ArticleThe Journal of clinical investigation2023
Multiomic screening of invasive GBM cells reveals targetable transsulfuration pathway alterations.
Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 31 citations in OpenAlex.
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- Heterogeneity, Measurement, and Clinical Implications of Oxygenation, Cell Signaling, and Redox Biology in Glioblastoma and Adult Diffuse Gliomas, with Context from Other Brain Tumors.Antioxidants (Basel, Switzerland) · 2026Review
- Dissecting the aberrant vasculature of glioblastoma: mechanisms and therapeutic targets.Cancer metastasis reviews · 2026Review
- Targeting Metabolic Vulnerabilities in Glioblastoma: a Framework for Multi-node Combination Therapy.Current oncology reports · 2026Review
- Hijacking the Hydrogen Sulfide Axis: A Novel 4-Trifluoromethylquinoline Derivative Suppresses Glioblastoma via Cystathionine γ-Lyase Suppression.Journal of medicinal chemistry · 2026Article
- Systemic cyst(e)inase administration induces ferroptosis and synergizes with temozolomide in glioblastoma.iScience · 2026Article
- Glutamate Drives Glioblastoma Invasion in Three-Dimensional Hyaluronic Acid Hydrogels.Tissue engineering. Part A · 2026Article
- Defining treatment-resistant brain cancer: Genetic screening to identify oncogene-driven immunomodulation and therapy resistance.Cancer gene therapy · 2026Review
- Bioinformatic analysis of metastasis-associated metabolic landscape reveals an oncogenic role for the transsulfuration pathway.Bioinformatics advances · 2026Article
- CAF-derived exosomes: orchestrators of dysregulated signaling pathways in breast cancer progression.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Single cell spatial profiling of the matrisome identifies region-specific adhesion and signaling networks in glioblastoma.Communications biology · 2025Article
- Bioenergetic responses to β-adrenergic stimulation in beige adipocyte depend on actomyosin driven forces.bioRxiv : the preprint server for biology · 2025Article
- Targeting macro- and micro-nutrient regulation of HNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Hyaluronic acid-based models of the brain microenvironment: Challenges and advances.Current opinion in biomedical engineering · 2025Article
- Suppression of cofilin-1 promotes invasion in 3D hyaluronic acid matrices by promoting actin-based protrusions.Molecular biology of the cell · 2025Article
- Article
- From Biomarker Discovery to Clinical Applications of Metabolomics in Glioblastoma.Metabolites · 2025Review
- The interplay of mitochondrial dysfunction and altered metabolic pathways in glioblastoma.Contemporary oncology (Poznan, Poland) · 2025Review
- A reactive oxygen species-related signature predicts the prognosis and immunosuppressive microenvironment in gliomas.Redox report : communications in free radical research · 2024Article
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
While the poor prognosis of glioblastoma arises from the invasion of a subset of tumor cells, little is known of the metabolic alterations within these cells that fuel invasion. We integrated spatially addressable hydrogel biomaterial platforms, patient site-directed biopsies, and multiomics analyses to define metabolic drivers of invasive glioblastoma cells. Metabolomics and lipidomics revealed elevations in the redox buffers cystathionine, hexosylceramides, and glucosyl ceramides in the invasive front of both hydrogel-cultured tumors and patient site-directed biopsies, with immunofluorescence indicating elevated reactive oxygen species (ROS) markers in invasive cells. Transcriptomics confirmed upregulation of ROS-producing and response genes at the invasive front in both hydrogel models and patient tumors. Among oncologic ROS, H2O2 specifically promoted glioblastoma invasion in 3D hydrogel spheroid cultures. A CRISPR metabolic gene screen revealed cystathionine γ-lyase (CTH), which converts cystathionine to the nonessential amino acid cysteine in the transsulfuration pathway, to be essential for glioblastoma invasion. Correspondingly, supplementing CTH knockdown cells with exogenous cysteine rescued invasion. Pharmacologic CTH inhibition suppressed glioblastoma invasion, while CTH knockdown slowed glioblastoma invasion in vivo. Our studies highlight the importance of ROS metabolism in invasive glioblastoma cells and support further exploration of the transsulfuration pathway as a mechanistic and 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.