Abstract: β-Catenin (CTNNB1  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 CTNNB1  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 CTNNB1  knockdown inhibited cell proliferation, migration, and invasion and induced apoptosis of A-498 cells. CTNNB1  overexpression promoted cell proliferation, migration, and invasion and inhibited apoptosis of 786-O cells. Moreover, knockdown of CTNNB1  decreased the levels of ICAM-1, VCAM-1, CXCR4, and CCL18 expression, but CTNNB1  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 CTNNB1  delayed the progress of tumor formation through inhibiting PCNA and Ki67 expression. These results indicate that CTNNB1  could act as an oncogene and may serve as a promising therapeutic strategy for RCC.
Keywords: kidney cancer, oncogene, β-catenin, survival time, tumor migration-related protein