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The human 18S rRNA m6A methyltransferase METTL5 promotes tumorigenesis via DEPDC1 in lung squamous cell carcinoma

  • 0Department of Cardiothoracic Surgery, Gaoxin Branch of The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.
Frontiers in Oncology +

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February 28, 2025

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February 28, 2025

View abstract on PubMed

Summary

This summary is machine-generated.

The N6-methyladenosine (m6A) methyltransferase METTL5 promotes lung squamous cell carcinoma (LUSC) by enhancing DEPDC1 translation. METTL5 is a risk factor and therapeutic target for LUSC.

Area Of Science

  • Oncology
  • Molecular Biology
  • Epigenetics

Background

  • N6-Methyladenosine (m6A) modifications are crucial in lung squamous cell carcinoma (LUSC) development.
  • The role of ribosomal RNA (rRNA) modifications in LUSC remains largely unknown.
  • Abnormal m6A is linked to cancer initiation, progression, and metastasis in LUSC.

Purpose Of The Study

  • To identify key m6A regulators in LUSC.
  • To elucidate the role of METTL5 in LUSC tumorigenesis.
  • To investigate the molecular mechanism of METTL5 in LUSC.

Main Methods

  • High-throughput library screening identified METTL5 as a key m6A regulator in LUSC.
  • Cell and animal experiments were conducted to assess METTL5's function.
  • Mechanistic studies focused on METTL5's role in DEPDC1 translation via m6A modification.

Main Results

  • METTL5 was identified as an independent risk factor for LUSC, associated with poor patient prognosis.
  • Overexpression of METTL5 promoted LUSC tumorigenesis through m6A modification.
  • METTL5 knockdown inhibited tumor cell proliferation and migration <i>in vitro</i> and <i>in vivo</i>.
  • METTL5 enhances DEPDC1 translation via m6A modification, promoting LUSC tumorigenesis.

Conclusions

  • METTL5 enhances DEPDC1 translation, contributing to LUSC tumorigenesis and poor prognosis.
  • METTL5 serves as a potential prognostic biomarker for LUSC.
  • METTL5 represents a potential therapeutic target for LUSC treatment.

Keywords:

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