β-Catenin promotes cell proliferation, migration, and invasion but induces apoptosis in renal cell carcinoma

Abstract

β-Catenin (<i>CTNNB1</i> gene coding protein) is a component of the Wnt signaling pathway that has been shown to play an important role in the formation of certain cancers. Abnormal accumulation of <i>CTNNB1</i> contributes to most cancers. This research studied the involvement of β-catenin in renal cell carcinoma (RCC) cell proliferation, apoptosis, migration, and invasion. Proliferation, cell cycle, and apoptosis were analyzed by using Cell Counting Kit-8 and by flow cytometry. Migration and invasion assays were measured by transwell analysis. Real-time polymerase chain reaction and Western blot analysis were used to detect the expression of CTNNB1, ICAM-1, VCAM-1, CXCR4, and CCL18 in RCC cell lines. It was found that <i>CTNNB1</i> knockdown inhibited cell proliferation, migration, and invasion and induced apoptosis of A-498 cells. <i>CTNNB1</i> overexpression promoted cell proliferation, migration, and invasion and inhibited apoptosis of 786-O cells. Moreover, knockdown of <i>CTNNB1</i> decreased the levels of ICAM-1, VCAM-1, CXCR4, and CCL18 expression, but <i>CTNNB1</i> overexpression increased the expression of ICAM-1, VCAM-1, CXCR4, and CCL18. Further in vivo tumor formation study in nude mice indicated that inhibition of <i>CTNNB1</i> delayed the progress of tumor formation through inhibiting PCNA and Ki67 expression. These results indicate that <i>CTNNB1</i> could act as an oncogene and may serve as a promising therapeutic strategy for RCC.