ArticleFrontiers in oncology2019
Dimethylaminomicheliolide (DMAMCL) Suppresses the Proliferation of Glioblastoma Cells via Targeting Pyruvate Kinase 2 (PKM2) and Rewiring Aerobic Glycolysis.
Article in Frontiers in oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 45 citations in OpenAlex.
- DMAMCL induces ferroptosis in neuroblastoma by targeting HMOX1 in MYCN-amplified subtypes whereas targeting STEAP3 in MYCN-nonamplified subtypes.Redox report : communications in free radical research · 2026Article
- Fatty Acid Metabolism Rewires Glioblastoma Progression and Treg-Mediated Immune Resistance.Cancers · 2026Review
- PKM2-Mediated Glycolytic Reprogramming in Thyroid Cancer: Mechanistic Insights and Therapeutic Potential.Molecules (Basel, Switzerland) · 2026Review
- Glioblastoma cells that evade chemoradiotherapy-induced cell death exhibit a bifurcated glycolytic program.Cell death & disease · 2026Article
- Targeting Metabolic Vulnerabilities in Glioblastoma: a Framework for Multi-node Combination Therapy.Current oncology reports · 2026Review
- The glioma microenvironment and its impact on antitumor immunity.Neuro-oncology advances · 2025Review
- Plant-derived terpenoids modulating cancer cell metabolism and cross-linked signaling pathways: an updated reviews.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- GLUT1 as a Potential Therapeutic Target in Glioblastoma.Brain sciences · 2025Review
- Glioblastoma multiforme: insights into pathogenesis, key signaling pathways, and therapeutic strategies.Molecular cancer · 2025Review
- Sesquiterpene Lactones as Promising Anti-Glioblastoma Drug Candidates Exerting Complex Effects on Glioblastoma Cell Viability and Proneural-Mesenchymal Transition.Biomedicines · 2025Review
- Metabolism of glioblastoma: a review of metabolic adaptations and metabolic therapeutic interventions.Frontiers in oncology · 2025Review
- Sesquiterpene lactones and cancer: new insight into antitumor and anti-inflammatory effects of parthenolide-derived Dimethylaminomicheliolide and Micheliolide.Frontiers in pharmacology · 2025Review
- Targeting metabolic reprogramming in glioblastoma as a new strategy to overcome therapy resistance.Frontiers in cell and developmental biology · 2025Review
- Targeting Mitochondria in Glioma: New Hopes for a Cure.Biomedicines · 2024Review
- Pharmacological potential of micheliolide: A focus on anti-inflammatory and anticancer activities.Heliyon · 2024Review
- Current Advances on Nanomaterials Interfering with Lactate Metabolism for Tumor Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Targeting glycolysis: exploring a new frontier in glioblastoma therapy.Frontiers in immunology · 2024Review
- Glioblastomas: Hijacking Metabolism to Build a Flexible Shield for Therapy Resistance.Antioxidants & redox signaling · 2023Review
- The Role of Ketone Bodies in Treatment Individualization of Glioblastoma Patients.Brain sciences · 2023Article
- The antitumor effect of the novel agent MCL/ACT001 in pancreatic ductal adenocarcinoma.Journal of cancer research and clinical oncology · 2023Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is the most prevalent malignant tumor in the central nervous system. Aerobic glycolysis, featured with elevated glucose consumption and lactate production, confers selective advantages on GBM by utilizing nutrients to support rapid cell proliferation and tumor growth. Pyruvate kinase 2 (PKM2), the last rate-limiting enzyme of glycolysis, is known to regulate aerobic glycolysis, and considered as a novel cancer therapeutic target. Herein, we aim to describe the cellular functions and mechanisms of a small molecular compound dimethylaminomicheliolide (DMAMCL), which has been used in clinical trials for recurrent GBM in Australia. Our results demonstrate that DMAMCL is effective on the inhibition of GBM cell proliferation and colony formation. MCL, the active metabolic form of DMAMCL, selectively binding to monomeric PKM2 and promoting its tetramerization, was also found to improve the pyruvate kinase activity of PKM2 in GBM cells. In addition, non-targeting metabolomics analysis reveals multiple metabolites involved in glycolysis, including lactate and glucose-6-phosphate, are decreased with DMAMCL treatment. The inhibitory effects of DMAMCL are observed to decrease in GBM cells upon PKM2 depletion, further confirming the importance of PKM2 in DMAMCL sensitivity. In conclusion, the activation of PKM2 by DMAMCL results in the rewiring aerobic glycolysis, which consequently suppresses the proliferation of GBM cells. Hence, DMAMCL represents a potential PKM2-targeted therapeutic agent against GBM.
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