promotes apoptosis and enhances chemosensitivity in breast cancer by acting as a novel transcriptional repressor targeting the signaling pathway.

Emerging evidence suggested that () was associated with immune activity and stem cell regulation in breast cancer. Whereas, the roles and molecular mechanisms of in oncogenesis remain unclear. expression was significantly diminished in breast cancer which was associated with promoter CpG methylation but not mutation. Ectopic over-expression of suppressed breast cancer cell proliferation and colony formation and promoted apoptosis , while knockdown of resulted in an opposite phenotype. Anti-proliferation effect of was verified . Bioinformatic analysis of public databases and transcriptome sequencing both showed that could enhance apoptosis through transcriptional regulation of the / pathway. ChIP and luciferase report assays demonstrated that ZNF831 could directly bind to one specific region of promoter and induce the transcriptional inhibition of . As a result, the attenuation of led to a restraint of the transcription of and thus accelerated the apoptotic progression. Augmentation of diminished the apoptosis-promoting effect of in breast cancer cell lines. Furthermore, could ameliorate the anti-proliferation effect of capecitabine and gemcitabine in breast cancer cell lines. Our findings demonstrate for the first time that is a novel transcriptional suppressor through inhibiting the expression of /2 and promoting the apoptosis process in breast cancer, suggesting as a novel biomarker and potential therapeutic target for breast cancer patients.