ArticleJournal of experimental & clinical cancer research : CR2019
Celastrol mediates autophagy and apoptosis via the ROS/JNK and Akt/mTOR signaling pathways in glioma cells.
Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 111 papers.
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Who cites it
111 citing papers in PubMed, 218 citations in OpenAlex.
- Bevacizumab induces apoptosis in glioblastoma cells by upregulating miR-4695-5p to inhibit PKMYT1.RNA biology · 2026Article
- Anoikis in cancer: molecular mechanisms, resistance, and therapeutic strategies.Apoptosis : an international journal on programmed cell death · 2026Review
- Celastrol induces apoptosis of myelodysplastic syndrome cells through a ROS-dependent pro-apoptotic endoplasmic-reticulum stress pathway.Cancer cell international · 2026Article
- Potential anti-glioma targets and mechanisms of Smilax china L. based on network pharmacological, molecular docking and experimental verification.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- The anticancer properties of dexmedetomidine in papillary thyroid cancer and its underlying mechanisms.Scientific reports · 2026Article
- Research on the molecular mechanism of celastrol targeting CTNNB1/STAT3 to inhibit uveal melanoma based on network pharmacology and multi-omics analysis.Scientific reports · 2026Article
- Celastrol overcomes 5-fluorouracil resistance in osteosarcoma cells through p53-mediated apoptotic pathway modulation and P-glycoprotein inhibition: A comprehensive mechanistic study.BioImpacts : BI · 2026Article
- Development of vascularized adipose organoids from PBMSCs and their application in evaluating Celastrol's effects.Adipocyte · 2025Article
- Traditional Chinese Medicinal Leech Induces Apoptosis and Autophagy in Glioblastoma by SGK1/Caspase-3 and PI3K/AKT/mTOR Pathway.CNS neuroscience & therapeutics · 2025Article
- Investigation into the synergistic effect of atorvastatin combined with ultrasound stimulation for anti-glioma therapy.Oncology letters · 2025Article
- Targeting the Mitochondria in High-Grade Gliomas.Cancers · 2025Review
- Potential of phytochemicals in the treatment of Alzheimer disease by modulating lysosomal dysfunction: a systematic review.Chinese medicine · 2025Review
- The role of JNK signaling pathway in organ fibrosis.Journal of advanced research · 2025Review
- A Nanosystem Alleviates Severe Acute Pancreatitis via Reactive Oxygen Species Scavenging and Enhancing Mitochondrial Autophagy.Nano letters · 2025Article
- Article
- Injectable celastrol-loading emulsion hydrogel for immunotherapy of low-immunogenic cancer.Journal of nanobiotechnology · 2025Article
- TUBB4A Inhibits Glioma Development by Regulating ROS-PINK1/Parkin-Mitophagy Pathway.Molecular neurobiology · 2025Article
- Celastrol promotes apoptotic cell death in thyroid cancer cells through a caspases-dependent pathway.Thyroid research · 2025Article
- Tailoring traditional Chinese medicine in cancer therapy.Molecular cancer · 2025Review
- Autophagy in brain tumors: molecular mechanisms, challenges, and therapeutic opportunities.Journal of translational medicine · 2025Review
51 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundCelastrol, a triterpene compound derived from the traditional Chinese medicine Tripterygium wilfordii, has been reported to possess potential antitumor activity towards various malignancies. However, the effect of celastrol on glioma cells and the underlying molecular mechanisms remain elusive.
methodsGlioma cells, including the U251, U87-MG and C6 cell lines and an animal model were used. The effects of celastrol on cells were evaluated by flow cytometry, confocal microscopy, reactive oxygen species production assay and immunoblotting after treatment of celastrol. Fisher's exact test, a one-way ANOVA and the Mann-Whitney U-test were used to compare differences between groups. All data were analyzed using SPSS version 21.0 software.
resultsHere, we found that exposure to celastrol induced G2/M phase arrest and apoptosis. Celastrol increased the formation of autophagosomes, accumulation of LC3B and the expression of p62 protein. Celastrol-treated glioma cells exhibited decreased cell viability after the use of autophagy inhibitors. Additionally, autophagy and apoptosis caused by celastrol in glioma cells inhibited each other. Furthermore, celastrol induced JNK activation and ROS production and inhibited the activities of Akt and mTOR kinases. JNK and ROS inhibitors significantly attenuated celastrol-trigged apoptosis and autophagy, while Akt and mTOR inhibitors had opposite effects.
conclusionsIn conclusion, our study revealed that celastrol caused G2/M phase arrest and trigged apoptosis and autophagy by activating ROS/JNK signaling and blocking the Akt/mTOR signaling pathway.
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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.