4.7 Review

The m6A RNA methylation regulates oncogenic signaling pathways driving cell malignant transformation and carcinogenesis

Journal

MOLECULAR CANCER
Volume 20, Issue 1, Pages -

Publisher

BMC
DOI: 10.1186/s12943-021-01356-0

Keywords

m(6)A; Epitranscriptomics; Cell transformation; Carcinogenesis; Signal transduction

Funding

  1. National Institutes of Health [R01ES026151, R01ES028256, R01ES029496, R01ES029942]

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m(6)A RNA methylation is a prevalent internal modification in mammalian mRNAs, dysregulation of which is frequently observed in pathological conditions, particularly in cancer. Recent studies have shown that oncogenic signaling pathways in cancer are modulated by m(6)A modifications in target mRNAs and noncoding RNA transcripts.
The m(6)A RNA methylation is the most prevalent internal modification in mammalian mRNAs which plays critical biological roles by regulating vital cellular processes. Dysregulations of the m(6)A modification due to aberrant expression of its regulatory proteins are frequently observed in many pathological conditions, particularly in cancer. Normal cells undergo malignant transformation via activation or modulation of different oncogenic signaling pathways through complex mechanisms. Accumulating evidence showing regulation of oncogenic signaling pathways at the epitranscriptomic level has added an extra layer of the complexity. In particular, recent studies demonstrated that, in many types of cancers various oncogenic signaling pathways are modulated by the m(6)A modification in the target mRNAs as well as noncoding RNA transcripts. m(6)A modifications in these RNA molecules control their fate and metabolism by regulating their stability, translation or subcellular localizations. In this review we discussed recent exciting studies on oncogenic signaling pathways that are modulated by the m(6)A RNA modification and/or their regulators in cancer and provided perspectives for further studies. The regulation of oncogenic signaling pathways by the m(6)A modification and its regulators also render them as potential druggable targets for the treatment of cancer.

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