Effect of ginsenoside CK combined with cisplatin on the proliferation and migration of human cervical cancer HeLa cells via Ras/ERK/MAPK pathway. (March 2023)

• Record Type: Journal Article
• Authors: Li, Xiao-Li; Yin, Qi; Wang, Wei; Ma, Run-Hui; Ni, Zhi-Jing; Thakur, Kiran; Zhang, Jian-Guo; Wei, Zhao-Jun
• Is Part Of: Journal of functional foods. Volume 102(2023)
• Publication Date: 2023-03
• Subjects: G-CK -- Antimetastatic -- EMT -- RAS/MEK/ERK -- PI3K/AKT -- Oxidative stress; CAT catalase -- CC cervical cancer -- CTX cyclophosphamide -- DDP cisplatin -- DMSO dimethyl sulfoxide -- EMT epithelial-mesenchymal transition -- FBS fetal bovine serum -- G-CK Ginsenoside CK -- GSH glutathione -- GSSG oxidized glutathione disulfide -- MDA malondialdehyde -- MTT 3-(4, 5-Dimethyl-2-Thiazolyl)-2, 5-Diphenyl Tetrazolium Bromide -- MTX methotrexate -- PBS phosphate buffer saline -- PC3 prostate cancer cell -- PS penicillin/streptomycin -- PTX paclitaxel -- ROS reactive oxygen species -- SOD Super Oxide Dismutase; Functional foods -- Analysis -- Periodicals; Food -- Biotechnology -- Periodicals; Nutrition -- Periodicals; 613.2
• DOI: 10.1016/j.jff.2023.105438
• Languages: English
• ISSNs: 1756-4646

Abstract

Graphical abstract: Highlights: G-CK and DDP inhibited the of HeLa cells proliferation in a concentration-dependent manner. Combination of both inhibited cell migration and epithelial-mesenchymal transition processes. G-CK combined with DDP inhibited cell migration via RAS/MEK/ERK and PI3K/AKT signaling pathways. G-CK treatment significantly reduced DDP-induced massive ROS production. G-CK attenuates DDP-induced oxidative stress damage by enhancing antioxidant enzymes. 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.