ArticleEBioMedicine2019
Blockade of miR-3614 maturation by IGF2BP3 increases TRIM25 expression and promotes breast cancer cell proliferation.
Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 55 papers.
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55 citing papers in PubMed, 105 citations in OpenAlex.
- Prognostic implications of immune-related eight-gene signature in pediatric brain tumors.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021Trial
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- Targeting IGF2BP3 in Cancer: From Molecular Structure and Biology to Early Drug Discovery.International journal of molecular sciences · 2026Review
- Antiviral regulator TRIM25 as a prognostic marker of better survival in Merkel cell carcinoma: Association with MCPyV status.International journal of cancer · 2026Article
- IGF2BP3 remodels the microRNA targeting landscape in MLL-AF4 leukemia.bioRxiv : the preprint server for biology · 2025Article
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- hsa_circ_0007376 Promotes Gastric Cancer Proliferation and Malignant Metastasis by Enhancing the Stability of IGF2BP3.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2025Article
- Epigenetic regulation in female reproduction: the impact of m6A on maternal-fetal health.Cell death discovery · 2025Review
- The Emerging Role of IGF2BP2 in Cancer Therapy Resistance: From Molecular Mechanism to Future Potential.International journal of molecular sciences · 2024Review
- RBM8A, a new target of TEAD4, promotes breast cancer progression by regulating IGF1R and IRS-2.Journal of translational medicine · 2024Article
- Oncofetal IGF2BP3-mediated control of microRNA structural diversity in the malignancy of early-stage lung adenocarcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Functions and mechanisms of RNA mInternational journal of oncology · 2024Review
- IGF2BPs as novel mGenes & diseases · 2024Review
- TEMINET: A Co-Informative and Trustworthy Multi-Omics Integration Network for Diagnostic Prediction.International journal of molecular sciences · 2024Article
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- The multifaceted role of Fragile X-Related Protein 1 (FXR1) in cellular processes: an updated review on cancer and clinical applications.Cell death & disease · 2024Review
- IGF2BP3 promotes the progression of colorectal cancer and mediates cetuximab resistance by stabilizing EGFR mRNA in an mCell death & disease · 2023Article
- miR-4796 enhances the sensitivity of breast cancer cells to ionising radiation by impairing the DNA repair pathway.Breast cancer (Tokyo, Japan) · 2023Article
- CircGNB1 facilitates the malignant phenotype of GSCs by regulating miR-515-5p/miR-582-3p-XPR1 axis.Cancer cell international · 2023Article
- CircNFATC3 promotes the proliferation of gastric cancer through binding to IGF2BP3 and restricting its ubiquitination to enhance CCND1 mRNA stability.Journal of translational medicine · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe cross-talk between RNA binding proteins (RBPs) and microRNAs (miRNAs) in the regulation of gene expression is a complex process. Here, we describe a new mode of regulation of TRIM25 expression mediated by an antagonistic interplay between IGF2BP3 and miR-3614-3p.
methodsThe expression level of TRIM25, IGF2BP3, pri-miR-3614 and miR-3614-3p in breast cancer (BC) tissues, non-tumor tissues and BC cell lines were detected by qRT-PCR, Western blot and Immunohistochemistry (IHC). Binding of miR-3614-3p and IGF2BP3 to TRIM25 RNA was verified using luciferase activation assays, RNA immunoprecipitation (RIP) and biotin pull-down assays. In vitro and in vivo loss- and gain-of-function studies were performed to reveal the effects and related mechanism of IGF2BP3-miR-3614-3p-TRIM25 axis in in breast cancer cells proliferation.
findingsWe found that an intragenic miRNA-3614-3p inhibits the expression of its host gene TRIM25 by binding to its 3'- untranslated region (UTR). Interestingly, IGF2BP3 can competitively occupy this binding site and inhibit miRNA-3614 maturation, thereby protecting TRIM25 mRNA from miR-3614-mediated degradation. The overexpression of miR-3614-3p dramatically inhibited breast cancer cell growth through the downregulation of TRIM25. Furthermore, the silencing of IGF2BP3 reduced TRIM25 expression, suppressed cell proliferation, and exhibited a synergistic effect with miR-3614-3p overexpression.
interpretationCollectively, these results demonstrate that control of TRIM25 RNA by an interplay between IGF2BP3 and miR-3614-3p represents a mechanism for breast cancer cell proliferation. FUND: The scientific research and sharing platform construction project of Shaanxi Province, Opening Project of Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, China Postdoctoral Science Foundation and The National Natural Science Foundation of China.
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