RNA methylation machinery and m6A target genes as circulating biomarkers of ulcerative colitis and Crohn’s disease: Correlation with disease activity, location, and inflammatory cytokines

Motawi, Tarek K.; Shaker, Olfat G.; Amr, Ghada; Senousy, Mahmoud A.

doi:10.1016/j.cca.2024.119831

Clinica Chimica Acta

2024

DOI: 10.1016/j.cca.2024.119831

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RNA methylation machinery and m6A target genes as circulating biomarkers of ulcerative colitis and Crohn’s disease: Correlation with disease activity, location, and inflammatory cytokines

Tarek K. Motawi,

Olfat G. Shaker,

Ghada Amr

et al.

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2024

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Cited by 2 publications

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m6A epitranscriptomic and epigenetic crosstalk in liver fibrosis: Special emphasis on DNA methylation and non-coding RNAs

Dong,

Yang,

Tao

et al. 2024

Cellular Signalling

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m6A epitranscriptomic and epigenetic crosstalk in liver fibrosis: Special emphasis on DNA methylation and non-coding RNAs

Dong,

Yang,

Tao

et al. 2024

Cellular Signalling

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Modulation of host N6-methyladenosine modification by gut microbiota in colorectal cancer

Jiang,

Wang,

Cheng

et al. 2024

World J Gastroenterol

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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.

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RNA methylation machinery and m6A target genes as circulating biomarkers of ulcerative colitis and Crohn’s disease: Correlation with disease activity, location, and inflammatory cytokines

Cited by 2 publications

References 44 publications

m6A epitranscriptomic and epigenetic crosstalk in liver fibrosis: Special emphasis on DNA methylation and non-coding RNAs

m6A epitranscriptomic and epigenetic crosstalk in liver fibrosis: Special emphasis on DNA methylation and non-coding RNAs

Modulation of host N6-methyladenosine modification by gut microbiota in colorectal cancer

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