Molecular mechanistic pathway of colorectal carcinogenesis associated with intestinal microbiota

The colon rectal portion of gastrointestinal tract (GI) is full of microorganisms with different complex community that plays important role in maintaining homeostasis. But now-a-days different literature indicated that microbiota cause development of colorectal cancer (CRC) with a disease and ultimately aggravates to death. The mechanism inside the colo-rectal portion of GI tract is not fully well-known and bacterial contribution inside it is also fully unclear. Therefore, there is certain evidence trying a target about the unclear mechanism between intestinal microbiota and CRC. Different reports revealed that colo-rectal microorganisms is playing a great role in inducing the onset and progression of CRC with different dynamic mechanisms viz. acceleration of chronic inflammatory state, the biosynthesis of genotoxins that interfere with cell cycle regulation, the production of toxic metabolites, or heterocyclic amine activation of pro-diet carcinogenic compounds. There is growing evidence that individuals with colonic adenomas and carcinomas harbor a distinct microbiota. Alterations to the gut microbiota may allow the outgrowth of bacterial populations that induce genomic mutations or exacerbate tumor-promoting inflammation. While cancer is largely considered to be a disease of genetic and environmental factors, increasing evidence has demonstrated a role for the microbiota in shaping inflammatory environments and promoting tumor growth and spread. Despite all these advances, different studies depicted the relationship between microbiota and CRC in humans and animal models and aid in developing alternate therapeutic approach based on gut microbiota manipulations. Alteration of the microbiota may be a useful to preventing and altering the trajectory of colorectal cancer. Therefore, the aim of the study is to identify the possible mechanistic mechanism regarding host-microbiota interaction in colorectal carcinogenesis. (C) 2017 Elsevier Ltd. All rights reserved.