Abstract

The m6A RNA methylation is the most prevalent internal modification in mammalian mRNAs which plays critical biological roles by regulating vital cellular processes. Dysregulations of the m6A 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 m6A modification in the target mRNAs as well as noncoding RNA transcripts. m6A 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 m6A RNA modification and/or their regulators in cancer and provided perspectives for further studies. The regulation of oncogenic signaling pathways by the m6A modification and its regulators also render them as potential druggable targets for the treatment of cancer.

Highlights

  • Carcinogenesis is a complex process stemming from genetic and epigenetic changes in a specific cell population

  • Epigenetic changes that are conventionally known for differential gene expression pattern leading to alternative phenotypic traits involve- altered DNA methylation, modification of histone or remodeling of chromatin structure

  • In mRNAs, m6A sites are highly enriched in 5′-untranslated regions (5′-UTRs), near the stop codons, in the 3′-untranslated regions (3′UTRs) and within long internal exons. m6A most frequently occurs in the consensus sequence RRACH (R = G/A/U, A = m6A, H=U/A/C) and such sequence occurs about every 85 nucleotides

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Summary

Introduction

Carcinogenesis is a complex process stemming from genetic and epigenetic changes in a specific cell population.

Results
Conclusion
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