Crosstalk between DNA Damage and Inflammation in the Multiple Steps of Carcinogenesis.

Publisher: MDPI Country of Publication: Switzerland NLM ID: 101092791 Publication Model: Electronic Cited Medium: Internet ISSN: 1422-0067 (Electronic) Linking ISSN: 14220067 NLM ISO Abbreviation: Int J Mol Sci Subsets: MEDLINE

Original Publication: Basel, Switzerland : MDPI, [2000-

Carcinogenesis/*genetics ; DNA Damage/*genetics ; Inflammation/*genetics ; Neoplasms/*genetics; 8-Hydroxy-2'-Deoxyguanosine ; Deoxyguanosine/analogs & derivatives ; Deoxyguanosine/metabolism ; Guanine/analogs & derivatives ; Guanine/metabolism ; Humans ; Inflammation/pathology ; Mutation ; Neoplasms/pathology ; Nitric Oxide Synthase Type II/genetics ; Reactive Nitrogen Species/metabolism ; Reactive Oxygen Species/metabolism ; Tumor Hypoxia/genetics

Inflammation can be induced by chronic infection, inflammatory diseases and physicochemical factors. Chronic inflammation is estimated to contribute to approximately 25% of human cancers. Under inflammatory conditions, inflammatory and epithelial cells release reactive oxygen (ROS) and nitrogen species (RNS), which are capable of causing DNA damage, including the formation of 8-oxo-7,8-dihydro-2'-deoxyguanosine and 8-nitroguanine. We reported that 8-nitroguanine was clearly formed at the sites of cancer induced by infectious agents including Helicobacter pylori , inflammatory diseases including Barrett's esophagus, and physicochemical factors including asbestos. DNA damage can lead to mutations and genomic instability if not properly repaired. Moreover, DNA damage response can also induce high mobility group box 1-generating inflammatory microenvironment, which is characterized by hypoxia. Hypoxia induces hypoxia-inducible factor and inducible nitric oxide synthase (iNOS), which increases the levels of intracellular RNS and ROS, resulting DNA damage in progression with poor prognosis. Furthermore, tumor-producing inflammation can induce nuclear factor-κB, resulting in iNOS-dependent DNA damage. Therefore, crosstalk between DNA damage and inflammation may play important roles in cancer development. A proposed mechanism for the crosstalk may explain why aspirin decreases the long-term risk of cancer mortality.
Competing Interests: The authors declare no conflict of interest.

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Keywords: cancer; inflammation; oxidative stress

0 (8-nitroguanine)
0 (Reactive Nitrogen Species)
0 (Reactive Oxygen Species)
5Z93L87A1R (Guanine)
88847-89-6 (8-Hydroxy-2'-Deoxyguanosine)
EC 1.14.13.39 (NOS2 protein, human)
EC 1.14.13.39 (Nitric Oxide Synthase Type II)
G9481N71RO (Deoxyguanosine)

Date Created: 20170822 Date Completed: 20180426 Latest Revision: 20240326

20240326

PMC5578195

10.3390/ijms18081808

28825631