Carcinogenesis, Teratogenesis & Mutagenesis ›› 2009, Vol. 21 ›› Issue (2): 93-097.doi: 10.3969/j.issn.1004-616x.2009.02.004

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Inhibition of Gastric Cancer Cells Apoptosis by Helicobacter Pylori L-form

XUAN Lan-lan1, YU Dong-hong1, CHENG Ze-nong 1, TANG Su-lan2   

  1. 1.Department of Pathology,The First Affiliated Hospital of Bengbu Medical College,Anhui Key Laboratory of Infection and Immunity, Bengbu 233003, Anhui; 2. Department of Microbiology, Bengbu Medical College, Bengbu 233003, Anhui, China
  • Received:2008-09-17 Revised:2008-11-17 Online:2009-03-30 Published:2009-03-30

Abstract: BACKGROUND AND AIM: To investigate the effects of helicobacter pylori L-form (Hp-L) on apoptosis of gastric cancer cells BGC-823 and the probable mechanisms involved. MATERIALS AND METHODS: The BGC-823 cells were co-incubated with Hp-L in different ratios (1∶20, 1∶100, 1∶500) and the followings were carried out at different time points: morphology changes of BGC-823 cells were examined by inversion microscope; the ultrastructure of cells and the apoptotic morphology by transmission electronic microscopy; the apoptotic rate by flow cytometry and immunohistochemical staining (SP method) to detect the expression of Livin, bcl-2 and p53 in BGC-823 cells. RESULTS: When BGC-823 cells were infected by Hp-L, the cells proliferated well, many tumor giant cells appeared indicating obvious inhibition of apoptosis. The number of apoptotic cells and the apoptotic rate were both reduced. The expressions of Livin, bcl-2 and p53 were all increased. All the effects were in a concentration- and time-dependent manner. CONCLUSION: Hp-L could inhibit the apoptosis of gastric cancer BGC-823 cells, its mechanisms might be related to up-regulation of Livin, bcl-2 and p53 expressions.

Key words: helicobacter pylori L-form, BGC-823, apoptosis, Livin