ArticleOncogene2016
WIF1 re-expression in glioblastoma inhibits migration through attenuation of non-canonical WNT signaling by downregulating the lncRNA MALAT1.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.
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Who cites it
84 citing papers in PubMed, 1 synthesis or guideline pooled it, 135 citations in OpenAlex.
- RNA Expression Signatures in Glioblastoma: A Systematic Review of Tumour Biology and Therapeutic Targets.Oncology research · 2025Pooled it
- Machine Learning-Based Classification of Gliomas and Tumor Grades with SHAP-Guided Feature Interpretation.Genes · 2026Article
- Review
- Wnt signaling pathways in biology and disease: mechanisms and therapeutic advances.Signal transduction and targeted therapy · 2025Review
- Innovative perspectives on glioblastoma: the emerging role of long non-coding RNAs.Functional & integrative genomics · 2025Review
- Immunological features of various molecular subtypes of cervical cancer and their prognostic implications in the context of disulfidptosis.Frontiers in oncology · 2025Article
- Inorganic and hybrid nanomaterials for NIR-II fluorescence imaging-guided therapy of Glioblastoma and perspectives.Theranostics · 2025Review
- Practical immunomodulatory landscape of glioblastoma multiforme (GBM) therapy.Journal of the Egyptian National Cancer Institute · 2024Review
- Article
- Wnt/β-catenin signaling components and mechanisms in bone formation, homeostasis, and disease.Bone research · 2024Review
- Regulation of Follicular Development in Chickens:International journal of molecular sciences · 2024Article
- Immune-related lncRNAs signature and radiomics signature predict the prognosis and immune microenvironment of glioblastoma multiforme.Journal of translational medicine · 2024Article
- PLEK2: a potential biomarker for metastasis and prognostic evaluation in uveal melanoma.Frontiers in medicine · 2024Article
- Roles of lncRNA-MALAT1 in the Progression and Prognosis of Gliomas.Mini reviews in medicinal chemistry · 2024Review
- Epigenetic silencing of HTATIP2 in glioblastoma contributes to treatment resistance by enhancing nuclear translocation of the DNA repair protein MPG.Molecular oncology · 2023Article
- BET protein inhibition sensitizes glioblastoma cells to temozolomide treatment by attenuating MGMT expression.Cell death & disease · 2022Article
- Review
- Neuroprotective effects of long noncoding RNAs involved in ischemic postconditioning after ischemic stroke.Neural regeneration research · 2022Article
- Review
- Mesenchymal stem cells-derived exosomes for drug delivery.Stem cell research & therapy · 2021Review
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma is the most aggressive primary brain tumor in adults and due to the invasive nature cannot be completely removed. The WNT inhibitory factor 1 (WIF1), a secreted inhibitor of WNTs, is systematically downregulated in glioblastoma and acts as strong tumor suppressor. The aim of this study was the dissection of WIF1-associated tumor-suppressing effects mediated by canonical and non-canonical WNT signaling. We found that WIF1 besides inhibiting the canonical WNT pathway selectively downregulates the WNT/calcium pathway associated with significant reduction of p38-MAPK (p38-mitogen-activated protein kinase) phosphorylation. Knockdown of WNT5A, the only WNT ligand overexpressed in glioblastoma, phenocopied this inhibitory effect. WIF1 expression inhibited cell migration in vitro and in an orthotopic brain tumor model, in accordance with the known regulatory function of the WNT/Ca(2+) pathway on migration and invasion. In search of a mediator for this function differential gene expression profiles of WIF1-expressing cells were performed. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a long non-coding RNA and key positive regulator of invasion, emerged as the top downregulated gene. Indeed, knockdown of MALAT1 reduced migration in glioblastoma cells, without effect on proliferation. Hence, loss of WIF1 enhances the migratory potential of glioblastoma through WNT5A that activates the WNT/Ca(2+) pathway and MALAT1. These data suggest the involvement of canonical and non-canonical WNT pathways in glioblastoma promoting key features associated with this deadly disease, proliferation on one hand and invasion on the other. Successful targeting will require a dual strategy affecting both canonical and non-canonical WNT pathways.
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