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IGF2BP3-TRIM37-P53 axis promotes tumor progression in LUAD.

Ting Ji1, Tingting Zhao1, Shuni Wang2

  • 1Ningxia Key Laboratory of Clinical and Pathogenic Microorganisms, Institute of Medical Science, General Hospital of Ningxia Medical University, Yinchuan 750004, Ningxia, China; Department of Respiratory and Critical Care Medicine, General Hospital of Ningxia Medical University, Yinchuan 750004, Ningxia, China.

Cellular Signalling
|March 14, 2026
PubMed
Summary

Insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) promotes lung adenocarcinoma (LUAD) by stabilizing TRIM37 mRNA, leading to p53 protein degradation. Silencing TRIM37 inhibits LUAD progression, offering a therapeutic target.

Keywords:
IGF2BP3LUADTRIM37m6A modificationp53

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Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • N6-methyladenosine (m6A) and ubiquitination modifications are key drivers of lung adenocarcinoma (LUAD) progression.
  • These modifications are closely linked to cellular context, including p53 status.
  • Understanding how these modifications regulate p53 in LUAD is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the role of IGF2BP3, a key m6A regulator, in LUAD pathogenesis.
  • To elucidate the mechanism by which IGF2BP3 influences p53 status and LUAD progression.
  • To identify potential therapeutic targets for LUAD based on the IGF2BP3-TRIM37-p53 axis.

Main Methods:

  • Utilized TCGA data to screen for IGF2BP3 and evaluate its expression and survival association in LUAD.
  • Performed colony formation and CCK8 assays to assess IGF2BP3's impact on cell proliferation.
  • Employed bioinformatics analysis of GEO data to identify TRIM37 as a downstream target of IGF2BP3.
  • Confirmed m6A enrichment of TRIM37 mRNA by IGF2BP3 using RIP-qPCR.
  • Validated the pro-tumor effects of IGF2BP3 in vitro and in vivo.

Main Results:

  • IGF2BP3 was found to be highly expressed in LUAD, correlating with poor patient prognosis.
  • IGF2BP3 was identified as an m6A reader that binds to the 3'UTR of TRIM37 mRNA, stabilizing its expression.
  • TRIM37 was shown to promote p53 protein degradation via ubiquitination.
  • Silencing TRIM37 effectively reversed the tumor-promoting effects of IGF2BP3 in both in vitro and in vivo models.

Conclusions:

  • IGF2BP3 promotes LUAD cell proliferation by acting as an m6A reader.
  • Mechanistically, IGF2BP3 facilitates p53 ubiquitination and degradation by binding to m6A-modified TRIM37 mRNA, thus driving LUAD tumorigenesis.
  • Targeting TRIM37 (shTRIM37) significantly inhibited IGF2BP3-driven tumor progression, highlighting its therapeutic potential.