Published online Nov 6, 2018. doi: 10.12998/wjcc.v6.i13.577
Peer-review started: June 20, 2018
First decision: August 29, 2018
Revised: September 15, 2018
Accepted: October 11, 2018
Article in press: October 12, 2018
Published online: November 6, 2018
Processing time: 139 Days and 8.3 Hours
Bile acids (BAs) are cholesterol derivatives synthesized in the liver and then secreted into the intestine for lipid absorption. There are numerous scientific reports describing BAs, especially secondary BAs, as strong carcinogens or promoters of colon cancers. Firstly, BAs act as strong stimulators of colorectal cancer (CRC) initiation by damaging colonic epithelial cells, and inducing reactive oxygen species production, genomic destabilization, apoptosis resistance, and cancer stem cells-like formation. Consequently, BAs promote CRC progression via multiple mechanisms, including inhibiting apoptosis, enhancing cancer cell proliferation, invasion, and angiogenesis. There are diverse signals involved in the carcinogenesis mechanism of BAs, with a major role of epidermal growth factor receptor, and its down-stream signaling, involving mitogen-activated protein kinase, phosphoinositide 3-kinase/Akt, and nuclear factor kappa-light-chain-enhancer of activated B cells. BAs regulate numerous genes including the human leukocyte antigen class I gene, p53, matrix metalloprotease, urokinase plasminogen activator receptor, Cyclin D1, cyclooxygenase-2, interleukin-8, and miRNAs of CRC cells, leading to CRC promotion. These evidence suggests that targeting BAs is an efficacious strategies for CRC prevention and treatment.
Core tip: Even though there is a close relationship between a high concentration of bile acids (BAs) and high risk of colorectal cancer (CRC), the mechanism of BAs promoting colon carcinogenesis is still not fully understood. In this review paper, we discuss molecular mechanisms of BAs as CRC promoters, their role in CRC progression, the oncogenic genes and signaling pathways involved, and important therapies against BA-related CRC.