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

Abstract

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.

Up-regulation of long non-coding RNA SNHG20 promotes ovarian cancer progression via Wnt/β-catenin signaling

“…For instance, lncRNA CASC2 regulates cell proliferation and metastasis of bladder cancer by activation of the Wnt/β-catenin signaling pathway [ 15 ], knockdown of UCA1 increases the tamoxifen sensitivity of breast cancer cells through inhibition of Wnt/β-catenin pathway [ 16 ]. Wnt/β-catenin signaling pathway regulates various biological events in ovarian cancer cells, such as gene expression, cell growth, metabolism, apoptosis, metastasis, and drug resistance [ 17 – 21 ]. To shed light on the precise mechanism underlying in SNHG20 promoted ovarian cancer cell growth, the effects of SNHG20 on Wnt/β-catenin signaling pathway were explored.…”

A systematic analysis of orphan cyclins reveals CNTD2 as a new oncogenic driver in lung cancer

“…S6a ), suggesting that CCNY might not play a role in lung cancer disease. On the other hand, the role of CCNY is clearly established in certain tumors, such as glioma 20 and ovarian cancer 21 indicating that its role in tumorigenesis might be tissue-specific. While previous reports have shown that CCNY is overexpressed in samples obtained from NSCLC patients 22 , we were unable to detect overexpression of CCNY in our samples (Fig.…”

Atypical cyclins: the extended family portrait

“…On the other hand, while additional cyclins are likely to be advantageous in a physiological context by providing additional regulatory flexibility, such diversity may actually be deleterious in a pathological context. For instance, the complexes of CCNY with either CDK14 or CDK16 have been shown to increase cell proliferation [85,100,101], suggesting that at least some atypical cyclins can use alternative CDKs to foster cell proliferation. Furthermore, atypical complexes may provide an escape route to the inhibitory actions of anticancer agents, in agreement with the observation that CCNG1 downregulation increased sensitivity to doxorubicin [102] or paclitaxel [103].…”