Gut Microbiota and Epigenetics in Colorectal Cancer: Implications for Carcinogenesis and Therapeutic Intervention

Abstract

Colorectal cancer (CRC) is a leading cause of cancer-related deaths worldwide. The occurrence of CRC is associated with various genetic and epigenetic mutations in intestinal epithelial cells that transform them into adenocarcinomas. There is increasing evidence indicating the gut microbiota plays a crucial role in the regulation of host physiological processes. Alterations in gut microbiota composition are responsible for initiating carcinogenesis through diverse epigenetic modifications, including histone modifications, ncRNAs and DNA methylation. This work was designed to comprehensively review recent findings to provide insight into the associations between the gut microbiota and CRC at an epigenetic level. These scientific insights can be used in the future to develop effective strategies for early detection and treatment of CRC.

Plain language summary

Colorectal cancer (CRC) is a major cause of cancer-related deaths worldwide. It happens when certain changes occur in the cells lining the intestine, turning them into cancerous growths. Recent studies suggest the collection of microbes in our gut, called the gut microbiota, plays a big role in how our body works. Dysregulation in gut microbiota composition is responsible for the development of colorectal cancer. This work provides a closer look at these recent discoveries to better understand how gut microbes might influence the development of colorectal cancer by affecting gene function. Understanding this connection may facilitate early diagnosis and treatment of colorectal cancer.

Tweetable abstract

The gut microbiota plays a crucial role in the regulation of host physiological processes, and an imbalance in microbiota composition is linked to the initiation of colorectal cancer. The gut microbiota regulates the initiation of colorectal cancer through various epigenetic modifications.

Keywords::

• colorectal cancer
• DNA methylation
• epigenetics
• gut microbiota
• histone modification
• ncRNA

Author contributions

M Pandey and J Bhattacharyya wrote the original draft and proofread and reviewed the manuscript. All authors agreed to the published version of the manuscript.

Acknowledgments

M Pandey acknowledges the Ministry of Human Resource Development IIT Delhi for providing a prime minister research fellowship for doctoral research.

Financial disclosure

The authors convey their sincere gratitude to the Indian Council of Medical Research (grant number: RP04467G) and the Indian Institute of Technology (grant number: MI02554) for supporting this work.

Competing interests disclosure

The authors have no competing interests or relevant affiliations with any organization or entity with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Writing disclosure

No writing assistance was utilized in the production of this manuscript.