Abstract
Background: Ovarian cancer (OC) is a common clinical gynecological disease, which seriously threatens women's health and life. We investigated the roles of SPOCK2 in OC and its associated molecular mechanism in the current study. Methods: The expressions and prognostic value of SPOCK2 in OC were identified using the clinical data and data from the GEPIA database. Then, SPOCK2 silence was implemented to search functions of SPOCK2 in OC cells. CCK-8 was used to examine cell proliferation. Cell apoptosis was detected by flow cytometry. The OC cell invasion and migration were evaluated by transwell assays. Results: Overexpressed SPOCK2 was identified in OC, which was correlated with poor prognosis and a shorter survival rate. SPOCK2 downregulation significantly suppressed OC cell proliferation, migration, and invasion, and cell apoptosis was markedly promoted by SPOCK2 silence. Meanwhile, SPOCK2 knockdown could effectively suppress Wnt/β-catenin. Conclusion: SPOCK2 exerted crucial functions in OC progression and could serve as a promising candidate for OC targeted therapy.