ArticleNature communications2023
IGFBP5 is an ROR1 ligand promoting glioblastoma invasion via ROR1/HER2-CREB signaling axis.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 44 citations in OpenAlex.
- miR-203 improves pressure overload-induced heart failure by targeting the IGFBP5/PI3K/AKT axis.Acta pharmacologica Sinica · 2026Article
- Insulin-like growth factor receptor signaling in physiology and disease.Signal transduction and targeted therapy · 2026Review
- Mechanisms and Manifestations of Ligand Bias in Signaling: Focus on Receptor Tyrosine Kinases.Chemical reviews · 2026Review
- PTBP1 knockdown reprograms glioma stem cells into neuronal-like cells and suppresses tumorigenesis via the DUSP5-ERK1/2 signaling pathway.Neuro-oncology · 2026Article
- Symbiotic exclusivity between CLOCK and TFPI2 drives stemness and immunosuppression in glioblastoma models.The Journal of clinical investigation · 2026Article
- Modeling blood-brain barrier-glioblastoma interactions: implications for chemoresistance and therapeutic targeting.Fluids and barriers of the CNS · 2026Review
- IGFBP in tumor immunity: a novel target for cancer immunotherapy.Journal of translational medicine · 2026Review
- IGFBP5 Restores Endometrial Receptivity and Rescues Implantation Failure in Polycystic Ovary Syndrome.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Multi-omics data reveal B cell regulated immune heterogeneity of MIF signaling pathway in uveal melanoma.Cancer cell international · 2026Article
- Two-dimensional NIR-II AIE nanotheranostic probes with ultralarge Stokes shifts for surgical navigation and ablation of glioma.Science advances · 2026Article
- Disruption of the NDC80-Nek2 axis suppresses glioblastoma stemness and enhances therapeutic efficacy.Journal of translational medicine · 2026Article
- Targeting MGAT4A-Mediated N-Glycosylation as a Therapeutic Strategy to Inhibit Glioblastoma Stem Cell Invasion.Exploration (Beijing, China) · 2026Article
- Spatially varying gene regulation network inference from spatial transcriptomics.Bioinformatics advances · 2026Article
- Inhibition of ICAM1 diminishes stemness and enhances antitumor immunity in glioblastoma via β-catenin/PD-L1 signaling.Nature communications · 2025Article
- Characterization of the extrinsic and intrinsic signatures and therapeutic vulnerability of small cell lung cancers.Signal transduction and targeted therapy · 2025Article
- Preadipocyte-induced upregulation of IGFBP5 enhances ovarian cancer tumorigenesis via CREB signaling.iScience · 2025Article
- The Role of Receptor Tyrosine Kinase-like Orphan Receptor 1 (ROR1) in Cancer Stem Cell Signaling.International journal of molecular sciences · 2025Review
- Regional profiling reveals a distinct glioblastoma infiltrative margin proteome.Scientific reports · 2025Article
- Single-Cell Analysis Clarifies Pathological Heterogeneity in Tenosynovial Giant Cell Tumor and Identifies Biomarkers for Predicting Disease Recurrence.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Identification of dynamic network biomarkerMolecular therapy. Oncology · 2025Article
Corrections and comments
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Authors and funding
23 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diffuse infiltration is the main reason for therapeutic resistance and recurrence in glioblastoma (GBM). However, potential targeted therapies for GBM stem-like cell (GSC) which is responsible for GBM invasion are limited. Herein, we report Insulin-like Growth Factor-Binding Protein 5 (IGFBP5) is a ligand for Receptor tyrosine kinase like Orphan Receptor 1 (ROR1), as a promising target for GSC invasion. Using a GSC-derived brain tumor model, GSCs were characterized into invasive or non-invasive subtypes, and RNA sequencing analysis revealed that IGFBP5 was differentially expressed between these two subtypes. GSC invasion capacity was inhibited by IGFBP5 knockdown and enhanced by IGFBP5 overexpression both in vitro and in vivo, particularly in a patient-derived xenograft model. IGFBP5 binds to ROR1 and facilitates ROR1/HER2 heterodimer formation, followed by inducing CREB-mediated ETV5 and FBXW9 expression, thereby promoting GSC invasion and tumorigenesis. Importantly, using a tumor-specific targeting and penetrating nanocapsule-mediated delivery of CRISPR/Cas9-based IGFBP5 gene editing significantly suppressed GSC invasion and downstream gene expression, and prolonged the survival of orthotopic tumor-bearing mice. Collectively, our data reveal that IGFBP5-ROR1/HER2-CREB signaling axis as a potential GBM therapeutic target.
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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.