ArticleOncogene2012
Regulation of IMP3 by EGFR signaling and repression by ERβ: implications for triple-negative breast cancer.
Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 102 citations in OpenAlex.
- Targeting IGF2BP3 in Cancer: From Molecular Structure and Biology to Early Drug Discovery.International journal of molecular sciences · 2026Review
- Estrogen receptor β target gene expression reveals novel repressive functions in aggressive breast cancer.NPJ breast cancer · 2026Article
- Estrogenic control of matrix metalloproteinases: a perspective on breast tumor invasion and metastasis.Molecular biology reports · 2025Review
- Altered ribosomal profile in acquired resistance and reversal associates with pathological response to chemotherapy in inflammatory breast cancer.NPJ breast cancer · 2024Article
- Estrogen Signals through ERβ in Breast Cancer; What We Have Learned since the Discovery of the Receptor.Receptors (Basel, Switzerland) · 2024Article
- IGF2BPs as novel mGenes & diseases · 2024Review
- A circular RNA activated by TGFβ promotes tumor metastasis through enhancing IGF2BP3-mediated PDPN mRNA stability.Nature communications · 2023Article
- Parkin regulates IGF2BP3 through ubiquitination in the tumourigenesis of cervical cancer.Clinical and translational medicine · 2023Article
- IGF2BP3 promotes the progression of colorectal cancer and mediates cetuximab resistance by stabilizing EGFR mRNA in an mCell death & disease · 2023Article
- Targeting IGF2BP3 in Cancer.International journal of molecular sciences · 2023Review
- Targeting CXCL16 and STAT1 augments immune checkpoint blockade therapy in triple-negative breast cancer.Nature communications · 2023Article
- Divergent features of ERβ isoforms in triple negative breast cancer: progress and implications for further research.Frontiers in cell and developmental biology · 2023Review
- Lipidomic and Membrane Mechanical Signatures in Triple-Negative Breast Cancer: Scope for Membrane-Based Theranostics.Molecular and cellular biochemistry · 2022Review
- Research progress on RNA-binding proteins in breast cancer.Oncology letters · 2022Review
- Chemotherapy and Physical Therapeutics Modulate Antigens on Cancer Cells.Frontiers in immunology · 2022Review
- Circular RNA circ-TNPO3 suppresses metastasis of GC by acting as a protein decoy for IGF2BP3 to regulate the expression of MYC and SNAIL.Molecular therapy. Nucleic acids · 2021Article
- The biological function of IGF2BPs and their role in tumorigenesis.Investigational new drugs · 2021Review
- The emerging role of RNA N6-methyladenosine methylation in breast cancer.Biomarker research · 2021Review
- Estrogen Receptor β-Mediated Inhibition of Actin-Based Cell Migration Suppresses Metastasis of Inflammatory Breast Cancer.Cancer research · 2021Article
- Estrogen receptor β and treatment with a phytoestrogen are associated with inhibition of nuclear translocation of EGFR in the prostate.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Insulin-like growth factor II (IGF-II) mRNA-binding protein 3 (IMP3) is emerging as a useful indicator of the progression and outcome of several cancers. IMP3 expression is associated with triple-negative breast carcinomas (TNBCs), which are aggressive tumors associated with poor outcome. In this study, we addressed the hypothesis that signaling pathways, which are characteristic of TNBCs, impact the expression of IMP3 and that IMP3 contributes to the function of TNBCs. The data obtained reveal that IMP3 expression is repressed specifically by estrogen receptor β (ERβ) and its ligand 3βA-diol but not by ERα. Epidermal growth factor receptor (EGFR) signaling and consequent activation of the mitogen-activated protein kinase pathway induce IMP3 transcription and expression. Interestingly, we discovered that the EGFR promoter contains an imperfect estrogen response element and that ERβ represses EGFR transcription. These data support a mechanism in which ERβ inhibits IMP3 expression indirectly by repressing the EGFR. This mechanism relates to the biology of TNBC, which is characterized by diminished ERβ and increased EGFR expression. We also demonstrate that IMP3 contributes to the migration and invasion of breast carcinoma cells. Given that IMP3 is an mRNA-binding protein, we determined that it binds several key mRNAs that could contribute to migration and invasion, including CD164 (endolyn) and MMP9. Moreover, expression of these mRNAs is repressed by ERβ and enhanced by EGFR signaling, consistent with our proposed mechanism for the regulation of IMP3 expression in breast cancer cells. Our findings show that IMP3 is an effector of EGFR-mediated migration and invasion and they provide the first indication of how this important mRNA-binding protein is regulated in cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.