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Chinese Journal of Oncology Prevention and Treatment ›› 2019, Vol. 11 ›› Issue (3): 233-238.doi: 10.3969/j.issn.1674-5671.2019.03.10

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Effect of silencing ERK5 on the biological function of gastric cancer SGC-7901 and BGC-823 cells

  

  • Online:2019-06-25 Published:2019-07-25
  • Supported by:
    国家自然科学基金项目(81120274);广西医疗卫生适宜技术开发与推广应用项目(S2017018)

Abstract: Objective To investigate the effects of extracellular signal regulated kinase 5 (ERK5) on the biological functions of gastric cancer SGC-7901 and BGC-823 cells. Methods Quantitative real-time PCR(qRT-PCR) was used to detect the expression levels of ERK5 mRNA in human gastric cancer cell lines and human gastric mucosal epithelial cell lines.The expression of ERK5 in gastric cancer cells SGC-7901 and BGC-823 was silenced by short hairpin RNA(shRNA) interference technology.After the ERK5 gene was knocked down in gastric cancer cells,cell growth and proliferation were detected by CCK-8 assay. Cell colony formation ability was detected by plate cloning assay,cell invasion and migration ability were detected by Transwell assay,cell apoptosis and cell cycle were detected by flow cytometry. Results Compared with GES-1 in gastric mucosal epithelial cells,ERK5 mRNA was highly expressed in gastric cancer cells SGC-7901,BGC-823,AGS,and HGC-27,the difference folds were 2.696±0.501,1.865±0.185,1.793±0.137 and 1.530±0.093,respectively(P<0.05). ERK5-shRNA effectively silenced the expression of ERK5 in gastric cancer cells SGC-7901 and BGC-823,and the silencing efficiency were(74.4±1.5)% and (69.1±3.9)%,respectively (P<0.05). Silencing ERK5 expression could effectively inhibit the proliferation,colony formation,migration and invasion of gastric cancer cells(P<0.05).Silencing ERK5 expression increased gastric cancer cell apoptosis rate(P<0.05),and induced cell cycle was arrested at the G0/G1 phase. Conclusions Silencing ERK5 significantly inhibit the proliferation and invasion of gastric cancer cell lines SGC-7901 and BGC-823.ERK5 may become a potential target for the treatment of gastric cancer in the future.

Key words: Gastric cancer, ERK5, Targeted therapy, SGC-7901 cell, BGC-823 cell