YY1-induced transcriptional activation of FAM111B contributes to the malignancy of breast cancer

Abstract Background: Family with sequence similarity 111 member B (FAM111B) is an oncoprotein associated with multiple malignancies. We investigated the potential mechanisms of FAM111B in breast cancer. Patients and Methods: We tested the expression of FAM111B in breast cancer tissues and the survival rate of breast cancer patients with high or low level of FAM111B through TCGA data. The expression of FAM111B in breast cancer tissues and adjacent tissues was detected using western blotting. Then we used siRNA to construct a low expression model of FAM111B in SKBR3 and MDA-MB-468. EdU, CCK-8, wound healing, and transwell assays were performed to monitor the proliferation, migration, and invasion of breast cancer cells. Western blotting was used to detect the expression of EMT-related indicators. Chromatin Immunoprecipitation (ChIP) and qPCR were used to evaluate the regulatory effect of Yin Yang 1 (YY1) on FAM111B. Results: The expression of FAM111B in breast cancer tissues was higher than that in normal tissues. Patients who had high FAM111B expression had a worse prognosis. Knockdown of FAM111B inhibited the proliferation, migration, and invasion of breast cancer cells. Knockdown of FAM111B resulted in increased expression of EMT-related protein E-cadherin and decreased expression of N-cadherin and Vimentin. ChIP-qPCR analysis demonstrated that YY1 could bind to the promoter of FAM111B gene and strengthen its transcription activity. Conclusion: YY1-induced transcriptional activation of FAM111B accelerated the progression of breast cancer.