Roles of DNA repair enzyme OGG1 in innate immunity and its significance for lung cancer

ABSTRACT Cytokines are pivotal mediators of the immune response, and their coordinated expression protects host tissue from excessive damage and oxidant stress. Nevertheless, the development of lung pathology, including asthma, chronic obstructive pulmonary disease, and ozone‐induced lung injury, is associated with oxidant stress; as evidence, there is a significant increase in levels of the modified guanine base 7,8‐dihydro‐8‐oxoguanine (8‐oxoG) in the genome. 8‐OxoG is primarily recognized by 8‐oxoguanine glycosylase 1 (OGG1), which catalyzes the first step in the DNA base excision repair pathway. However, oxidant stress in the cell transiently halts enzymatic activity of substrate‐bound OGG1. The stalled OGG1 facilitates DNA binding of transactivators, including NF‐&kgr;B, to their cognate sites to enable expression of cytokines and chemokines, with ensuing recruitments of inflammatory cells. Hence, defective OGG1 will modulate the coordination between innate and adaptive immunity through excessive oxidant stress and cytokine dysregulation. Both oxidant stress and cytokine dysregulation constitute key elements of oncogenesis by KRAS, which is mechanistically coupled to OGG1. Thus, analysis of the mechanism by which OGG1 modulates gene expression helps discern between beneficial and detrimental effects of oxidant stress, exposes a missing functional link as a marker, and yields a novel target for lung cancer.

• Publication year

  2019

• Venue

  Pharmacology and Therapeutics

• Publication date

  2019-02-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1016/j.pharmthera.2018.09.004PMID 30240635PMCID PMC6504182
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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