Abstract
Previous studies have demonstrated that calpain small subunit 4 (Capn4) is able to regulate the viability and metastasis of cancer cells. However, the regulatory effects and underlying molecular mechanism of Capn4 in ovarian carcinoma cells are not well understood. The purpose of the present study was to investigate the role of Capn4 in ovarian carcinoma cells and analyze the possible mechanism mediated by Capn4. The expression levels of Capn4 and osteopontin (OPN) were determined and the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway was analyzed in ovarian carcinoma cells. The results of the present study revealed that Capn4 and OPN were overexpressed in clinical ovarian carcinoma tissues and ovarian carcinoma cells. Capn4 silencing downregulated OPN expression, and suppressed ovarian carcinoma cell viability and migration. Capn4 silencing enhanced apoptosis of ovarian carcinoma cells by increasing activity of the capase-3 apoptosis signaling pathway. Capn4 promoted the metastasis of ovarian carcinoma cells by interacting with the PI3K/AKT signaling pathway via upregulation of OPN expression. In conclusion, the results of the present study indicate that Capn4 may be a potential therapeutic target for the treatment of ovarian carcinoma.