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©The Author(s) 2023.
World J Gastrointest Oncol. Aug 15, 2023; 15(8): 1317-1331
Published online Aug 15, 2023. doi: 10.4251/wjgo.v15.i8.1317
Published online Aug 15, 2023. doi: 10.4251/wjgo.v15.i8.1317
Figure 1 Different mechanisms of colitis-associated colorectal carcinogenesis.
Recent advances underlying colitis-associated colorectal carcinogenesis include a variety of mechanisms, including genetics and epigenetics, immunity and inflammation, and microbiota. Their subtle and complex interactions contribute to the development of colorectal cancer (CAC): (1) DNA mutations, oxidative damage, DNA methylation and histone modifications promote colitis-associated colorectal carcinogenesis; (2) Classical signaling pathways such as NF-κB, Wnt/β-catenin, STAT3/IL-6 promote colitis-associated colorectal carcinogenesis. In addition, TIMs and macrophage polarization are also involved in carcinogenesis; and (3) Several bacteria (e.g., E. coli, ETBF, and Fn) and metabolites may cause DNA damage, inflammation, activation of several oncogenic signaling pathways and EMT, thereby promoting CAC. BFT: Bacteroides fragilis toxin; DSBs: Double-strand breaks; EMT: Epithelial-mesenchymal transition; E. coli: Escherichia coli; ETBF: Enterotoxigenic Bacteroides fragilis; Fn: Fusobacterium nucleatum; IKK: IκB kinase; MEL18: Polycomb group ring finger 2; NFATc3: Nuclear factor of activated T cells 3; NF-Κb: Nuclear factor-κB; ODC: Ornithine decarboxylase; PI3K: Phosphoinositide 3-kinase; Pou3f1: POU class 3 homeobox 1; STAT3: Signal transducer and activator of transcription 3; TIMs: Tumor-infiltrating myeloid cells; TLR4: Toll-like receptor 4.
- Citation: Dan WY, Zhou GZ, Peng LH, Pan F. Update and latest advances in mechanisms and management of colitis-associated colorectal cancer. World J Gastrointest Oncol 2023; 15(8): 1317-1331
- URL: https://www.wjgnet.com/1948-5204/full/v15/i8/1317.htm
- DOI: https://dx.doi.org/10.4251/wjgo.v15.i8.1317