GINS2 regulates cell proliferation and apoptosis in human epithelial ovarian cancer.

Go-Ichi-Ni-San 2 (GINS2), also known as partner of Sld five 2, is involved in the initiation of DNA replication and cell cycle progression. GINS2 is abundantly expressed in a number of malignant solid tumors, including breast cancer, melanoma and hepatic carcinoma. However, the functions of GINS2 in epithelial ovarian cancer (EOC) remain unclear. The aim of the present study was to investigate these functions. GINS2 expression was detected in EOC and normal ovarian tissues using immunohistochemistry. To investigate the functions of GINS2 in EOC, GINS2 expression was stably knocked down in SKOV-3 cells using lentiviral short hairpin RNA (shRNA). The expression of GINS2 mRNA and protein in SKOV-3 cells was examined using reverse-transcription quantitative polymerase chain reaction (RT-qPCR) and western blot analyses, respectively. Cell proliferation was determined using high-content screening and MTT assays. Cell cycle progression and apoptosis were detected using flow cytometry. Compared with normal ovarian tissues, EOC tissues expressed increased levels of GINS2 expression (16.7 vs. 58.3%). Increased expression of GINS2 mRNA was also observed in SKOV-3 and OVCAR3 cells. In the investigation of GINS2 functions in EOC, GINS2 expression at the mRNA and protein levels was significantly inhibited by specific GINS2 shRNA. GINS2 knockdown significantly inhibited the proliferation and viability of SKOV-3 cells and induced cell cycle arrest in S phase. Furthermore, GINS2 knockdown in SKOV-3 cells significantly increased cell apoptosis. GINS2 is markedly expressed in EOC tissues and cell lines. Stable GINS2 knockdown in SKOV-3 cells significantly inhibited cell proliferation and induced cell cycle arrest and cell apoptosis. Therefore, GINS2 may be involved in EOC progression.