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Updated: Jun 26, 2025

Assessment of Selective mRNA Translation in Mammalian Cells by Polysome Profiling
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Assessment of Selective mRNA Translation in Mammalian Cells by Polysome Profiling

Published on: October 28, 2014

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FTO blocks RNA translational activity via the loss of N6-methyladenosine methylation at 5' UTR regulated by RBM5 in

Liantao Li1,2, Debao Qu1,2, Bo Wang3

  • 1The First School of Clinical Medicine, Xuzhou Medical University, Xuzhou, Jiangsu, China.

Journal of Cellular Physiology
|May 14, 2024
PubMed

Insights

FTO alpha-ketoglutarate dependent dioxygenase (FTO) downregulation in non-small cell lung cancer (NSCLC) promotes tumor resistance. FTO regulates gene translation via m6A methylation, impacting cancer progression.

Area of Science:

  • Molecular Biology
  • Oncology
  • Epigenetics

Background:

  • N6-methyladenosine (m6A) methylation plays roles in biological functions.
  • The role of m6A methylation in chemoresistance (CR) of non-small cell lung cancer (NSCLC) remains unclear.

Purpose of the Study:

  • To investigate the molecular mechanism of m6A methylation in chemoresistant NSCLC.
  • To identify key regulators involved in this process.

Main Methods:

  • Analysis of FTO expression in CR NSCLC tissues and cells.
  • RNA immunoprecipitation sequencing (RIP-seq) to assess m6A methylation.
  • Investigation of FTO's interaction with eIF3A and RBM5.
  • Assessment of RNA-binding motif protein 5 (RBM5) role in FTO function.

Main Results:

  • FTO expression was downregulated in CR NSCLC.
  • Loss of FTO increased m6A methylation in 5'-untranslated regions, enhancing tumor resistance and malignancy.
  • FTO inhibited eIF3A recruitment to target genes, reducing their translation.
  • RBM5 deficiency impaired FTO's transcript recognition, leading to translation silencing of CR-associated genes.

Conclusions:

  • FTO acts as a novel translation regulator in CR NSCLC.
  • FTO's mechanism involves synergistic effects with RBM5 and m6A methylation.
  • Understanding this pathway offers potential therapeutic targets for chemoresistant NSCLC.
Keywords:
FTON6‐methyladenosine methylationcisplatin resistancegene translationnon‐small cell lung cancer

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