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CagA promotes proliferation and inhibits apoptosis of GES-1 cells by upregulating TRAF1/4-1BB

  • Authors:
    • Fen Wang
    • Nanfang Qu
    • Jin Peng
    • Chun Yue
    • Lingzhi Yuan
    • Yi Yuan
  • View Affiliations / Copyright

    Affiliations: Department of Gastroenterology, The Third Xiangya Hospital, Central South University, Changsha, Hunan 410013, P.R. China, Department of Gastroenterology, The Affiliated Hospital of Guilin Medical College, Guilin, Guangxi 541001, P.R. China, Department of Neurology, The Third Xiangya Hospital, Central South University, Changsha, Hunan 410013, P.R. China
    Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1262-1268
    |
    Published online on: June 12, 2017
       https://doi.org/10.3892/mmr.2017.6757
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Abstract

Cytotoxin-associated gene A (CagA) is one of the most important virulence factors of Helicobacter pylori, and serves a role in H. pylori‑mediated tumorigenesis in gastric cancer. However, the underlying molecular mechanism remains to be elucidated. The present study aimed to investigate the effects of CagA on the proliferation and apoptosis of GES‑1 cells, and the underlying mechanism. A CagA eukaryotic expression plasmid was constructed and transfected into GES‑1 cells. The mRNA and protein levels of CagA, tumor necrosis factor receptor‑associated factor 1 (TRAF1) and tumor necrosis factor receptor superfamily member 9 (4‑1BB) were determined using the reverse transcription‑quantitative polymerase chain reaction and western blot analysis, respectively. Western blot and ELISA analysis was used to detect the release of interleukin (IL)‑8. An MTT assay and flow cytometric analysis was used to assess cell viability and apoptosis, respectively. Ectopic expression of CagA markedly increased TRAF1 and 4‑1BB mRNA and protein levels in GES‑1 cells. CagA increased the expression and release of IL‑8 in GES‑1 cells. The expression of CagA significantly promoted the proliferation (P<0.05) and inhibited the apoptosis (P<0.05) of GES‑1 cells. In conclusion, CagA upregulated TRAF1/4‑1BB, thereby promoting the proliferation and inhibiting the apoptosis of GES-1 cells.
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Copy and paste a formatted citation
Spandidos Publications style
Wang F, Qu N, Peng J, Yue C, Yuan L and Yuan Y: CagA promotes proliferation and inhibits apoptosis of GES-1 cells by upregulating TRAF1/4-1BB. Mol Med Rep 16: 1262-1268, 2017.
APA
Wang, F., Qu, N., Peng, J., Yue, C., Yuan, L., & Yuan, Y. (2017). CagA promotes proliferation and inhibits apoptosis of GES-1 cells by upregulating TRAF1/4-1BB. Molecular Medicine Reports, 16, 1262-1268. https://doi.org/10.3892/mmr.2017.6757
MLA
Wang, F., Qu, N., Peng, J., Yue, C., Yuan, L., Yuan, Y."CagA promotes proliferation and inhibits apoptosis of GES-1 cells by upregulating TRAF1/4-1BB". Molecular Medicine Reports 16.2 (2017): 1262-1268.
Chicago
Wang, F., Qu, N., Peng, J., Yue, C., Yuan, L., Yuan, Y."CagA promotes proliferation and inhibits apoptosis of GES-1 cells by upregulating TRAF1/4-1BB". Molecular Medicine Reports 16, no. 2 (2017): 1262-1268. https://doi.org/10.3892/mmr.2017.6757
Copy and paste a formatted citation
x
Spandidos Publications style
Wang F, Qu N, Peng J, Yue C, Yuan L and Yuan Y: CagA promotes proliferation and inhibits apoptosis of GES-1 cells by upregulating TRAF1/4-1BB. Mol Med Rep 16: 1262-1268, 2017.
APA
Wang, F., Qu, N., Peng, J., Yue, C., Yuan, L., & Yuan, Y. (2017). CagA promotes proliferation and inhibits apoptosis of GES-1 cells by upregulating TRAF1/4-1BB. Molecular Medicine Reports, 16, 1262-1268. https://doi.org/10.3892/mmr.2017.6757
MLA
Wang, F., Qu, N., Peng, J., Yue, C., Yuan, L., Yuan, Y."CagA promotes proliferation and inhibits apoptosis of GES-1 cells by upregulating TRAF1/4-1BB". Molecular Medicine Reports 16.2 (2017): 1262-1268.
Chicago
Wang, F., Qu, N., Peng, J., Yue, C., Yuan, L., Yuan, Y."CagA promotes proliferation and inhibits apoptosis of GES-1 cells by upregulating TRAF1/4-1BB". Molecular Medicine Reports 16, no. 2 (2017): 1262-1268. https://doi.org/10.3892/mmr.2017.6757
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