Gut microbiota, epigenetic modification and colorectal cancer

Micro-organisms contain 90% of cells in human body and trillions foreign genes versus less than 30 thousand of their own. The human colon host various species of microorganisms, appraised at more than 10 microbiota and contained of over a thousand species. Although each one's profile is separab...

Full description

Saved in:
Bibliographic Details
Published inIranian journal of microbiology Vol. 9; no. 2; pp. 55 - 63
Main Authors Rezasoltani, Sama, Asadzadeh-Aghdaei, Hamid, Nazemalhosseini-Mojarad, Ehsan, Dabiri, Hossein, Ghanbari, Reza, Zali, Mohammad Reza
Format Journal Article
LanguageEnglish
Published Iran Tehran University of Medical Sciences 01.04.2017
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Micro-organisms contain 90% of cells in human body and trillions foreign genes versus less than 30 thousand of their own. The human colon host various species of microorganisms, appraised at more than 10 microbiota and contained of over a thousand species. Although each one's profile is separable, the relative abundance and distribution of bacterial species is the same between healthy ones, causing conservation of each person's overall health. Germline DNA mutations have been attributed to the less than 5% of CRC occurrence while more than 90% is associated with the epigenetic regulation. The most ubiquitous environmental factor in epigenetic modification is gut microbiota. Disruptive changes in the gut microbiome strongly contributed to the improvement of colorectal cancer. Gut microbiota may play critical role in progression of CRC via their metabolite or their structural component interacting with host intestinal epithelial cell (IEC). Herein we discuss the mechanism of epigenetic modification and its implication in CRC development, progression even metastasis by gut microbiota induction.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
content type line 23
ObjectType-Review-1
ISSN:2008-3289
2008-4447