期刊
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
卷 10, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fcell.2022.931493
关键词
cancer; inflammation; epigenetics; histone modifications; high-order genome organization; super-enhancer; senescence
资金
- National Research Foundation (NRF), Singapore [NRF-NRFF2016-06]
- Singapore National Medical Research Council
- NMRC [OFIRG19nov-0015, CIRG21jun-0047]
This review discusses the interplay between epigenetics and inflammation. External and internal microenvironments contribute to epigenetic processes, and dysregulation of these processes can lead to cancer. Chronic inflammation plays a crucial role in the tumor microenvironment, and inflammatory signaling can modulate changes in the global epigenetic landscape.
Epigenetics comprise a diverse array of reversible and dynamic modifications to the cell's genome without implicating any DNA sequence alterations. Both the external environment surrounding the organism, as well as the internal microenvironment of cells and tissues, contribute to these epigenetic processes that play critical roles in cell fate specification and organismal development. On the other hand, dysregulation of epigenetic activities can initiate and sustain carcinogenesis, which is often augmented by inflammation. Chronic inflammation, one of the major hallmarks of cancer, stems from proinflammatory cytokines that are secreted by tumor and tumor-associated cells in the tumor microenvironment. At the same time, inflammatory signaling can establish positive and negative feedback circuits with chromatin to modulate changes in the global epigenetic landscape. In this review, we provide an in-depth discussion of the interconnected crosstalk between epigenetics and inflammation, specifically how epigenetic mechanisms at different hierarchical levels of the genome control inflammatory gene transcription, which in turn enact changes within the cell's epigenomic profile, especially in the context of inflammation-induced cancer.
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