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METTL3-mediated the m6A modification of SF3B4 facilitates the development of non-small cell lung cancer by enhancing

Guangsi He1,2, Kangsheng Gu1, Jie Wei3

  • 1Department of Oncology, the First Affiliated Hospital of Anhui Medical University, Hefei, China.

Thoracic Cancer
|March 11, 2024
PubMed
Abstract

Insights

Methyltransferase-like 3 (METTL3) stabilizes Splicing factor B subunit 4 (SF3B4), promoting non-small cell lung cancer (NSCLC) growth and metastasis. Targeting this pathway may offer new therapeutic strategies for NSCLC.

Area of Science:

  • Molecular Oncology
  • Cancer Biology
  • Epigenetics

Background:

  • Splicing factor B subunit 4 (SF3B4) is implicated in various cancers.
  • SF3B4 is a potential therapeutic target for non-small cell lung cancer (NSCLC).
  • The precise role and molecular mechanisms of SF3B4 in NSCLC require further investigation.

Purpose of the Study:

  • To elucidate the role and molecular mechanism of SF3B4 in NSCLC progression.
  • To investigate the interaction between SF3B4, METTL3, and LSM4 in NSCLC.

Main Methods:

  • Quantitative real-time PCR and western blot for SF3B4, LSM4, and METTL3 expression.
  • Functional assays including proliferation, apoptosis, invasion, migration, and stemness.
  • RNA immunoprecipitation (MeRIP, RIP, Co-IP) and mice xenograft models.

Main Results:

  • SF3B4 is highly expressed in NSCLC and correlates with poor survival.
  • SF3B4 knockdown inhibits NSCLC cell proliferation, invasion, migration, and stemness, while inducing apoptosis.
  • METTL3 enhances SF3B4 mRNA stability via m6A modification, promoting NSCLC progression; SF3B4 interacts with LSM4.

Conclusions:

  • METTL3-stabilized SF3B4 promotes NSCLC cell growth, metastasis, and stemness.
  • This promotion is mediated through the positive regulation of LSM4.
  • The METTL3-SF3B4-LSM4 axis represents a potential therapeutic target for NSCLC.
Keywords:
LSM4METTL3SF3B4non‐small cell lung cancer

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