RTKN2 knockdown alleviates the malignancy of breast cancer cells by regulating the Wnt/β-catenin pathway

Abstract

Abstract RTKN2 is a new effector protein of Rho GTPase, and has been indicated to be a tumor inhibitor in colon cancer. In this article, we explored the function of RTKN2 in BC cell development. RTKN2 expression in BC tissues and BC cell lines was evaluated by RT-qPCR and Western blot assay. CCK-8, Wound-healing and Transwell assays were carried out to examine the role of RTKN2 knockdown on proliferation, the migratory ability and the invasive ability of BC cells. FCM and Western blot assay were performed to measure the function of RTKN2 silencing on BC cell apoptosis. In addition, the regulatory effect of RTKN2 on Wnt/β-catenin pathway was studied via Western blot assay. RTKN2 expression was elevated in BC tissues and BC cells. Down-regulation of RTKN2 restrained BC cell progression by suppressing cell proliferation, migratory ability, invasive ability, and inducing apoptosis. In addition, reduced of RTKN2 sharply reduced the expressing levels of Wnt3A, β-catenin, C-Myc, and Cyclin D1, suggesting that RTKN2 silencing blocked the motivation of Wnt/β-catenin pathway in BC development. The in vivo experiment also confirmed the inhibitory effect of RTKN2 on BC tumors. Our study confirmed that RTKN2 was highly expressed in BC. Moreover, RTKN2 knockdown suppressed the development of BC through affecting the Wnt/β-catenin pathway. Hence, we deduced that RTKN2 was a possible treatment target for BC.