Related Experiment Video

Updated: Jul 16, 2025

Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors
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Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors

Published on: August 5, 2022

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N6-methyladenosine-induced METTL1 promotes tumor proliferation via CDK4

Chunyan Zhang1, Yuanbo Cui2

  • 1Department of Clinical Laboratory, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou 450007, China.

Biological Chemistry
|September 11, 2023
PubMed

Insights

N6-methyladenosine (m6A) and N7-methylguanosine (m7G) RNA modifications regulate gene expression. METTL1, elevated by m6A, promotes head and neck cancer via m7G modification of CDK4, offering a potential therapeutic target.

Area of Science:

  • Epigenetics
  • Molecular Biology
  • Cancer Research

Background:

  • N6-methyladenosine (m6A) and N7-methylguanosine (m7G) are key RNA epigenetic modifications regulating gene expression.
  • The interplay between m6A and m7G in cancer development is not well understood.

Purpose of the Study:

  • To investigate the role of m6A methyltransferase METTL3-mediated METTL1 in head and neck squamous cell carcinoma (HNSC).
  • To elucidate the mechanism by which METTL1 influences cancer cell proliferation through crosstalk with m7G modification.

Main Methods:

  • Database mining (GEPIA) to analyze METTL1 expression and clinical correlation.
  • Investigating the m6A-mediated regulation of METTL1 by METTL3.
  • Assessing the functional impact of METTL1 and CDK4 on HNSC cell proliferation and cell cycle.
  • Analyzing the m7G modification of CDK4 by METTL1.

Main Results:

  • METTL1 is upregulated in various cancers, including HNSC, and correlates with poor patient outcomes.
  • METTL3 enhances METTL1 expression in HNSC via m6A modification.
  • METTL1 promotes HNSC cell proliferation and cell cycle progression by stabilizing CDK4 through m7G modification.
  • Overexpression of CDK4 mitigates the inhibitory effects of METTL1 knockdown on cancer cell proliferation.

Conclusions:

  • The METTL1/CDK4 axis plays a crucial role in HNSC tumorigenesis.
  • This study reveals a novel crosstalk mechanism between m6A and m7G modifications in cancer.
  • The METTL1/CDK4 pathway represents a potential therapeutic target for HNSC and other digestive system tumors.
Keywords:
METTL1METTL3N6-methyladenosineN7-methylguanosinecancer proliferation

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