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A Method for Measuring RNA N6-methyladenosine Modifications in Cells and Tissues
08:56

A Method for Measuring RNA N6-methyladenosine Modifications in Cells and Tissues

Published on: December 5, 2016

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N6-methyladenosine modification of ITGA6 mRNA promotes the development and progression of bladder cancer

Huan Jin1, Xiaoling Ying2, Biao Que3

  • 1Center for Translational Medicine, The First Affiliated Hospital, Sun Yat-sen University, 510080 Guangzhou, China; Department of Physiology, Zunyi Medical College, Guizhou 563000, China.

Ebiomedicine
|August 15, 2019
PubMed
Abstract

Insights

N6-methyladenosine (m6A) modification of Integrin Subunit Alpha 6 (ITGA6) promotes bladder cancer (BC) progression. Targeting m6A-modified ITGA6 offers a potential therapeutic strategy for BC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • N6-methyladenosine (m6A) mRNA modification plays a crucial role in various cancers.
  • The specific functions and regulatory mechanisms of m6A in bladder cancer (BC) remain largely unexplored.

Purpose of the Study:

  • To investigate the role and regulatory mechanisms of m6A modification in bladder cancer (BC).
  • To assess the impact of m6A-modified Integrin Subunit Alpha 6 (ITGA6) on BC progression.
  • To identify ITGA6 as a potential therapeutic target for BC.

Main Methods:

  • Cell phenotype analysis and in vivo mouse xenograft models were employed to evaluate the effects of m6A-modified ITGA6 on BC.
  • Methylated RNA immunoprecipitation (MeRIP), RNA immunoprecipitation, luciferase reporter assays, and mutagenesis assays were utilized to elucidate the regulatory mechanism.
  • Immunohistochemical analysis correlated METTL3 and ITGA6 expression in human BC tissues.

Main Results:

  • METTL3 and ALKBH5 modulated BC cell adhesion by regulating ITGA6 expression.
  • Increased ITGA6 expression correlated with higher METTL3 levels and poorer survival rates in BC patients.
  • m6A enrichment in ITGA6 mRNA promoted its translation via YTHDF1/YTHDF3, driving BC growth, adhesion, migration, and invasion.

Conclusions:

  • m6A-modified ITGA6 exhibits an oncogenic role in BC development and progression.
  • The study elucidates the regulatory mechanisms of m6A-ITGA6 in BC.
  • ITGA6 represents a promising therapeutic target for bladder cancer.
Keywords:
Bladder cancerITGA6METTL3N(6)-methyladenosineProgression

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