The effect of DUSP2 on proliferation and apoptosis of gastric cancer cells and its mechanism
- VernacularTitle:双特异性磷酸酶2对胃癌细胞增殖凋亡的 影响及机制研究
- Author:
Shi-wei LIU
1
Author Information
1. Department of Internal Medicine, Xianshuigu Hospital of Jinnan District, Tianjin 300350, China
- Publication Type:Journal Article
- Keywords:
dual specificity phosphatase 2;
stomach neoplasms;
extracellular signal-regulated MAP kinases (ERK);
p38 mitogen-activated protein kinases (P38)
- From:
Tianjin Medical Journal
2018;46(9):923-927
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of dual-specificity phosphatase-2 (DUSP2) on the cell proliferation
and apoptosis in the gastric cancer and its mechanisms. Methods Firstly, the effects of different expressions of DUSP2 on
the overall survival of 876 gastric cancer patients were analyzed by online analysis tool KM plotter, and the expressions of
DUSP2 in various gastric cancer cell lines (MKN-45, SGC-7901, HGC-27 and N-87) were verified. Secondly, DUSP2
overexpressed lentiviral vector was constructed, and MKN-45 was transfected by packaged virus. DUSP2-overexpression
gastric cancer cell line was gained by drug screening. Meanwhile, gastric cancer cells infected with empty vector virus were
used as control. Then the effect of DUSP2 upregulation on the proliferation ability of gastric cancer cells was evaluated by
MTS cell proliferation assay, and the apoptosis was determined by Annexin V-FITC / PI double staining. The protein
expressions of DUSP2, ERK, p-ERK (Thr202/Tyr204), P38 and p-P38 were tested by the Western blot analysis. Results
Gastric cancer patients with high DUSP2 expression showed a significant survival advantage compared with those with low
DUSP2 expression, and DUSP2 levels were decreased in several gastric cancer cell lines. The Western blot analysis revealed
that the expression of DUSP2 markedly increased in overexpressed DUSP2 group (experimental group) compared with that of
control group. The MTS experiment showed that the cell viability was significantly decreased in experimental group than that of the control group. Correspondingly, the cell apoptosis test showed that the cell apoptosis rate was obviously higher in the
experimental group than that of the control group. The results of Western blot assay indicated that p-ERK (Thr202/Tyr204)
and p-38 were significantly down-regulated in the experimental group compared with those of control group. Conclusion
The over-expression of DUSP2 can efficiently inhibit cell proliferation and promote its apoptosis in gastric cancer cells, and
the mechanism is related to DUSP2 inhibiting the phosphorylation levels of ERK and P38.
