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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.
Background:
m6A and ubiquitination modifications critically drive lung adenocarcinoma (LUAD) progression and are closely linked to cellular context-such as p53 status. Thus, elucidating how these modifications regulate p53's role in LUAD pathogenesis is vital for targeted therapy.
Methods:
TCGA was used to screen for IGF2BP3, a key m6A regulator in LUAD, and its survival and differential expression were evaluated. Colony formation and CCK8 assays were used to assess the effects of IGF2BP3 on cell proliferation. TRIM37 was identified as a downstream target of IGF2BP3 using the Gene Expression Omnibus (GEO) database for bioinformatics analysis. RIP-qPCR experiments confirmed m6a enrichment of TRIM37 mRNA by IGF2BP3. The pro-tumor effects of IGF2BP3 were validated both in vivo and in vitro.
Results:
IGF2BP3 was highly expressed in lung adenocarcinoma (LUAD) and associated with poor patient prognosis. IGF2BP3 recognizes the m6A modification site in the 3'UTR of TRIM37 mRNA, stabilizing its expression. TRIM37 promotes p53 protein degradation through ubiquitination. Silencing TRIM37 reversed IGF2BP3-driven LUAD progression in vivo and in vitro.
Conclusion:
Here, we found that IGF2BP3, acting as an m6A reader, promotes LUAD cell proliferation both in vivo and in vitro. Mechanistically, IGF2BP3 mediates the ubiquitination and degradation of p53 by reading the m6A-modified TRIM37 mRNA 3'UTR, thereby promoting tumorigenesis in LUAD. Importantly, shTRIM37 significantly inhibited IGF2BP3-driven tumor progression.
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