期刊
CANCER JOURNAL
卷 19, 期 6, 页码 468-472出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/PPO.0000000000000004
关键词
Inflammasome; IL-1; IL-18; carcinogenesis
类别
资金
- German Research Society (DFG) [DR 817/2-1, YA-182/2-1]
The central role of chronic inflammation in the promotion of tumor growth is supported by a broad range of experimental and clinical evidence. However, the molecular mechanisms converting transient inflammatory tissue reactions into a tumor-promoting microenvironment remain largely elusive. Because inflammasomes have been shown to regulate the proinflammatory cytokines interleukin 1 beta (IL-1 beta) and IL-18, they have been implicated in the relationship between tumor genesis/progression and inflammation. For instance, many cancers have been directly linked to inflammasome-mediated sterile inflammation, where a blockade of IL-1 beta and IL-18 has been shown to inhibit tumor growth. On the other hand, inflammasome activation also has potent antitumorigenic effects, where malignant precursor cells are eliminated through pyroptotic cell death. Indeed, inflammasome activity can even increase the efficacy of certain chemotherapies. Here, we review the current understanding on the complex and sometimes contradictory role of inflammasomes in carcinogenesis.
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