• Medicine · Nov 2023

    Review

    Research progress of N6-methyladenosine in colorectal cancer: A review.

    • Yu Lin, Hongjun Shi, Lianping Wu, Linyang Ge, and Zengqing Ma.
    • Department of Respiratory, Nanjing Gaochun People's Hospital, Nanjing, China.
    • Medicine (Baltimore). 2023 Nov 24; 102 (47): e36394e36394.

    AbstractColorectal cancer is the third most common malignant tumor worldwide, causing serious harm to human health. Epigenetic modification, especially RNA methylation modification, plays a critical role in the occurrence and development of colorectal cancer via post-transcriptional regulation of mRNA and non-coding RNA expression. Among these, N6-methyladenosine (m6A) is the most common chemical modification in mammals, which plays an important role in the progress of cancer, including colorectal cancer. m6A is a dynamic and reversible process and is mainly regulated by m6A methyltransferase ("writers"), m6A demethylases ("erasers"), and m6A binding proteins ("readers"). Herein, we reviewed recent advances in the role of m6A modification in colorectal cancer and focused on the factors affecting m6A modification. Furthermore, we discussed the clinical application of m6A modifications for colorectal cancer diagnosis, prognosis, and treatment and provided guides in clinical practice. m6A modification and m6A regulators play significant roles in the occurrence and development of colorectal cancer by regulating the stability and translation of mRNAs, the maturation of miRNAs, and the function of lncRNAs. m6A regulators can play biological roles in colorectal cancer through m6A-dependent manner or m6A-independent manner. Multiplies of internal factors, including miRNAs and lncRNAs, and external factors can also regulate the m6A modification by completing with m6A regulators in a base complement manner, regulating the expression of m6A and mutating the m6A site. m6A regulators and m6A modificantion are diagnostic and prognostic markers for CRC. Therefore, m6A regulators and m6A modificantion may be potential therapeutic target for CRC in the future.Copyright © 2023 the Author(s). Published by Wolters Kluwer Health, Inc.

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