ArticleJournal of neuro-oncology2024
Inhibition of BMP signaling pathway induced senescence and calcification in anaplastic meningioma.
Article in Journal of neuro-oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 1 citations in OpenAlex.
- Immune-Enriched Versus Matrix-Remodeling Microenvironments in Psammoma Body-Rich and Psammoma Body-Poor WHO Grade I Meningiomas: An Exploratory Transcriptomic Study.Neuropathology : official journal of the Japanese Society of Neuropathology · 2026Article
- Extent of resection and adjuvant radiotherapy in intracranial anaplastic meningioma: improved disease control with no statistically significant overall survival benefit.Frontiers in surgery · 2026Article
- Targeting fibroblasts in pathological bone formation: mechanisms and treatments.Frontiers in cell and developmental biology · 2025Review
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
purposeMeningiomas are the most common type of brain tumors and are generally benign, but malignant atypical meningiomas and anaplastic meningiomas frequently recur with poor prognosis. The metabolism of meningiomas is little known, so few effective treatment options other than surgery and radiation are available, and the targets for treatment of recurrence are not well defined. The Aim of this paper is to find the therapeutic target.
methodsThe effects of bone morphogenetic protein (BMP) signal inhibitor (K02288) and upstream regulator Gremlin2 (GREM2) on meningioma's growth and senescence were examined. In brief, we examined as follows: 1) Proliferation assay by inhibiting BMP signaling. 2) Comprehensive analysis of forced expression GREM2.3) Correlation between GREM2 mRNA expression and proliferation marker in 87 of our clinical samples. 4) Enrichment analysis between GREM2 high/low expressed groups using RNA-seq data (42 cases) from the public database GREIN. 5) Changes in metabolites and senescence markers associated with BMP signal suppression.
resultsInhibitors of BMP receptor (BMPR1A) and forced expression of GREM2 shifted tryptophan metabolism from kynurenine/quinolinic acid production to serotonin production in malignant meningiomas, reduced NAD + /NADH production, decreased gene cluster expression involved in oxidative phosphorylation, and caused decrease in ATP. Finally, malignant meningiomas underwent cellular senescence, decreased proliferation, and eventually formed psammoma bodies. Reanalyzed RNA-seq data of clinical samples obtained from GREIN showed that increased expression of GREM2 decreased the expression of genes involved in oxidative phosphorylation, similar to our experimental results.
conclusionsThe GREM2-BMPR1A-tryptophan metabolic pathway in meningiomas is a potential new therapeutic target.
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