m6A RNA modification modulates gene expression and cancer-related pathways in clear cell renal cell carcinoma

Yimeng Chen1, Cuixing Zhou1, Yangyang Sun1

  • 1Department of Urology, The Third Affiliated Hospital of Soochow University, Changzhou 213003, Jiangsu, China.

Epigenomics
|December 21, 2019
PubMed

Insights

This study maps N6-methyladenosine (m6A) modifications in clear cell renal cell carcinoma (ccRCC), revealing significant changes in m6A patterns and identifying novel m6A-related genes involved in cancer pathways.

Area of Science:

  • Molecular Biology
  • Genomics
  • Cancer Research

Background:

  • N6-methyladenosine (m6A) is the most prevalent internal mRNA modification.
  • Dysregulation of m6A modification is implicated in various cancers, including renal cell carcinoma.
  • Understanding m6A patterns in clear cell renal cell carcinoma (ccRCC) is crucial for elucidating its oncogenic mechanisms.

Purpose of the Study:

  • To systematically profile the global m6A modification landscape in ccRCC.
  • To identify differentially methylated m6A peaks and associated genes in ccRCC.
  • To explore the role of m6A-mediated gene regulation in ccRCC development.

Main Methods:

  • m6A-seq and RNA-seq were performed on ccRCC and normal tissues.
  • Bioinformatics analysis was used to identify m6A peaks and differentially expressed genes.
  • Quantitative real-time PCR (qPCR) was employed for validation of m6A-related RNAs.

Main Results:

  • A total of 6919 new m6A peaks emerged, and 5020 peaks disappeared in ccRCC samples.
  • Unique m6A-related genes in ccRCC were found to be associated with cancer-related pathways.
  • Differentially expressed mRNA transcripts with hyper- or hypo-methylated m6A peaks were identified in ccRCC.

Conclusions:

  • This study provides the first comprehensive transcriptome-wide m6A map for human ccRCC.
  • The findings offer insights into potential mechanisms of m6A-driven gene expression regulation in ccRCC.
  • This m6A map may serve as a foundation for future research into ccRCC pathogenesis and therapeutic strategies.

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