The regulation of ERK and p-ERK expression by cisplatin and sorafenib in gastric cancer cells

•Cisplatin and sorafenib inhibited gastric cell growth and induced apoptosis.•Inhibited MKN-45 cell proliferation and induced G0/G1 phase arrest•Cisplatin and sorafenib promoted the phosphorylation ERK.•Cisplatin and sorafenib played a synergistic antitumor effect.•Cisplatin and sorafenib play the antitumor activity by suppressing ERK pathway.

Previous studies have reported strong antitumor effects of cisplatin and sorafenib. Our results indicated that cisplatin and sorafenib exhibited anti-tumor effects on gastric cancer cells. They significantly inhibited gastric cell growth and induced apoptosis. They effectively inhibited gastric cancer cell proliferation and induced G0/G1 phase arrest. Western blotting analysis indicated that it also promoted the phosphorylation extracellular signal regulated kinase (p-ERK). Moreover, cisplatin and sorafenib played a synergistic antitumor effect. These results suggested that the antitumor mechanism of cisplatin and sorafenib involved altering the cell cycle and stimulating ERK phosphorylation in the ERK signaling pathway.