Effect of ginsenoside CK combined with cisplatin on the proliferation and migration of human cervical cancer HeLa cells via Ras/ERK/MAPK pathway

Abstract

Ginsenoside (G-CK) has good chemo preventive and anticancer effects. However, its antimetastatic effects and underlying mechanisms on cervical cancer (CC) are still not clear. This study found that both G-CK and DDP inhibited the proliferation of HeLa cells in a concentration-dependent manner, and the combination blocked cell growth and colony-forming ability, and inhibited cell migration and EMT processes. The signature molecule of EMT, E-cadherin, was up-regulated, and both N-cadherin and vimentin were down-regulated and cell migration was affected through inhibition of RAS/MEK/ERK and PI3K/AKT signaling pathways. DDP could induce oxidative stress damage in HEK293 cells, as evidenced by the accumulation of ROS, decrease in GSH levels and oxidative stress antioxidant enzymes (CAT, SOD and GSH-Px) and increase in GSSG and MDA levels, which proved that G-CK exerted inhibitory on HeLa cell proliferation and EMT in combination with traditional anti-cancer drug and protected normal cells from DDP-induced oxidative stress damage.

Keywords

• G-CK
• Antimetastatic
• EMT
• RAS/MEK/ERK
• PI3K/AKT
• Oxidative stress