期刊
MEDICAL ONCOLOGY
卷 39, 期 9, 页码 -出版社
HUMANA PRESS INC
DOI: 10.1007/s12032-022-01728-6
关键词
MORC2; beta-catenin; c-Myc; Proliferation; Migration
类别
资金
- DBT
- IISER Tirupati
The expression of MORC2 is positively correlated with beta-catenin in breast cancer, and overexpression of MORC2 increases beta-catenin and its target genes. The target gene of beta-catenin, c-Myc, regulates the MORC2-beta-catenin signaling axis through a feedback mechanism. MORC2 regulates beta-catenin expression and function by modulating AKT phosphorylation, promoting proliferation and migration of breast cancer cells.
Although Microrchidia 2 (MORC2) is overexpressed in many types of human cancer, its role in breast cancer progression remains unknown. Here, we report that the chromatin remodeler MORC2 expression positively correlates with beta-catenin expression in breast cancer cell lines and patients. Overexpression of MORC2 augmented the expression of beta-catenin and its target genes, cyclin D1 and c-Myc. Consistent with these results, we found MORC2 knockdown resulted in decreased expression of beta-catenin and its target genes. Surprisingly, we observed that c-Myc, the target gene of beta-catenin, regulated the MORC2-beta-catenin signaling axis through a feedback mechanism. We demonstrated that MORC2 regulates beta-catenin expression and function by modulating the phosphorylation of AKT. In addition, we observed reduced proliferation and migration of MORC2 overexpressing breast cancer cells upon beta-catenin inhibition. Overall, our results demonstrate that MORC2 promotes breast cancer cell proliferation and migration by regulating beta-catenin signaling.
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