Downregulated Wnt2B Expression Suppresses Proliferation, Invasion, and Angiogenesis of Ovarian Cancer Cells Through Inhibiting the Wnt/β-Catenin Signaling Pathway

Ovarian cancer (OC) is known to be the most malignant gynecologic cancers. Wnt2B, a member of the Wnt family, plays a critical role in tumor development. However, the effect of Wnt2B on the occurrence and development of OC remains largely uncharacterized. In this study, immunohistochemistry assay indicated that Wnt2B was increased in our study cohort (OC). In addition, the expression of Wnt2B was positively correlated with TNM stages and metastasis of OC patients. Wnt2B markedly mediated the regulation of OC proliferation, invasion, and angiogenesis. Moreover, Wnt2B knockdown inactivated the Wnt/beta-catenin signaling pathway. More importantly, the Wnt/beta-catenin signaling pathway activator LiCl reversed the effect of Wnt2B knockdown on OC cell proliferation, angiogenesis, and invasion. Our data indicated that Wnt2B silencing could inhibit the proliferation, invasion, and angiogenesis of OC cells through downregulating the activity of Wnt/beta-catenin pathway.