新加坡国立大学的科研人员日前宣布，他们发现细菌感染与癌症之间的关系也许比目前科学界所知道的更为密切，细菌在某种程度上可能是癌症的“帮凶”。
据新加坡《联合早报》3月26日报道，新加坡国立大学药剂学系副教授俞振纲介绍说，人体内大约有150万亿个细菌，其中99%不属于病原体，也就是没有能力引发人类疾病的寄生物。在其余仅1%的细菌中，有70%到90%属于侵袭性细菌。虽然它们与人体内细菌总数相比微不足道，但却往往带给人类不小的麻烦。
俞振纲的研究团队发现，侵入人类肠道的侵袭性细菌――如沙门氏菌等，可能具有阻止癌细胞“自杀”的能力。
他解释说，人体细胞受感染或遭遇基因变异后往往会“自杀”，以求保存其他细胞正常运作。与修补细胞相比，这是比较“经济”的做法。而俞振纲的团队经研究发现，侵袭性细菌――沙门氏菌所分泌的FimA蛋白能启动人体细胞中线粒体上的“电压依赖性阴离子通道”（VDAC）与己糖激酶的复合体，从而阻止细胞“自杀”，保住细胞“性命”。细菌也得以在细胞内繁殖，导致胃肠炎等病症。如果遭到入侵的是癌细胞，FimA蛋白也可能保住癌细胞的性命，使其继续增殖，形成肿瘤。
俞振纲表示，侵袭性细菌阻止细胞“自杀”的机理在现有医学文献中极少提及，这是制药企业研制抗癌药物的潜在线索。
这项研究已经发表在最新一期美国学术期刊《分子细胞》（Molecular Cell）上。
更多阅读
《分子细胞》发表论文摘要（英文）
Molecular Cell, Volume 37, Issue 6, 768-783, 26 March 2010 | Copyright 2010 Elsevier Inc. All rights reserved. | 10.1016/j.molcel.2010.02.015
A Soluble Form of the Pilus Protein FimA Targets the VDAC-Hexokinase Complex at Mitochondria to Suppress Host Cell Apoptosis
Sunil K. Sukumaran, Nai Yang Fu, Chua Boon Tin, Kah Fei Wan, San San Lee, Victor C. YuSee
Highlights
Enteroinvasive bacteria block Bax integration and cytochrome c release in host cells
A soluble form of the pilus protein FimA is a potent suppressor of cytochrome c release
FimA targets to mitochondria through binding to VDAC1
FimA stabilizes VDAC1-hexokinase complex to inhibit apoptosis of host cells
Summary
Inhibition of apoptotic response of host cells during an early phase of infection is a strategy used by many enteroinvasive bacterial pathogens to enhance their survival. Here, we report the identification of a soluble form of the pilus protein FimA from the culture supernatants of E. coli K1, Salmonella, and Shigella that can potently inhibit Bax-mediated release of cytochrome c from isolated mitochondria. Similar to the infected cells, HCT116 cells stably expressing FimA display a delay in the integration of Bax into outer mitochondrial membrane induced by apoptotic stimuli. FimA targets to mitochondria through binding to VDAC1, which is a prerequisite step for E. coli K1 to render the short-term blockade of apoptotic death in the host cells. Interestingly, FimA strengthens the VDAC1-hexokinase interaction and prevents dissociation of hexokinase from VDAC1 triggered by apoptotic stimuli. Together, these data thus reveal a paradigm of antiapoptosis mechanism undertaken by the enteroinvasive bacteria.
