Ginsenoside Rg3 enhances the radiosensitivity of lung cancer A549 and H1299 cells via the PI3K/AKT signaling pathway.

Abstract

Lung cancer is one of the most common cancers and the leading cause of cancer-related deaths in the world. Radiation is widely used for the treatment of lung cancer. However, radioresistance and toxicity limit its effectiveness. Ginsenoside Rg3 (Rg3) is a positive monomer extracted from ginseng and has been shown to the anti-cancer ability on many tumors. The aim of the present study was to ascertain whether Rg3 is able to enhance the radiosensitivity of lung cancer cells and investigate the underlying mechanisms. The effect of Rg3 on cell proliferation was examined by Cell Counting Kit-8 (CCK-8) and radiosensitivity was measured by colony formation assay. Flow cytometry, transwell, and wound healing assay were used to determine apoptosis, cell cycle, and metastasis. Western blot was used to detect the main protein levels of the PI3K/AKT signaling pathway. We found that Rg3 inhibited cell proliferation, promoted apoptosis, and suppressed migration and invasion in radio-induced lung cancer cells. In addition, Rg3 increased the proportion of G2/M phase cells and inhibited the formation of cell colonies. Moreover, Rg3 decreased the expression levels of PI3K, p-AKT, and PDK1 in radio-induced cells. These findings indicate that Rg3 may be able to enhance the radiosensitivity in lung cancer cells by the PI3K/AKT signaling pathway. These results demonstrate the therapeutic potential of Rg3 as a radiosensitizer for lung cancer.