ArticleBioMed research international2015
Effect of celastrol on growth inhibition of prostate cancer cells through the regulation of hERG channel in vitro.
Article in BioMed research international, 2015. 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, 31 citations in OpenAlex.
- The Antitumor Potential of Celastrol: Research Progress on Antitumor Mechanisms and Strategies for Toxicity Reduction with Efficacy Enhancement.Biomolecules · 2026Review
- Targeting Ion Channels for Cancer Therapy: From Pathophysiological Mechanisms to Clinical Translation.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Identification and assessment of hub genes and miRNAs coregulatory associated with immune infiltrations and drug interactions in latent tuberculosis based on MicroarrayData analysis, molecular docking, and dynamic simulation.Biochemistry and biophysics reports · 2025Article
- Carrier-Free Nanomedicine Based on Celastrol and Methotrexate for Synergistic Treatment of Breast Cancer via Folate Targeting.International journal of nanomedicine · 2025Article
- Recent advances in drug delivery of celastrol for enhancing efficiency and reducing the toxicity.Frontiers in pharmacology · 2024Review
- Withaferin A and Celastrol Overwhelm Proteostasis.International journal of molecular sciences · 2023Review
- Natural Compounds in Sex Hormone-Dependent Cancers: The Role of Triterpenes as Therapeutic Agents.Frontiers in endocrinology · 2020Review
- Effects of diclofenac on the pharmacokinetics of celastrol in rats and its transport.Pharmaceutical biology · 2018Article
- Celastrol suppresses the proliferation of lung adenocarcinoma cells by regulating microRNA-24 and microRNA-181b.Oncology letters · 2018Article
- Celastrol induces apoptosis in hepatocellular carcinoma cells via targeting ER-stress/UPR.Oncotarget · 2017Article
- Celastrol-induced apoptosis in human nasopharyngeal carcinoma is associated with the activation of the death receptor and the mitochondrial pathway.Oncology letters · 2017Article
- Natural Products Discovered in a High-Throughput Screen Identified as Inhibitors of RGS17 and as Cytostatic and Cytotoxic Agents for Lung and Prostate Cancer Cell Lines.Journal of natural products · 2017Article
- Compounds From Celastraceae Targeting Cancer Pathways and Their Potential Application in Head and Neck Squamous Cell Carcinoma: A Review.Current genomics · 2017Review
- Celastrol: A Spectrum of Treatment Opportunities in Chronic Diseases.Frontiers in medicine · 2017Review
- Marine compound rhizochalinin shows high in vitro and in vivo efficacy in castration resistant prostate cancer.Oncotarget · 2016Article
- Pivotal Cytoprotective Mediators and Promising Therapeutic Strategies for Endothelial Progenitor Cell-Based Cardiovascular Regeneration.Stem cells international · 2016Review
- Celastrol and Its Role in Controlling Chronic Diseases.Advances in experimental medicine and biology · 2016Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo explore the antiprostate cancer effects of Celastrol on prostate cancer cells' proliferation, apoptosis, and cell cycle distribution, as well as the correlation to the regulation of hERG.
methodsDU145 cells were treated with various concentrations of Celastrol (0.25-16.0 μmol/L) for 0-72 hours. MTT assay was used to evaluate the inhibition effect of Celastrol on the growth of DU145 cells. Cell apoptosis was detected through both Annexin-V FITC/PI double-labeled cytometry and Hoechst 33258. Cell cycle regulation was examined by a propidium iodide method. Western blot and RT-PCR technologies were applied to assess the expression level of hERG in DU145 cells.
resultsCelastrol presented striking growth inhibition and apoptosis induction potency on DU145 cells in vitro in a time- and dose-dependent manner. The IC50 value of Celastrol for 24 hours was 2.349 ± 0.213 μmol/L. Moreover, Celastrol induced DU145 cell apoptosis in a cell cycle-dependent manner, which means Celastrol could arrest DU145 cells in G0/G1 phase; accordingly, cells in S phase decreased gradually and no obvious changes were found in G2/M phase cells. Through transmission electron microscope, apoptotic bodies containing nuclear fragments were found in Celastrol-treated DU145 cells. Overexpression of hERG channel was found in DU145 cells, while Celastrol could downregulate it at both protein and mRNA level in a dose-dependent manner (P < 0.01).
conclusionsCelastrol exhibits its antiprostate cancer effects partially through the downregulation of the expression level of hERG channel in DU145 cells, suggesting that Celastrol may be a potential agent against prostate cancer with a mechanism of blocking the hERG channel.
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