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Methods to Study Mrp4-containing Macromolecular Complexes in the Regulation of Fibroblast Migration
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DMDRMR-Mediated Regulation of m6A-Modified CDK4 by m6A Reader IGF2BP3 Drives ccRCC Progression

Yinmin Gu1,2, Shaoxi Niu3, Yang Wang4

  • 1CAS Key Laboratory of Bio-medical Diagnostics, Suzhou Institute of Biomedical Engineering and Technology, Chinese Academy of Sciences, Suzhou, China.

Cancer Research
|December 9, 2020
PubMed

Insights

Aberrant N6-methyladenosine (m6A) modification drives cancer. A novel long noncoding RNA (lncRNA), DMDRMR, cooperates with IGF2BP3 to promote clear cell renal cell carcinoma (ccRCC) growth and metastasis by stabilizing target genes in an m6A-dependent manner.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Aberrant N6-methyladenosine (m6A) modification is implicated in tumor initiation and progression.
  • The role of long noncoding RNAs (lncRNAs) in regulating m6A modification is largely unknown.
  • Understanding these regulatory mechanisms is crucial for cancer research.

Purpose of the Study:

  • To identify lncRNAs deregulated by DNA methylation across 12 cancer types.
  • To investigate the function of a novel lncRNA, DMDRMR, in clear cell renal cell carcinoma (ccRCC).
  • To elucidate the molecular mechanism by which DMDRMR influences ccRCC progression.

Main Methods:

  • Analysis of The Cancer Genome Atlas (TCGA) data for 12 cancer types.
  • Identification of DNA methylation-deregulated lncRNAs.
  • Mechanistic studies involving DMDRMR, IGF2BP3, and target genes (CDK4, COL6A1, LAMA5, FN1).
  • Assessment of m6A-dependent stabilization of target genes.

Main Results:

  • A novel lncRNA, DMDRMR, was identified as DNA methylation-deregulated and cooperating with m6A readers.
  • DMDRMR facilitates tumor growth and metastasis in ccRCC by binding IGF2BP3.
  • DMDRMR enhances IGF2BP3 activity to stabilize target genes (CDK4, COL6A1, LAMA5, FN1) in an m6A-dependent manner, promoting G1-S transition and cell proliferation.
  • High coexpression of DMDRMR and IGF2BP3 correlates with poor prognosis in ccRCC patients.

Conclusions:

  • The lncRNA DMDRMR acts as a cofactor for IGF2BP3, stabilizing target genes via an m6A-dependent mechanism.
  • DMDRMR plays a significant oncogenic role in ccRCC.
  • DMDRMR and IGF2BP3 represent potential diagnostic, prognostic, and therapeutic targets for ccRCC.

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