PNAS:癌症又一重大突破:支原体感染通过影响表观遗传促进癌症发生发展!

2018-12-07 佚名 转化医学网

抗生素的应用和发现使人类的平均寿命延长了15年。但细菌进化的速度却超出了人类的预想,这种“意外之外”不仅导致了超级细菌的出现,而且近年来,越来越多的研究将癌症与细菌感染联系在了一起。国际癌症研究中心曾指出,世界上约1/6癌症的罪魁祸首是细菌和病毒。在炎症见怪不怪的时代,这种统计学数据听起来简直让人“毛骨悚然”!那么,细菌感染与癌症之间的关系为什么如此“缠绵悱恻”呢?

抗生素的应用和发现使人类的平均寿命延长了15年。但细菌进化的速度却超出了人类的预想,这种“意外之外”不仅导致了超级细菌的出现,而且近年来,越来越多的研究将癌症与细菌感染联系在了一起。国际癌症研究中心曾指出,世界上约1/6癌症的罪魁祸首是细菌和病毒。在炎症见怪不怪的时代,这种统计学数据听起来简直让人“毛骨悚然”!那么,细菌感染与癌症之间的关系为什么如此“缠绵悱恻”呢?

马里兰大学医学院人类病毒学研究所给我们以答疑解惑:细菌支原体的蛋白质DnaK会干扰感染支原体的细胞对已知癌症来源的DNA损伤的反应和修复能力,该研究以“Mycoplasma promotes malignant transformation in vivo, and its DnaK, a bacterial chaperon protein, has broad oncogenic properties”为题发表在顶级医学期刊《PNAS》杂志上。

科学家们早就证明了癌与幽门螺旋杆菌感染的相关性。支原体感染(如HIV)也与淋巴瘤似乎“沾亲带故”。在感染了某种血清型幽门螺杆菌的患者中,黏膜里许多基因启动子的甲基化水平是未感染人群的5倍~300倍。在感染的粘膜中,异常甲基化和随后抑癌基因的沉默被发现与随后发生癌症的风险有很强的相关性。

受此启发,研究人员从表观遗传层面入手,利用免疫受损小鼠作为模型,分析支原体感染对淋巴瘤发生的影响。他们比较了未感染的免疫受损小鼠和支原体感染的免疫受损小鼠的淋巴瘤进展速度。结果发现,与未感染的免疫缺陷小鼠相比,支原体感染在小鼠生命早期便导致淋巴瘤发生,而且不是所有的癌细胞都有细菌DNA。在癌细胞中只发现少量的细菌DNA,这表明感染不一定会持续引发癌症。

在对细菌DNA序列进行分析时,他们将研究重点放在一种名为DnaK的蛋白质,它作为其他蛋白质的“伴侣”,通过帮助它们折叠保护它们免受损害。然而,在上述研究中,他们发现DnaK降低了参与DNA修复和抗癌活性的重要细胞蛋白的活性,如p53。因此,感染支原体的细胞将不能适当修复受损的DNA,而DNA修复机制在肿瘤的发生和进展过程中其到关键的作用。如此,便会潜在地增加癌症发展的风险。

DnaK蛋白对p53等相关基因的影响

不仅如此,遗传氨基酸序列分析显示,其他与癌症相关的细菌中也携带类似的DnaK蛋白,这与通过DNA修复机制缺失、断裂和p53失调介导的细胞转化机制是一致的。该机制也为理解感染干扰某些癌症药物提供了基础,综上,Gallo和Zella博士领导的研究团队作出结论:某些细菌的致癌特性是DnaK介导的[3]。

微生物和肿瘤之间的相关性仍在不断地被揭露。随着从表观遗传现象的认识到对表观遗传学的深入研究,在未来通过改变表观遗传来治疗炎症、肿瘤将不再是一个概念,而是真正可以为人类所用。既然细菌感染促进癌症发生发展的机制已经明确,那接下来我们面临的问题便是:能否通过治愈细菌感染来阻断癌症的发展,或许这是未来3-5年在癌症精准医学研究前沿领域的热点之一。

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    2019-07-07 drwjr
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    2018-12-17 1215028fm42暂无昵称

    支原体感染(如HIV),这个有问题吧

    0

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    2018-12-08 kafei

    学习了谢谢

    0

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