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BIOMARKER:

RUNX3 overexpression

i
Other names: RUNX3, RUNX Family Transcription Factor 3, AML2, Runt-Related Transcription Factor 3, PEBP2A3, CBFA3, Polyomavirus Enhancer-Binding Protein 2 Alpha C Subunit, SL3/AKV Core-Binding Factor Alpha C Subunit, SL3-3 Enhancer Factor 1 Alpha C Subunit, Runt Related Transcription Factor 3, Core-Binding Factor Subunit Alpha-3, Acute Myeloid Leukemia 2 Protein, Oncogene AML-2, CBF-Alpha-3, Core-Binding Factor, Runt Domain, Alpha Subunit 3, Acute Myeloid Leukemia Gene 2, Transcription Factor AML2, PEBP2 Alpha C, PEBP2-Alpha C, PEA2 Alpha C, PEA2-Alpha C, PEBP2aC
Entrez ID:
Related biomarkers:
2years
MiR-600 mediates EZH2/RUNX3 signal axis to modulate breast cancer cell viability and sorafenib sensitivity. (PubMed, J Biochem Mol Toxicol)
EZH2 knockdown or RUNX3 overexpression could offset the effect of miR-600 inhibitor on the malignant behavior and sorafenib sensitivity of BC cells. MiR-600 can hinder the malignant behavior of BC cells and foster sensitivity of BC cells to sorafenib via EZH2/RUNX3 axis, exhibiting the miR-600/EZH2/RUNX3 axis as a feasible therapeutic target for BC patients.
Journal
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EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • RUNX3 (RUNX Family Transcription Factor 3)
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EZH2 overexpression • RUNX3 overexpression
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sorafenib
almost3years
Enforced Expression of Runx3 Improved CAR-T Cell Potency in Solid Tumor via Enhancing Resistance to Activation-induced Cell Death. (PubMed, Mol Ther)
Further studies revealed that Runx3 could bind to the TNF promoter and suppress its gene transcription after T-cell activation. In conclusion, Runx3-armored CAR-T cells showed increased antitumor activities and could be a new modality for the treatment of solid tumors.
Journal • CAR T-Cell Therapy • IO biomarker
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TNFA (Tumor Necrosis Factor-Alpha) • RUNX3 (RUNX Family Transcription Factor 3)
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RUNX3 overexpression
almost3years
Runx3-overexpression cooperates with ex vivo AKT inhibition to generate receptor-engineered T cells with better persistence, tumor-residency, and antitumor ability. (PubMed, J Immunother Cancer)
Runx3-overexpression cooperated with ex vivo AKTi to generate CAR-T cells with both tissue-resident and central memory characteristics, which equipped CAR-T cells with better persistence, cytotoxic potential, and tumor-residency ability to overcome roadblocks in the treatment of solid tumors.
Preclinical • Journal • PD(L)-1 Biomarker • IO biomarker
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CD8 (cluster of differentiation 8) • AKT1 (V-akt murine thymoma viral oncogene homolog 1) • PD-1 (Programmed cell death 1) • CD4 (CD4 Molecule) • TCF3 (Transcription Factor 3) • CA9 (Carbonic anhydrase 9) • AKT2 (V-akt murine thymoma viral oncogene homolog 2) • RUNX3 (RUNX Family Transcription Factor 3)
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RUNX3 overexpression
3years
RUNX3 improves CAR-T cell phenotype and reduces cytokine release while maintaining CAR-T function. (PubMed, Med Oncol)
In re-challenge experiments, CAR-T cells overexpressing RUNX3 (Runx3-OE CAR-T) were safer than conventional CAR-T cells, while RUNX3 could also maintain the anti-tumor efficacy of CAR-T cells in vivo. Collectively, we found that Runx3-OE CAR-T cells can improve CAR-T phenotype and reduce cytokines release while maintaining CAR-T cells function, which may improve the safety of CAR-T therapy in clinical trials.
Journal • CAR T-Cell Therapy • IO biomarker
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RUNX3 (RUNX Family Transcription Factor 3)
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RUNX3 overexpression
3years
Increased transcription of hsa_circ_0000644 upon RUNX family transcription factor 3 downregulation participates in the malignant development of bladder cancer. (PubMed, Cell Signal)
This study demonstrates that transcriptional activation of circ_644 upon RUNX3 downregulation drives the malignant development of BCa through the miR-143-3p/MSI2 axis. RUNX3 restoration or specific inhibition of circ_644 or MSI2 may help block BCa progression.
Journal
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TCF3 (Transcription Factor 3) • RUNX3 (RUNX Family Transcription Factor 3) • MIR143 (MicroRNA 143) • MSI2 (Musashi RNA Binding Protein 2)
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MSI2 overexpression • RUNX3 overexpression
3years
Antitumor activity of RUNX3: Upregulation of E-cadherin and downregulation of the epithelial-mesenchymal transition in clear-cell renal cell carcinoma. (PubMed, Open Life Sci)
In conclusion, RUNX3 overexpression increased the level of E-cadherin and inhibited the proliferation, invasion, and migration of CCRCC in vitro and in vivo. RUNX3 has potential use as a biomarker for prognostic monitoring of CCRCC and as a therapeutic target for the treatment of this cancer.
Journal
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CDH1 (Cadherin 1) • RUNX3 (RUNX Family Transcription Factor 3)
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CDH1 expression • RUNX3 overexpression
over3years
Increased expression of RUNX3 inhibits normal human myeloid development. (PubMed, Leukemia)
RNA-sequencing showed that RUNX3 overexpression downregulates key developmental genes, such as KIT and RUNX1, while upregulating lymphoid genes, such as KLRB1 and TBX21. Overall, these data show that increased RUNX3 expression observed in AML could contribute to the developmental arrest characteristic of this disease, possibly by driving a competing transcriptional program favoring a lymphoid fate.
Journal
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RUNX1 (RUNX Family Transcription Factor 1) • TBX21 (T-Box Transcription Factor 21) • RUNX3 (RUNX Family Transcription Factor 3) • KLRB1 (Killer Cell Lectin Like Receptor B1)
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RUNX3 overexpression