From: Influences of diet and the gut microbiome on epigenetic modulation in cancer and other diseases
Cancer | Link to gut microbiome | Link to epigenetics | Possible therapy | Reference |
---|---|---|---|---|
Gastric | H. pylori causes gastric pathology by injecting about 128 kDa Cytotoxin-associated gene A (Cag A) protein which enhanced c-Myc and DNMT3B expression | H. pylori increased histone H4 acetylation in the promoter region of p21 thereby increasing p21 expression | Dietary compounds that have HAT-inhibiting activities | (Hayashi, Tsujii et al. 2012) [26] |
(Ding, Goldberg et al. 2010) [13] | ||||
(Fehri, Rechner et al. 2009) [21] | ||||
Colon | Elevated TNF-α expression in the colon | TNF-α-suppressed differentiation and potentiated cell death induced by butyrate (NaBt) in both adenocarcinoma HT-29 and fetal FHC human colon cells in vitro | Sodium butyrate which is an HDAC inhibitor can induce TNF-α to potentiate cell death | (Hýžd’alová, Hofmanova et al. r2008) [35] |
(Erdman, Rao et al. 2009) [17] | ||||
Estrogen-dependent cancers | Bacterial species possess β-glucuronidases and β-glucuronides that participate in estrogen conjugation and deconjugation | Phase II hepatic conjugation reactions of E1 and E2 include methylation via catechol-O-methyltransferase, glucuronidation via uridine 5′-diphospho-glucuronosyltransferase | Certain plant-based dietary compounds contain O-methyltransferase enzymes that can inactivate catechol estrogens | (Plottel and Blaser 2011) [68] |
(Mageroy, Tieman et al. 2012) [50] | ||||
Liver | TLR4 activation by LPS from gut bacteria contributes to tumor promotion | Epigenetic regulation of TLR4 gene expression in intestinal epithelial cells (IECs) can act as one mechanism for maintaining intestinal homeostasis by suppressing excessive responses to the commensals and regulating mucosal inflammation in the gut | (Dapito, Mencin et al. 2012) [11] | |
(Takahashi, Sugi et al. 2011) [87] | ||||
Lung | SCFAs produced by gut microbiota bind GPCR43 which affects inflammatory responses. GPR43-deficient (Gpr43 −/−) mice showed exacerbated or unresolving inflammation in models of colitis, arthritis, and asthma | SCFAs are known to have HDAC-inhibiting activities | SCFAs are produced by fermentation of carbohydrates by gut microbiota | (Maslowski, Vieira et al. 2009) [54] |