Sodium selenite inhibits the proliferate of cervical cancer cells through PI3K/AKT pathway

Selenium can inhibit cervical cancers, but the specific mechanism of anti-cervical cancer is not fully understood. In this study, we investigated the effect of sodium selenite (SS) on cervical cancer cell lines HeLa and SiHa and examined the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway to reveal the mechanism of SS against cervical cancer. We detected cell viability by MTT [3-(4, 5dimethylthiazol-2-yl)-2, 5- diphenyltetrazolium bromide] assay, and apoptosis by Annexin V-FITC/PI staining. The levels of PI3K, AKT, phosphorylated PI3K (p-PI3K), and phosphorylated Akt (p-AKT) were measured by Western Blot. The results showed that SS reduced the viability and increased apoptosis of HeLa and SiHa cells and suppressed the activation of the PI3K/AKT signaling pathway in a dose-dependent manner. To verify the role of PI3K/AKT signaling pathway in this, we treated HeLa and SiHa cells with LY294002 (LY, a specific PI3K inhibitor) and established control, LY-treated, SS-treated, and combined LY + SS-treated groups. The results showed that the combined LY + SS treatment group enhanced the inhibitory effect of SS on the PI3K/AKT signaling pathway, which further inhibiting cervical cancer cell viability and increasing apoptosis. In conclusion, SS exerted its anti-cervical cancer effects by inhibiting cell proliferation, promoting apoptosis, and inhibiting PI3K/AKT signaling pathway.