Biotechnology Bulletin ›› 2015, Vol. 31 ›› Issue (10): 242-248.doi: 10.13560/j.cnki.biotech.bull.1985.2015.10.035

• Research report • Previous Articles     Next Articles

A Study on the Regulation Mechanism of ERK1/2 Promoting Proliferation and Inhibiting Apoptosis in Esophageal Squamous Carcinoma

Liu Fengxia, Liu Wenjuan, Li Jianyong, Chen Shenguo   

  1. Department of Anatomy, College of Basic Medicine, Xinjiang University of Medical Science, Urumqi 830011
  • Received:2015-03-16 Online:2015-10-28 Published:2015-10-28

Abstract: This study aims to explore the role of ERK1/2 MAPK in the regulation mechanism of cell proliferation and apoptosis concerning of esophageal squamous carcinoma(ESCC). The results of plate colony, cell apoptosis and cycle revealed that the inhibition of ERK1/2 MAPK pathway eliminated the clone formation and proliferation of Eca109 cells, promoted cell apoptosis, and slowed down cell cycle; in addition, the inhibition of ERK1/2 MAPK pathway reversed the changes of proliferation, apoptosis and cycle induced by miR-21 overexpression. The results of qRT-PCR and Western blot showed that the inhibition of ERK1/2 MAPK pathway downregulated endogenous miR-21 expression, and also reversed the activation of ERK1/2 MAPK signal pathway induced by exogenous miR-21. The findings demonstrated that the inhibition of ERK1/2 MAPK pathway hindered Eca109 cell proliferation, promoted cell apoptosis, and retarded cell cycle via downregulation of miR-21 expression in Eca109 cell.

Key words: esophageal squamous cell carcinoma(ESCC), ERK1/2 MAPK, Eca 109 cell proliferation, cell apoptosis, miR-21