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METTL3 as a master regulator of translation in cancer: mechanisms and implications

Margalida Esteva-Socias1,2, Francesca Aguilo1,2

  • 1Department of Molecular Biology, Umeå University, SE-901 85Umeå, Sweden.

NAR Cancer
|March 6, 2024
PubMed

Insights

N6-methyladenosine (m6A) and its writer METTL3 regulate protein translation in cancer. This review explores how m6A and METTL3 impact cancer cell survival and metastasis.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Epigenetics

Background:

  • Gene expression control is crucial in cancer.
  • Translational regulation impacts tumor progression.
  • N6-methyladenosine (m6A) is a key mRNA modification affecting translation.

Purpose of the Study:

  • To review the role of m6A and METTL3 in cancer translational regulation.
  • To explore the impact of m6A and METTL3 on oncogenes and tumor suppressors.
  • To discuss cytoplasmic METTL3's role in protein synthesis.

Main Methods:

  • Literature review of m6A mapping tools and functional investigations.
  • Analysis of m6A and METTL3 involvement in cancer-related gene translation.
  • Examination of METTL3's catalytic-independent functions.

Main Results:

  • m6A and METTL3 influence the translation of both oncogenes and tumor suppressor genes.
  • The effect of m6A modification is context-dependent in cancer.
  • Cytoplasmic METTL3 participates in protein synthesis independently of its enzymatic activity.

Conclusions:

  • m6A and METTL3 are critical regulators of translational control in cancer.
  • Understanding this interplay provides insights into tumorigenesis mechanisms.
  • Targeting m6A and METTL3 pathways may offer therapeutic strategies.

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