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A Method to Define the Effects of Environmental Enrichment on Colon Microbiome Biodiversity in a Mouse Colon Tumor Model
Published on: February 28, 2018
Modulation of host N6-methyladenosine modification by gut microbiota in colorectal cancer
Tian-Qi Jiang1,2, Hao Wang1,2, Wang-XinJun Cheng3
1Department of Gastroenterology, Jiangxi Provincial Key Laboratory of Digestive Diseases, Jiangxi Clinical Research Center for Department of Gastroenterology, Digestive Disease Hospital, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, Jiangxi Province, China.
Abstract:
As a research hotspot in the field of molecular biology, N6-methyladenosine (m6A) modification has made progress in the treatment of colorectal cancer (CRC), leukemia and other cancers. Numerous studies have demonstrated that the tumour microenvironment (TME) regulates the level of m6A modification in the host and activates a series of complex epigenetic signalling pathways through interactions with CRC cells, thus affecting the progression and prognosis of CRC. However, with the diversity in the composition of TME factors, this action is reciprocal and complex. Encouragingly, some studies have experimentally revealed that the intestinal flora can alter CRC cell proliferation by directly acting on m6A and thereby altering CRC cell proliferation. This review summarizes the data, supporting the idea that the intestinal flora can influence host m6A levels through pathways such as methyl donor metabolism and thus affect the progression of CRC. We also review the role of m6A modification in the diagnosis, treatment, and prognostic assessment of CRC and discuss the current status, limitations, and potential clinical value of m6A modification in this field. We propose that additional in-depth research on m6A alterations in CRC patients and their TME-related targeted therapeutic issues will lead to better therapeutic outcomes for CRC patients.
Insights
The gut microbiome influences colorectal cancer (CRC) progression by altering N6-methyladenosine (m6A) levels. Understanding this interaction offers new therapeutic strategies for CRC patients.
Area of Science:
- Molecular Biology
- Epigenetics
- Cancer Research
Background:
- N6-methyladenosine (m6A) modification is a key epigenetic mechanism with emerging roles in cancer.
- The tumor microenvironment (TME) significantly impacts colorectal cancer (CRC) progression via complex interactions.
- The gut microbiome's influence on CRC through m6A modification is an area of active investigation.
Purpose of the Study:
- To review the current understanding of how intestinal flora affects host m6A levels and CRC progression.
- To explore the role of m6A modification in CRC diagnosis, treatment, and prognosis.
- To discuss the limitations and future clinical potential of targeting m6A pathways in CRC.
Main Methods:
- Literature review and synthesis of existing research on m6A, TME, gut microbiome, and CRC.
- Analysis of pathways linking gut microbiota to host m6A levels (e.g., methyl donor metabolism).
- Evaluation of the diagnostic, therapeutic, and prognostic implications of m6A in CRC.
Main Results:
- Intestinal flora can directly impact CRC cell proliferation by modulating m6A levels.
- Gut microbes influence host m6A levels through mechanisms like methyl donor metabolism.
- m6A modification plays a multifaceted role in CRC development and progression.
Conclusions:
- The interplay between gut microbiota, m6A modification, and the TME is crucial for CRC progression.
- Targeting m6A pathways presents potential for novel therapeutic strategies in CRC.
- Further research into m6A alterations and TME-targeted therapies is essential for improving CRC patient outcomes.
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