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炎症诱导的 DNA 损伤、突变与癌症。

Inflammation-induced DNA damage, mutations and cancer.

机构信息

Department of Biological Engineering, United States.

Department of Biological Engineering, United States.

出版信息

DNA Repair (Amst). 2019 Nov;83:102673. doi: 10.1016/j.dnarep.2019.102673. Epub 2019 Jul 25.

Abstract

The relationships between inflammation and cancer are varied and complex. An important connection linking inflammation to cancer development is DNA damage. During inflammation reactive oxygen and nitrogen species (RONS) are created to combat pathogens and to stimulate tissue repair and regeneration, but these chemicals can also damage DNA, which in turn can promote mutations that initiate and promote cancer. DNA repair pathways are essential for preventing DNA damage from causing mutations and cytotoxicity, but RONS can interfere with repair mechanisms, reducing their efficacy. Further, cellular responses to DNA damage, such as damage signaling and cytotoxicity, can promote inflammation, creating a positive feedback loop. Despite coordination of DNA repair and oxidative stress responses, there are nevertheless examples whereby inflammation has been shown to promote mutagenesis, tissue damage, and ultimately carcinogenesis. Here, we discuss the DNA damage-mediated associations between inflammation, mutagenesis and cancer.

摘要

炎症与癌症之间的关系是多种多样且复杂的。将炎症与癌症发展联系起来的一个重要环节是 DNA 损伤。在炎症过程中,会产生活性氧和氮物种(RONS)来对抗病原体并刺激组织修复和再生,但这些化学物质也会损伤 DNA,进而促进引发和促进癌症的突变。DNA 修复途径对于防止 DNA 损伤导致突变和细胞毒性至关重要,但 RONS 可以干扰修复机制,降低其功效。此外,细胞对 DNA 损伤的反应,如损伤信号和细胞毒性,也可以促进炎症,形成正反馈循环。尽管 DNA 修复和氧化应激反应之间存在协调,但仍有一些例子表明炎症可以促进突变、组织损伤,并最终导致癌变。在这里,我们讨论了炎症、突变和癌症之间与 DNA 损伤相关的关联。

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