based on RNA-sequencing analysis. (PubMed, J Mol Histol)
Knockdown of MYBL2 promoted the senescence of control-NPCs, and overexpression of MYBL2 inhibited the senescence of IDD-NPCs. The study found that upregulation of MYBL2 ameliorated the senescence of IDD-NPCs, providing a potential way to inhibit the senescence of NPCs.
Journal
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CAV1 (Caveolin 1) • MYBL2 (MYB Proto-Oncogene Like 2) • CCNB1 (Cyclin B1)
2ms
Maternal undernutrition inhibits fetal rumen development: novel miRNA-736-mediated dual targeting of E2F2 and MYBL2 in sheep. (PubMed, J Anim Sci Biotechnol)
In summary, maternal undernutrition disrupted male fetal rumen metabolism and elevated novel miR-736, which targeted and downregulated E2F2 and MYBL2 to inhibit cell cycle progression and promote apoptosis, finally inhibited male fetal rumen development. This study provides new insights into the epigenetic mechanisms underlying maternal undernutrition-induced male fetal rumen developmental deficits.
Journal
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JAK3 (Janus Kinase 3) • MYBL2 (MYB Proto-Oncogene Like 2) • E2F2 (E2F Transcription Factor 2)
2ms
FBXW7 Inhibited M2 Macrophage Polarization in Endometrial Cancer by Reducing CCL2 Secretion Through Ubiquitination of MYBL2 Subtitle: The Role of FBXW7 on M2 Macrophage Polarization in EC. (PubMed, Biochem Genet)
In vivo functional assays demonstrated that FBXW7 overexpression significantly suppressed EC xenograft growth and enhanced tumor cell apoptosis. FBXW7 enhanced the ubiquitination and degradation of MYBL2 to reduce CCL2 secretion from EC, which inhibited macrophage polarization to the M2 type.
Journal
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FBXW7 (F-Box And WD Repeat Domain Containing 7) • CD163 (CD163 Molecule) • IL10 (Interleukin 10) • CCL2 (Chemokine (C-C motif) ligand 2) • MRC1 (Mannose Receptor C-Type 1) • MYBL2 (MYB Proto-Oncogene Like 2)