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幽门螺杆菌热休克蛋白 60 在胃癌发生中的潜在作用。

A potential role for Helicobacter pylori heat shock protein 60 in gastric tumorigenesis.

机构信息

Department of Biological Science and Technology, National Chiao-Tung University, Hsin-Chu, Taiwan.

出版信息

Biochem Biophys Res Commun. 2010 Feb 5;392(2):183-9. doi: 10.1016/j.bbrc.2010.01.010. Epub 2010 Jan 7.

DOI:10.1016/j.bbrc.2010.01.010
PMID:20060384
Abstract

Helicobacter pylori has been found to promote the malignant process leading to gastric cancer. Heat shock protein 60 of H. pylori (HpHSP60) was previously been identified as a potent immunogene. This study investigates the role of HpHSP60 in gastric cancer carcinogenesis. The effect of HpHSP60 on cell proliferation, anti-death activity, angiogenesis and cell migration were explored. The results showed that HpHSP60 enhanced migration by gastric cancer cells and promoted tube formation by umbilical vein endothelial cells (HUVECs); however, HpHSP60 did not increase cell proliferation nor was this protein able to rescue gastric cancer cells from death. Moreover, the results also indicated HpHSP60 had different effects on AGS gastric cancer cells or THP-1 monocytic cells in terms of their expression of pro-inflammatory cytokines, which are known to be important to cancer development. We propose that HpHSP60 may trigger the initiation of carcinogenesis by inducing pro-inflammatory cytokine release and by promoting angiogenesis and metastasis. Thus, this extracellular pathogen-derived HSP60 is potentially a vigorous virulence factor that can act as a carcinogen during gastric tumorigenesis.

摘要

幽门螺杆菌已被发现可促进导致胃癌的恶性进程。幽门螺杆菌的热休克蛋白 60(HpHSP60)先前被鉴定为一种有效的免疫基因。本研究调查了 HpHSP60 在胃癌发生中的作用。探讨了 HpHSP60 对细胞增殖、抗死亡活性、血管生成和细胞迁移的影响。结果表明,HpHSP60 增强了胃癌细胞的迁移,并促进了脐静脉内皮细胞(HUVEC)的管形成;然而,HpHSP60 并未增加细胞增殖,也不能使胃癌细胞免于死亡。此外,结果还表明,HpHSP60 对 AGS 胃癌细胞或 THP-1 单核细胞的促炎细胞因子表达有不同的影响,这些细胞因子已知对癌症的发展很重要。我们提出,HpHSP60 可能通过诱导促炎细胞因子的释放以及促进血管生成和转移来引发癌变的发生。因此,这种源自细胞外病原体的 HSP60 可能是一种强有力的毒力因子,可在胃肿瘤发生过程中充当致癌物。

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