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

Gene. 2014 Nov 15;552(1):106-15. doi: 10.1016/j.gene.2014.09.019. Epub 2014 Sep 16.

Abstract

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.

Keywords: Apoptosis; Phosphorylation ERK; Proliferation.

MeSH terms

  • Antineoplastic Agents / pharmacology
  • Apoptosis / drug effects
  • Apoptosis / genetics
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cisplatin / pharmacology*
  • G1 Phase Cell Cycle Checkpoints / drug effects
  • G1 Phase Cell Cycle Checkpoints / genetics
  • Humans
  • MAP Kinase Signaling System / drug effects*
  • MAP Kinase Signaling System / genetics*
  • Niacinamide / analogs & derivatives*
  • Niacinamide / pharmacology
  • Phenylurea Compounds / pharmacology*
  • Phosphorylation / drug effects
  • Phosphorylation / genetics
  • Resting Phase, Cell Cycle / drug effects
  • Resting Phase, Cell Cycle / genetics
  • Sorafenib
  • Stomach Neoplasms / drug therapy*
  • Stomach Neoplasms / genetics*

Substances

  • Antineoplastic Agents
  • Phenylurea Compounds
  • Niacinamide
  • Sorafenib
  • Cisplatin