ArticleActa pharmacologica Sinica2023
Involvement of cell shape and lipid metabolism in glioblastoma resistance to temozolomide.
Article in Acta pharmacologica Sinica, 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, 42 citations in OpenAlex.
- Label-Free Raman Spectroscopy Reveals Metabolic Signatures Associated with MGMT Promoter Methylation Status in Glioblastoma.Analytical chemistry · 2026Article
- SOAT1 expression associates with prognosis, immune environment and biochemical indicators in glioma.Discover oncology · 2026Article
- Cryogenic Electron Microscopy of Extracellular Vesicles from Temozolomide-Treated Glioblastoma Cells Reveals Great Morphological Heterogeneity.Nanomaterials (Basel, Switzerland) · 2026Article
- UCHL1 promotes temozolomide resistance in glioblastoma by inhibiting the ubiquitination-mediated degradation of keratin 8.Translational oncology · 2026Article
- GPR40 Attenuates Glioma TMZ-Resistance Through Ferroptosis Inhibition.Neurochemical research · 2026Article
- The Natural Triterpenoid Alisol B Overcomes Temozolomide Resistance in Glioblastoma Through Multi-Target Mechanisms: Coordinated Epigenetic, Metabolic, and Cell-Cycle Reprogramming.International journal of molecular sciences · 2026Article
- Targeting metabolic mechanisms to overcome temozolomide resistance in glioblastoma.Discover oncology · 2026Review
- Live Metabolomics with NMR.Analytical chemistry · 2026Review
- Defining treatment-resistant brain cancer: Genetic screening to identify oncogene-driven immunomodulation and therapy resistance.Cancer gene therapy · 2026Review
- Lipid metabolic plasticity in glioblastoma: mechanisms, tumor microenvironment remodeling, and therapeutic opportunities.Frontiers in oncology · 2026Review
- Review
- Lipids: Driving Forces in the Underlying Biology of Carcinogenesis.ACS pharmacology & translational science · 2025Review
- Investigating potential drug targets for the treatment of glioblastoma: a Mendelian randomization study.BMC cancer · 2025Article
- Utilization of nanotechnology to surmount the blood-brain barrier in disorders of the central nervous system.Materials today. Bio · 2025Review
- Lipid metabolism: the potential therapeutic targets in glioblastoma.Cell death discovery · 2025Review
- Targeted Glioma Therapy via TMVP1 Peptide-Modified FLT4 Liposomes: A Novel Molecular Probe Strategy.International journal of nanomedicine · 2025Article
- Identification and validation of TSPAN13 as a novel temozolomide resistance-related gene prognostic biomarker in glioblastoma.PloS one · 2025Article
- SREBP2 as a central player in cancer progression: potential for targeted therapeutics.Frontiers in pharmacology · 2025Review
- LAT4 drives temozolomide induced radiotherapy resistance in glioblastoma by enhancing mTOR pathway activation.Cancer cell international · 2024Article
- The Role and Applied Value of Mitochondria in Glioma-Related Research.CNS neuroscience & therapeutics · 2024Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Temozolomide (TMZ) has been used as standard-of-care for glioblastoma multiforme (GBM), but the resistance to TMZ develops quickly and frequently. Thus, more studies are needed to elucidate the resistance mechanisms. In the current study, we investigated the relationship among the three important phenotypes, namely TMZ-resistance, cell shape and lipid metabolism, in GBM cells. We first observed the distinct difference in cell shapes between TMZ-sensitive (U87) and resistant (U87R) GBM cells. We then conducted NMR-based lipid metabolomics, which revealed a significant increase in cholesterol and fatty acid synthesis as well as lower lipid unsaturation in U87R cells. Consistent with the lipid changes, U87R cells exhibited significantly lower membrane fluidity. The transcriptomic analysis demonstrated that lipid synthesis pathways through SREBP were upregulated in U87R cells, which was confirmed at the protein level. Fatostatin, an SREBP inhibitor, and other lipid pathway inhibitors (C75, TOFA) exhibited similar or more potent inhibition on U87R cells compared to sensitive U87 cells. The lower lipid unsaturation ratio, membrane fluidity and higher fatostatin sensitivity were all recapitulated in patient-derived TMZ-resistant primary cells. The observed ternary relationship among cell shape, lipid composition, and TMZ-resistance may be applicable to other drug-resistance cases. SREBP and fatostatin are suggested as a promising target-therapeutic agent pair for drug-resistant glioblastoma.
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