ArticleCancer letters2023
A complex of Wnt/planar cell polarity signaling components Vangl1 and Fzd7 drives glioblastoma multiforme malignant properties.
Article in Cancer letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
The trial behind it
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
16 citing papers in PubMed, 14 citations in OpenAlex.
- Phosphorylated HPV‑16 E7 disrupts planar cell polarity in cervical cancer cells through vangl1 dysregulation.PLoS pathogens · 2026Article
- Epigenetic Silencing of miR-124 Drives KITENIN Activation in Colorectal Cancer.Biomolecules & therapeutics · 2026Article
- Role of epithelial-mesenchymal transition (EMT) in malignancies: current status and future prospects.Signal transduction and targeted therapy · 2026Review
- Targeting frizzled receptors (FZDs) for anti-tumor therapy: From orthosteric to allosteric inhibition.Acta pharmaceutica Sinica. B · 2026Review
- Targeting KITENIN signaling in cancer progression and therapeutic resistance: mechanistic insights and future directions.Cancer cell international · 2026Review
- GPCR signaling systems facilitate precision interventions for multi-oncology therapy.Frontiers in systems biology · 2026Review
- VANGL1 links angiogenesis-stemness programs and tumor microenvironment remodeling: a pan-cancer, multi-omics study with translational validation.Frontiers in oncology · 2026Article
- LINC00888 Promotes Gastric Cancer Growth and Metastasis by Sponging miR-145-5p to Regulate FZD7 Expression.Combinatorial chemistry & high throughput screening · 2026Article
- Tracing the enteric neural crest cell pathway from origin to colonization: insights into Hirschsprung's disease.Molecular biology reports · 2025Review
- WNT signaling in cancer: molecular mechanisms and potential therapies.Molecular biomedicine · 2025Review
- Key genes altered in glioblastoma based on bioinformatics (Review).Oncology letters · 2025Review
- Wnt signaling pathways in biology and disease: mechanisms and therapeutic advances.Signal transduction and targeted therapy · 2025Review
- Chrysophanol inhibits of colorectal cancer cell motility and energy metabolism by targeting the KITENIN/ErbB4 oncogenic complex.Cancer cell international · 2024Article
- Unveiling cancer dormancy: Intrinsic mechanisms and extrinsic forces.Cancer letters · 2024Review
- The Physiological Function of nNOS-Associated CAPON Proteins and the Roles of CAPON in Diseases.International journal of molecular sciences · 2023Review
- Nuclear and membrane-bound hormone receptors in glioblastoma: Expression, functionality, and therapeutic implications.Neuro-oncology advancesReview
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Targeting common oncogenic drivers of glioblastoma multiforme (GBM) in patients has remained largely ineffective, raising the possibility that alternative pathways may contribute to tumor aggressiveness. Here we demonstrate that Vangl1 and Fzd7, components of the non-canonical Wnt planar cell polarity (Wnt/PCP) signaling pathway, promote GBM malignancy by driving cellular proliferation, migration, and invasiveness, and engage Rho GTPases to promote cytoskeletal rearrangements and actin dynamics in migrating GBM cells. Mechanistically, we uncover the existence of a novel Vangl1/Fzd7 complex at the leading edge of migrating GBM cells and propose that this complex is critical for the recruitment of downstream effectors to promote tumor progression. Moreover, we observe that depletion of FZD7 results in a striking suppression of tumor growth and latency and extends overall survival in an intracranial mouse xenograft model. Our observations support a novel mechanism by which Wnt/PCP components Vangl1 and Fzd7 form a complex at the leading edge of migratory GBM cells to engage downstream effectors that promote actin cytoskeletal rearrangements dynamics. Our findings suggest that interference with Wnt/PCP pathway function may offer a novel therapeutic strategy for patients diagnosed with GBM.
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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.