ArticleOncogene2016
IMP3 promotes stem-like properties in triple-negative breast cancer by regulating SLUG.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
44 citing papers in PubMed, 85 citations in OpenAlex.
- A positive feedback loop between Periostin and TGFβ1 induces and maintains the stemness of hepatocellular carcinoma cells via AP-2α activation.Journal of experimental & clinical cancer research : CR · 2021Trial
- Targeting IGF2BP3 in Cancer: From Molecular Structure and Biology to Early Drug Discovery.International journal of molecular sciences · 2026Review
- Combinatorial inhibition of IGF2BP3-regulated receptor tyrosine kinases offers a new therapeutic strategy for triple-negative breast cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- The role of pluripotency regulators in triple-negative breast cancer immune response.Frontiers in genetics · 2026Review
- Regulation of Energy Metabolism and Lipid Metabolites by IMP3 in Cervical Cancer.Current issues in molecular biology · 2025Article
- Deciphering the crucial role of IGF2BP3 in modulating stemness traits of salivary adenoid cystic carcinoma.Medical oncology (Northwood, London, England) · 2025Article
- Exosomal circSIPA1L3-mediated intercellular communication contributes to glucose metabolic reprogramming and progression of triple negative breast cancer.Molecular cancer · 2024Article
- NRF2 activation by cysteine as a survival mechanism for triple-negative breast cancer cells.Oncogene · 2024Article
- Hepatic Snai1 and Snai2 promote liver regeneration and suppress liver fibrosis in mice.Cell reports · 2024Article
- IGF2BPs as novel mGenes & diseases · 2024Review
- Atractylodes macrocephala III suppresses EMT in cervical cancer by regulating IGF2BP3 through ETV5.Journal of cellular and molecular medicine · 2024Article
- IGF2BP3 as a Prognostic Biomarker in Well-Differentiated/Dedifferentiated Liposarcoma.Cancers · 2023Article
- IGF2BP3 mediates the mRNA degradation of NF1 to promote triple-negative breast cancer progression via an m6A-dependent manner.Clinical and translational medicine · 2023Article
- Targeting IGF2BP3 in Cancer.International journal of molecular sciences · 2023Review
- Regulatory mechanisms and therapeutic implications of insulin-like growth factor 2 mRNA-binding proteins, the emerging crucial mTheranostics · 2023Review
- Review
- The Contributions of Cancer-Testis and Developmental Genes to the Pathogenesis of Keratinocyte Carcinomas.Cancers · 2022Review
- Research progress on RNA-binding proteins in breast cancer.Oncology letters · 2022Review
- METTL3/IGF2BP3 axis inhibits tumor immune surveillance by upregulating NMolecular cancer · 2022Article
- A pan-cancer landscape of IGF2BPs and their association with prognosis, stemness and tumor immune microenvironment.Frontiers in oncology · 2022Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
IMP3 (insulin-like growth factor-2 mRNA binding protein 3) is an oncofetal protein whose expression is prognostic for poor outcome in several cancers. Although IMP3 is expressed preferentially in triple-negative breast cancer (TNBC), its function is poorly understood. We observed that IMP3 expression is significantly higher in tumor initiating than in non-tumor initiating breast cancer cells and we demonstrate that IMP3 contributes to self-renewal and tumor initiation, properties associated with cancer stem cells (CSCs). The mechanism by which IMP3 contributes to this phenotype involves its ability to induce the stem cell factor SOX2. IMP3 does not interact with SOX2 mRNA significantly or regulate SOX2 expression directly. We discovered that IMP3 binds avidly to SNAI2 (SLUG) mRNA and regulates its expression by binding to the 5' UTR. This finding is significant because SLUG has been implicated in breast CSCs and TNBC. Moreover, we show that SOX2 is a transcriptional target of SLUG. These data establish a novel mechanism of breast tumor initiation involving IMP3 and they provide a rationale for its association with aggressive disease and poor outcome.
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What OpenQuestion holds
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.