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- W3041383485 abstract "MORC4 has recently been characterized as a breast cancer-associated anti-apoptotic oncoprotein. In the current study, we explored its downstream regulation in luminal A/B breast tumors.Bioinformatic prediction was performed using data from The Cancer Genome Atlas (TCGA)-breast cancer (BRCA). Cellular and molecular studies were conducted using luminal A/B representative MCF-7 and BT-474 cell lines.ENST00000355610.8 (encoding MORC4a isoform) was the dominant transcript in breast cancer. ChIP-qPCR and dual-luciferase assay confirmed two STAT3-binding sites in the MID2 promoter in both MCF-7 and BT-474 cells. Co-IP confirmed an interaction between MORC4 and STAT3. ChIP-qPCR data indicated that MORC4 inhibition led to remarkably decreased enrichment of the STAT3-binding MID2 promoter segments. MORC4 overexpression significantly elevated BCL-2 expression in MCF-7 cells and increased their resistance to adriamycin (ADM), 5-fluorouracil (5-FU), and cisplatin (DDP). MID2 inhibition largely abrogated MORC4-induced drug-resistance. However, the drug-resistant phenotype was rescued by overexpressing MID2-MT that was resistant to MID2 siRNA.This study revealed a novel regulatory mechanism of MORC4 on MID2 expression via STAT3-mediated transcriptional activation. This regulatory axis might confer increased chemoresistance to breast cancer cells." @default.
- W3041383485 created "2020-07-16" @default.
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- W3041383485 date "2020-07-01" @default.
- W3041383485 modified "2023-10-16" @default.
- W3041383485 title "<p>MORC4 Promotes Chemoresistance of Luminal A/B Breast Cancer via STAT3-Mediated <em>MID2</em> Upregulation</p>" @default.
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- W3041383485 doi "https://doi.org/10.2147/ott.s260509" @default.
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