Cyclin Y regulates the proliferation, migration, and invasion of ovarian cancer cells via Wnt signaling pathway.

This study is designated to investigate the roles of cyclin Y (CCNY) and Wnt signaling pathway in regulating ovarian cancer (OC) cell proliferation, migration, and invasion. Quantitative real-time PCR (qRT-PCR), Western blot, MTT assay, cell scratch, and transwell test were used in our study, and transplanted tumor model was constructed on nude mice. C-Myc, cyclin D1, PFTK1, ki67, OGT, and β-catenin protein expressions in tumor tissues were detected. CCNY was significantly upregulated in OC cell lines and tissues (both P < 0.05); significant association was observed between CCNY expression and clinicopathological stage, lymph node metastasis (LNM) (P < 0.05); and the CCNY expression in stages III to IV was higher than that in stages I to II, and patients with LNM had higher CCNY expression when compared with those in patients without LNM (P < 0.05); expressions of c-Myc, cyclin D, PFTK1, ki67, and OGT were upregulated in OC tissues compared with ovarian benign tissues, suggesting that these expressions were significantly different between the two groups (P < 0.05); CCNY significantly exacerbated proliferation, migration, and invasion of A2780 cells; c-Myc and cyclin D1 protein expressions increased as the expression of CCNY increased (P < 0.001); β-catenin expressions in A2780 cells with over-expression of CCNY were significantly increased in the nucleus, but significantly decreased in the cytoplasm (both P < 0.05); high expressions of CCNY exacerbated the proliferation of A2780 cells in nude mice and significantly increased c-Myc, cyclin D1, PFTK1, ki67, and OGT protein expressions in tumor tissues which were transplanted into nude mice (P < 0.01). CCNY might exacerbate the proliferation, migration, and invasion of OC cells via activating the Wnt signaling pathway. Thus, this study provides a theoretical foundation for the development of therapeutic drugs that are able to cure OC by targeting CCNY.