吴莺, 孙海波, 艾宽宽, 李翔, 蒋晓猛, 周红. 幽门螺杆菌上调Bcl-xL基因的表达促进胃癌BGC-823细胞的增殖[J]. 中国肿瘤临床, 2012, 39(18): 1342-1345. DOI: 10.3969/j.issn.1000-8179.2012.18.003
引用本文: 吴莺, 孙海波, 艾宽宽, 李翔, 蒋晓猛, 周红. 幽门螺杆菌上调Bcl-xL基因的表达促进胃癌BGC-823细胞的增殖[J]. 中国肿瘤临床, 2012, 39(18): 1342-1345. DOI: 10.3969/j.issn.1000-8179.2012.18.003
Ying WU, Haibo SUN, Kuankuan AI, Xiang LI, Xiaomeng JIANG, Hong ZHOU. Upregulation of Bcl-xL mRNA Cellular Expression by Helicobacter pylori Leads to the Proliferation of Gastric Cancer BGC-823 Cells[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2012, 39(18): 1342-1345. DOI: 10.3969/j.issn.1000-8179.2012.18.003
Citation: Ying WU, Haibo SUN, Kuankuan AI, Xiang LI, Xiaomeng JIANG, Hong ZHOU. Upregulation of Bcl-xL mRNA Cellular Expression by Helicobacter pylori Leads to the Proliferation of Gastric Cancer BGC-823 Cells[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2012, 39(18): 1342-1345. DOI: 10.3969/j.issn.1000-8179.2012.18.003

幽门螺杆菌上调Bcl-xL基因的表达促进胃癌BGC-823细胞的增殖

Upregulation of Bcl-xL mRNA Cellular Expression by Helicobacter pylori Leads to the Proliferation of Gastric Cancer BGC-823 Cells

  • 摘要:
      目的  探讨幽门螺杆菌(H.pylori)对胃癌细胞BGC-823 Bcl-xL基因表达的影响。
      方法  分别用东、西方型H.Pylori裂解液处理胃癌细胞,MTT法检测细胞增殖情况,荧光定量PCR法检测细胞Bcl-xL基因mRNA表达水平的变化;Bcl-xL短发夹RNA(short hairpin,shRNA)质粒沉默Bcl-xL基因,MTT法检测胃癌细胞增殖能力。
      结果  H.pylori裂解液处理胃癌细胞24h后,与对照组相比,处理组均出现细胞的增殖(P均<0.01),并且东亚型处理组的增殖作用比西方型处理组更明显(P<0.01);Bcl-xL基因的mRNA表达水平也均出现上调(P均<0.01),东亚型处理组的上调水平比西方型处理组更明显(P<0.01);Bcl-xL shRNA质粒转染胃癌细胞BGC-823后,与对照组、Bcl-xL shRNA阴性对照组相比,细胞增殖受到抑制。
      结论  H.pylori的生物活性物质通过上调Bcl-xL基因的表达促进胃癌细胞BGC-823的增殖,东亚型H.pylori的生物活性作用比西方型强。Bcl-xL shRNA质粒在一定程度上可抑制胃癌细胞BGC-823的增殖。

     

    Abstract:
      Objective  This study aims to investigate the effect of Helicobacter pylori on the expression of the Bcl-xL gene and its potential effect on human gastric cancer BGC-823 cell lines.
      Methods  Human gastric cancer BGC-823 cell lines were treated with extracts from East Asian-type andWestern-type H. pylori. Cell proliferation was evaluated by MTT assay. The mRNA level of Bcl-xL was detected by real-time quantitative PCR. The Bcl-xL-mediated RNA interference technique was employed to inhibit Bcl-xL gene expression and BGC-823 cell proliferation. The mRNA level, Bcl-xL protein expression, and inhibitory percentage of BGC-823 cells were detected by RT-PCR, western blot, and MTT assay, respectively.
      Results  The proliferation of BGC-823 cells treated with H. pylori extract was observed after 24 hours (P<0.01) in relation to the control group. The enhanced cellular proliferation in the East Asian type was higher than that in the Western type (P<0.01). The expression of Bcl-xL mRNA in the groups treated with H. pylori extract was significantly elevated (all P<0.01) compared with the control group. Statistical difference in Bcl-xL mRNA expression was also found between the East Asian type group and theWestern type group (P<0.01). Bcl-xL shRNA significantly reduced Bcl-xL mRNA and protein expressions as well as BGC-823 proliferation.
      Conclusion  The biologically active elements in H. pylori extract induced the proliferation of gastric epithelial cells by upregulating the expression of Bcl-xL mRNA in human gastric cancer cells. The East Asian-type H. pylori showed stronger influence on cell proliferation and Bcl-xL mRNA expression compared with the Western type. This result implies that the East Asian-type H. pylori had much more biological activity than the Western type. Moreover, Bcl-xL shRNA inhibited Bcl-xL expression and BGC-823 cell proliferation.

     

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