Conclusions
Our results support that CCDC3 promotes EOC tumorigenesis through the Wnt/β-catenin pathway and that CCDC3 may serve as a novel prognostic biomarker and therapeutic target for metastatic EOC.
Material and methods
Initially, a Kaplan-Meier plot was applied to evaluate the prognostic value of CCDC3 expression in patients with EOC. A bioinformatics analysis was next used to explore the biological function of CCDC3 in EOC. Western blot, quantitative real-time polymerase chain reaction, and in vitro invasion and migration assays were performed using SKOV3 cells and CCDC3 secreted by rat adipocytes to analyzes the impact of CCDC3 on EOC and the underlying mechanism.
Methods
Initially, a Kaplan-Meier plot was applied to evaluate the prognostic value of CCDC3 expression in patients with EOC. A bioinformatics analysis was next used to explore the biological function of CCDC3 in EOC. Western blot, quantitative real-time polymerase chain reaction, and in vitro invasion and migration assays were performed using SKOV3 cells and CCDC3 secreted by rat adipocytes to analyzes the impact of CCDC3 on EOC and the underlying mechanism.
Results
Overexpression of CCDC3 was associated with poor prognosis of EOC. CCDC3 interacted with multiple key signalling pathways, including the Wnt/β-catenin pathway. EOC cellular proliferation, migration, and invasion were promoted in vitro when co-cultured with CCDC3 enriched conditioned medium, and this tumour-promoting effect was induced by activating the Wnt/β-catenin pathway. Furthermore, the epithelial-mesenchymal transition of EOC cells was reversed after CCDC3 silencing. Conclusions: Our results support that CCDC3 promotes EOC tumorigenesis through the Wnt/β-catenin pathway and that CCDC3 may serve as a novel prognostic biomarker and therapeutic target for metastatic EOC.