| Abstrakt: |
Background and aim: "Inflammatory bowel disease" (IBD) is a chronic, relapsing inflammatory disease of the intestinal tract that typically begins at a young age and might transit to colorectal cancer (CRC). In this manuscript, we discussed the epigenetic and metabolic change to present a extensive view of IBDs transition to CRC. This study discusses the possible biomarkers for evaluating the condition of IBDs patients, especially before the transition to CRC. Research approach: We searched "PubMed" and "Google Scholar" using the keywords from 2000 to 2022. Discussion: In this manuscript, interesting titles associated with IBD and CRC are discussed to present a broad view regarding the epigenetic and metabolic reprogramming and the biomarkers. Conclusion: Epigenetics can be the main reason in IBD transition to CRC, and Hypermethylation of several genes, such as VIM, OSM4, SEPT9, GATA4 and GATA5, NDRG4, BMP3, ITGA4 and plus hypomethylation of LINE1 can be used in IBD and CRC management. Epigenetic, metabolisms and microbiome-derived biomarkers, such as Linoleic acid and 12 hydroxy 8,10-octadecadienoic acid, Serum M2-pyruvate kinase and Six metabolic genes (NAT2, XDH, GPX3, AKR1C4, SPHK and ADCY5) expression are valuable biomarkers for early detection and transition to CRC condition. Some miRs, such as miR-31, miR-139-5p, miR -155, miR-17, miR-223, miR-370-3p, miR-31, miR -106a, miR -135b and miR-320 can be used as biomarkers to estimate IBD transition to CRC condition. Highlights: Inflammatory signals, cytokines and immune cell interaction lead to epigenetic reprogramming in IBD. The imprinting profile of IGF2, NOD2, ATG16L1 and IRGM is considerable in IBD. Microbiota plays an essential role in IBD transition to CRC via NF-kB and STAT3 signaling pathways. TLR4 activates β-catenin via PI3K then it interacts with Wnt pathway and leads to a metabolic and neoplastic reprograming in IBD. [ABSTRACT FROM AUTHOR] |
