ArticleOncoTargets and therapy2019
ROS generation and autophagosome accumulation contribute to the DMAMCL-induced inhibition of glioma cell proliferation by regulating the ROS/MAPK signaling pathway and suppressing the Akt/mTOR signaling pathway.
Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Immune molecular mechanisms of PANoptosis in sepsis-induced acute kidney injury.Inflammation and regeneration · 2026Review
- ROS homeostasis in cell fate, pathophysiology, and therapeutic interventions.Molecular biomedicine · 2025Review
- Research advances in natural sesquiterpene lactones: overcoming cancer drug resistance through modulation of key signaling pathways.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- Sesquiterpene lactones and cancer: new insight into antitumor and anti-inflammatory effects of parthenolide-derived Dimethylaminomicheliolide and Micheliolide.Frontiers in pharmacology · 2025Review
- A Zeolitic Imidazolate Framework-Based Antimicrobial Peptide Delivery System with Enhanced Anticancer Activity and Low Systemic Toxicity.Pharmaceutics · 2024Article
- Pharmacological potential of micheliolide: A focus on anti-inflammatory and anticancer activities.Heliyon · 2024Review
- Hirudin inhibits glioma growth through mTOR-regulated autophagy.Journal of cellular and molecular medicine · 2023Article
- The antitumor effect of the novel agent MCL/ACT001 in pancreatic ductal adenocarcinoma.Journal of cancer research and clinical oncology · 2023Article
- ACT001 inhibits pituitary tumor growth by inducing autophagic cell death via MEK4/MAPK pathway.Acta pharmacologica Sinica · 2022Article
- Potential targets and treatments affect oxidative stress in gliomas: An overview of molecular mechanisms.Frontiers in pharmacology · 2022Review
- Sesquiterpene Lactones and Cancer: New Insight into Antitumor and Anti-inflammatory Effects of Parthenolide-Derived Dimethylaminomicheliolide and Micheliolide.Computational and mathematical methods in medicine · 2022Review
- Dimethylaminomicheliolide Sensitizes Cancer Cells to Radiotherapy for Synergistic Combination with Immune Checkpoint Blockade.Advanced therapeutics · 2022Article
- Anti-Cancer Pectins and Their Role in Colorectal Cancer Treatment.Onco therapeutics · 2022Article
- Antitumor effects of the small molecule DMAMCL in neuroblastoma via suppressing aerobic glycolysis and targeting PFKL.Cancer cell international · 2021Article
- Micheliolide suppresses the viability, migration and invasion of U251MG cells via the NF-κB signaling pathway.Oncology letters · 2020Article
- IMMUNEPOTENT CRP induces DAMPS release and ROS-dependent autophagosome formation in HeLa and MCF-7 cells.BMC cancer · 2020Article
- Dimethylaminomicheliolide (DMAMCL) Suppresses the Proliferation of Glioblastoma Cells via Targeting Pyruvate Kinase 2 (PKM2) and Rewiring Aerobic Glycolysis.Frontiers in oncology · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeChemotherapy after surgery can prolong the survival of patients with gliomas. Dimethylaminomicheliolide (DMAMCL), a novel chemotherapeutic agent, exhibited antitumor properties in acute myeloid leukemia stem cells and showed an increased drug concentration in the brain. This study aims to investigate the specific anticancer activities and mechanisms of DMAMCL in glioma cells. MATERIALS AND
methodsIn this study, the effects of DMAMCL were evaluated and characterized in U87-MG and U251 glioma cells. Cell viability was assessed by Cell Counting Kit-8. Apoptosis, mitochondrial membrane potential, and intracellular reactive oxygen species (ROS) generation were assessed by fluorescence microscopy. Autophagosome formation was observed with transmission electron microscopy, and the autophagy flux was measured by transfecting cells with mRFP-GFP-LC3 adenoviral vectors. Immunofluorescence and Western blot analyses were used to determine the expression of proteins.
resultsIn the present study, treatment with DMAMCL decreased cell viability and induced apoptosis in U87-MG and U251 glioma cells. Additionally, DMAMCL activated autophagy-mediated cell death as evidenced by the formation of autophagosomes, accumulation of LC3B-II, inhibition of autophagy flux, and increase in cell viability after cotreatment with an autophagy inhibitor. Subsequent experiments showed that the DMAMCL-induced apoptosis and autophagy were possibly mediated by ROS generation and Akt/mTOR signaling pathway inhibition. On the other hand, the ROS scavenger N-acetyl-L-cysteine and the Akt activator insulin-like growth factor-1 attenuated the DMAMCL-induced autophagy and cell death.
conclusionOur findings revealed that DMAMCL induced apoptosis and autophagic cell death by regulating the ROS/mitogen-activated protein kinase signaling pathway and suppressing the Akt/mTOR signaling pathway in human glioma cells. DMAMCL may be a novel effective anticancer agent, which can target gliomas.
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