ArticleCancer science2023
Feedforward loop between IMP1 and YAP/TAZ promotes tumorigenesis and malignant progression in glioblastoma.
Article in Cancer science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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
18 citing papers in PubMed, 0 citations in OpenAlex.
- Overcoming IGF1R-mediated resistance to oncolytic HSV1 and radiotherapy via triple combination therapy.Cell death & disease · 2026Article
- Circulating placental small extracellular vesicles miR-2110 depletion drives maternal-fetal endothelial injury in preeclampsia.Cell communication and signaling : CCS · 2026Article
- Arylsulfatase D promotes malignant phenotypes in glioblastoma cells and is linked to altered Hippo pathway phosphorylation.Frontiers in oncology · 2026Article
- Extracellular matrix stiffness conditions glioblastoma cells for long-term migration: Mechanical memory as a driver of invasion and recurrence in glioblastoma.Neuro-oncology · 2026Review
- Overcoming IGF1R-Mediated Resistance to Oncolytic HSV1 and Radiotherapy via Triple Combination Therapy.Research square · 2025Article
- Imp1 acts as a dosage- and stage-dependent temporal rheostat orchestrating radial glial fate transitions and cortical morphogenesis.bioRxiv : the preprint server for biology · 2025Article
- Phenotypic variations in glioma stem cells: regulatory mechanisms and implications for therapeutic strategies.Journal of translational medicine · 2025Review
- β-adrenergic receptor inhibits heart regeneration by downregulating Yap m6A modification.Cell death & disease · 2025Article
- The IGF2BP1 oncogene is a druggable mNAR cancer · 2025Article
- YAP/TAZ-associated cell signaling - at the crossroads of cancer and neurodevelopmental disorders.Frontiers in cell and developmental biology · 2025Review
- Targeting Hippo-YAP/TAZ signaling pathway: an updated review demonstrating the therapeutic potential of key plant derived anticancer compounds.Frontiers in pharmacology · 2025Review
- Insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) in hematological diseases.Molecular medicine (Cambridge, Mass.) · 2024Review
- Comprehensive understanding of glioblastoma molecular phenotypes: classification, characteristics, and transition.Cancer biology & medicine · 2024Review
- STAT3-mediated up-regulation of DAB2 via SRC-YAP1 signaling axis promotes Helicobacter pylori-driven gastric tumorigenesis.Biomarker research · 2024Article
- Emerging Roles and Mechanisms of RNA Modifications in Neurodegenerative Diseases and Glioma.Cells · 2024Review
- Article
- Feedforward loop between IMP1 and YAP/TAZ promotes tumorigenesis and malignant progression in glioblastoma.Cancer science · 2023Article
- Regulatory mechanisms and therapeutic implications of insulin-like growth factor 2 mRNA-binding proteins, the emerging crucial mTheranostics · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
YAP/TAZ have been identified as master regulators in malignant phenotypes of glioblastoma (GBM); however, YAP/TAZ transcriptional disruptor in GBM treatment remains ineffective. Whether post-transcriptional dysregulation of YAP/TAZ improves GBM outcome is currently unknown. Here, we report that insulin-like growth factor 2 (IGF2) mRNA-binding protein 1 (IGF2BP1 or IMP1) is upregulated in mesenchymal GBM compared with proneural GBM and correlates with worse patient outcome. Overexpression of IMP1 in proneural glioma stem-like cells (GSCs) promotes while IMP1 knockdown in mesenchymal GSCs attenuates tumorigenesis and mesenchymal signatures. IMP1 binds to and stabilizes m6A-YAP mRNA, leading to activation of YAP/TAZ signaling, depending on its m6A recognition and binding domain. On the other hand, TAZ functions as enhancer for IMP1 expression. Collectively, our data reveal a feedforward loop between IMP1 and YAP/TAZ maintaining GBM/GSC tumorigenesis and malignant progression and a promising molecular target in GBM.
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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.