The link between inflammation and cancer is well established. Chronic inflammation promotes cancer initiation and progression. Various studies showed that the underlying mechanisms involve epigenetic alterations. These epigenetic alterations might culminate into an epigenetic switch that transforms premalignant cells into tumor cells or non-invasive into invasive tumor cells, thereby promoting metastasis. Epigenetic switches require an initiating event, which can be inflammation, whereas the resulting phenotype is inherited without the initiating signal. Epigenetic switches are induced and maintained by DNA methylation, histone modifications, polycomb group (PcG)/trithorax group (TrxG) proteins, and feedback loops consisting of transcription factors and microRNAs. Since epigenetic switches are reversible, they might represent an important basis for the design of novel anticancer therapeutics. This review summarizes published evidence of epigenetic switches in cancer development that are induced by inflammation.
Keywords: Cancer; Cytokine; Epigenetic switch; Epigenetics; Epithelial-mesenchymal transition; Histone modifications; IL-6; Inflammation; Interleukin; Metastasis; Methylation; MicroRNA; NF-κB; Polycomb group proteins; STAT3; TGF-β; Tumor; Tumor microenvironment; miR-200; miR-34; p53.