ArticleCancer research2014
Changes in pyruvate metabolism detected by magnetic resonance imaging are linked to DNA damage and serve as a sensor of temozolomide response in glioblastoma cells.
Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 73 citations in OpenAlex.
- Targeting metabolic mechanisms to overcome temozolomide resistance in glioblastoma.Discover oncology · 2026Review
- Integrated screening for small molecules interfering with PKM2: a drug repurposing strategy against glioblastoma.Journal of translational medicine · 2025Article
- Hyperpolarized Carbon-13 Metabolic Imaging Differentiates Distinctive Molecular Phenotypes in Diffuse Midline Gliomas.Molecules (Basel, Switzerland) · 2025Article
- Hypoxic microenvironment-induced exosomes confer temozolomide resistance in glioma through transfer of pyruvate kinase M2.Discover oncology · 2024Article
- Inhibitory effect of temozolomide on apoptosis induction of cinnamaldehyde in human glioblastoma multiforme T98G cell line.Anatomy & cell biology · 2024Article
- Article
- Neurons require glucose uptake and glycolysis in vivo.Cell reports · 2023Article
- Hyperpolarized δ-[1-Scientific reports · 2023Article
- The potential of advanced MR techniques for precision radiotherapy of glioblastoma.Magma (New York, N.Y.) · 2022Review
- A Clinical PET Imaging Tracer ([Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- Characterization of Distinctive In Vivo Metabolism between Enhancing and Non-Enhancing Gliomas Using Hyperpolarized Carbon-13 MRI.Metabolites · 2021Article
- Detection of metabolic change in glioblastoma cells after radiotherapy using hyperpolarizedNMR in biomedicine · 2021Article
- Differentiating Radiation Necrosis from Brain Tumor Using Hyperpolarized Carbon-13 MR Metabolic Imaging.Molecular imaging and biology · 2021Article
- In Vivo Assessment of Metabolic Abnormality in Alport Syndrome Using Hyperpolarized [1-Metabolites · 2021Article
- Tumor treating fields (TTFields) impairs aberrant glycolysis in glioblastoma as evaluated by [Neoplasia (New York, N.Y.) · 2021Article
- Glutamate Is a Noninvasive Metabolic Biomarker of IDH1-Mutant Glioma Response to Temozolomide Treatment.Cancer research · 2020Article
- Evaluation of Glycolytic Response to Multiple Classes of Anti-glioblastoma Drugs by Noninvasive Measurement of Pyruvate Kinase M2 Using [Molecular imaging and biology · 2020Article
- Overexpression of CXCL14 Alleviates Ventilator-Induced Lung Injury through the Downregulation of PKM2-Mediated Cytokine Production.Mediators of inflammation · 2020Article
- MR-detectable metabolic biomarkers of response to mutant IDH inhibition in low-grade glioma.Theranostics · 2020Article
- Optimized monoclonal antibody treatment against ELTD1 for GBM in a G55 xenograft mouse model.Journal of cellular and molecular medicine · 2020Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Recent findings show that exposure to temozolomide (TMZ), a DNA-damaging drug used to treat glioblastoma (GBM), can suppress the conversion of pyruvate to lactate. To understand the mechanistic basis for this effect and its potential utility as a TMZ response biomarker, we compared the response of isogenic GBM cell populations differing only in expression of the DNA repair protein methyltransferase (MGMT), a TMZ-sensitivity determinant, after exposure to TMZ in vitro and in vivo. Hyperpolarized [1-((13))C]-pyruvate-based MRI was used to monitor temporal effects on pyruvate metabolism in parallel with DNA-damage responses and tumor cell growth. TMZ exposure decreased conversion of pyruvate to lactate only in MGMT-deficient cells. This effect coincided temporally with TMZ-induced increases in levels of the DNA-damage response protein pChk1. Changes in pyruvate to lactate conversion triggered by TMZ preceded tumor growth suppression and were not associated with changes in levels of NADH or lactate dehydrogenase activity in tumors. Instead, they were associated with a TMZ-induced decrease in the expression and activity of pyruvate kinase PKM2, a glycolytic enzyme that indirectly controls pyruvate metabolism. PKM2 silencing decreased PK activity, intracellular lactate levels, and conversion of pyruvate to lactate in the same manner as TMZ, and Chk1 silencing blocked the TMZ-induced decrease in PKM2 expression. Overall, our findings showed how TMZ-induced DNA damage is linked through PKM2 to changes in pyruvate metabolism, and how these changes can be exploited by MRI methods as an early sensor of TMZ therapeutic response.
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