Kulvinder Kochar Kaur*, Gautam Nand K Allahbadia, Mandeep Singh
Bile Acids (BAs) possess a considerable significant part in the form of emulsifiers in digestion besides absorption of dietary lipids as well as cholesterol. BAs represent amphiphilic molecules whose formation take place by the response of enzymes with cholesterol in the form of a substrate, with them being the primary metabolites. Earlier the BAs were believed to be tumor repressors. The tumor repressive actions of BAs are correlated with Programmed Cell Death (PCD). Furthermore, dependent on this observation different Synthetic BAs products have been generated along with their utilization regarding induction of PCD (in the form of apoptosis, autophagy or necropolis in variable kinds of human cancers Thus we conducted a narrative review utilizing search engine PubMed, Google scholar ;web of science; embase; Cochrane review library utilizing the MeSH terms like cell death modes; apoptosis; autophagy; necroptosis; BAs; colorectal cancer; leukaemia; breast cancer; thyroid carcinoma cells ;CDCA; DCA; LCA;UDCA; GCDCA; TCDCA; synthetic BAs; other GIT cancers; NFκB;Bcl-2 family members from 1940 till 2022 till date in 2022. We found a total of 7000 articles out of which we selected 140 articles for this review. No meta-analysis was done. Thus here we start in this review with description of PCD (in the form of apoptosis, autophagy or necroptosis in considerable details pertinent to this topic. Further we highlight the significance of the different drug generation in the form of synthetic BAs obtained substances for the treatment of various human cancers besides how BAs might be implicated in the generation of certain GIT cancers like the colorectal cancers. That might form the basis of generation of such innovative therapies even for cancers/tumors that are cisplatin resistant. Gradually this might be extended to therapy of Neurodege Nerative Diseases (NDD), along with amyotrophic sclerosis, besides many metabolic diseases, hematological diseases like use of TUDCA.