Overexpression of NCAPG in ovarian cancer is associated with ovarian cancer proliferation and apoptosis via p38 MAPK signaling pathway

Abstract

Abstract Background Non-SMC condensin I complex subunit G (NCAPG), a member of the subunit of condensin complex, is significantly overexpressed in various cancers and involved in the pathogenesis of cancers. However, the roles of NCAPG in ovarian cancer remain unclear. Methods The mRNA expression, overall survival, and disease-free survival of NCAPG in ovarian cancer were analyzed by GEPIA and KM plotter database, and the expression levels of NCAPG in OC tissues and cell lines were determined by qPCR and immunohistochemistry analysis. shRNA targeting NCAPG gene (sh-NCAPG) was utilized to knock down NCAPG expression in OVCAR3 and SKOV3 cells. Subsequently, CCK-8 assay, colony formation assay, transwell invasion assay and flow cytometric analysis were performed to detect the effect of NCAPG on OC cell proliferation, apoptosis, and invasion. Finally, western blot assays were performed to detect the mechanism of NCAPG in ovarian cancer. Results Analysis using GEPIA and KM plotter database showed NCAPG was upregulated in ovarian cancer and negatively associated with the survival of OC patients. qPCR and immunohistochemistry analysis confirmed it was highly expressed in both ovarian cancer tissues and cells. The silencing of NCAPG inhibited OC cell proliferation and invasion, and induced cell apoptosis. Additionally, flow cytometric analysis revealed that NCAPG knockdown arrested the cell cycle at G2 and S phases. Furthermore, we also found that downregulation of NCAPG could suppress OC cell proliferation and invasion via activating the p38 MAPK signaling pathway. Conclusion Our results suggest that NCAPG exhibits an important role in the development and progression of ovarian cancer and implicates NCAPG as a potential therapeutic target in ovarian cancer.