β-inducible gene-h3 promotes human breast carcinoma cell metastasis by activating the phosphatidylinositol 3-kinase/protein kinase B signaling pathway

Metastatic breast cancer is one of the most common metastatic tumors. Although studies have validated the role of beta-inducible gene-h3 (beta ig-h3) in human biology and disease, the detailed mechanisms mediated by beta ig-h3 in breast carcinoma metastasis remain unclear. Thus, the present study investigated the role and potential mechanism of beta ig-h3 during breast carcinoma cell metastasis. The results indicated that the upregulation of beta ig-h3 significantly promotes the growth and inhibits the cisplatin-induced apoptosis of breast carcinoma cells. It was also demonstrated that beta ig-h3 promoted the migration and invasion of human breast carcinoma cells in vitro and in vivo. Furthermore, the results demonstrated that beta ig-h3 upregulated the overall expression and phosphorylation of phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt) in human breast carcinoma cells. By contrast, beta ig-h3 knockdown reversed the beta ig-h3-mediated characteristics of breast carcinoma cells. Thus, the current study demonstrated that the PI3K/Akt signaling pathway serves a role in beta ig-h3-induced human breast cancer cell metastasis and that beta ig-h3 transfection enhances the metastatic potential of human breast carcinoma cells via the PI3K/Akt signaling pathway. These observations contribute to the understanding of the potential mechanism of human breast carcinoma cell growth and metastasis and suggest that beta ig-h3 may be a promising therapeutic target for the treatment of human breast carcinoma.