ArticleMolecules (Basel, Switzerland)2014
Celastrol induces apoptosis in gefitinib-resistant non-small cell lung cancer cells via caspases-dependent pathways and Hsp90 client protein degradation.
Article in Molecules (Basel, Switzerland), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 52 citations in OpenAlex.
- Integrated bioinformatics analyses and cell line experiments implicate miR-33a-5p/HIF1A in the cellular response to celastrol in lung adenocarcinoma.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Natural compounds for non-small cell lung cancer treatment: focus on the EGFR signaling pathway.Frontiers in pharmacology · 2026Review
- The emerging role of mitochondria in the pharmacological and toxicological effects of Tripterygium wilfordii Hook F: functions, targets and new therapeutic applications.Chinese medicine · 2025Review
- Traditional Chinese Medicines as Anticancer Agents for Non-Small Cell Lung Cancer with EGFR Mutations: A Review.Drug design, development and therapy · 2025Review
- Celastrol elicits antitumor effects by inhibiting the STAT3 pathway through ROS accumulation in non-small cell lung cancer.Journal of translational medicine · 2022Article
- Review
- Celastrol Inhibits Canine Mammary Tumor Cells by Inducing ApoptosisFrontiers in veterinary science · 2021Article
- Article
- Circ_SATB2 Attenuates the Anti-Tumor Role of Celastrol in Non-Small-Cell Lung Carcinoma Through Targeting miR-33a-5p/E2F7 Axis.OncoTargets and therapy · 2020Article
- Gefitinib induces non-small cell lung cancer H1650 cell apoptosis through downregulating tumor necrosis factor-related apoptosis-inducing ligand expression levels.Oncology letters · 2018Article
- A Mechanistic Overview of Triptolide and Celastrol, Natural Products fromFrontiers in pharmacology · 2018Review
- Synthesis and characterisation of celastrol derivatives as potential anticancer agents.Journal of enzyme inhibition and medicinal chemistry · 2017Article
- Celastrol inhibits migration and invasion through blocking the NF-κB pathway in ovarian cancer cells.Experimental and therapeutic medicine · 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
- Mutations Y493G and K546D in human HSP90 disrupt binding of celastrol and reduce interaction with Cdc37.FEBS open bio · 2016Article
- SCD1 is associated with tumor promotion, late stage and poor survival in lung adenocarcinoma.Oncotarget · 2016Article
- Compound Library Screening Identified Cardiac Glycoside Digitoxin as an Effective Growth Inhibitor of Gefitinib-Resistant Non-Small Cell Lung Cancer via Downregulation of α-Tubulin and Inhibition of Microtubule Formation.Molecules (Basel, Switzerland) · 2016Article
- (Z)3,4,5,4'-trans-tetramethoxystilbene, a new analogue of resveratrol, inhibits gefitinb-resistant non-small cell lung cancer via selectively elevating intracellular calcium level.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Celastrol, a triterpene extracted from the Chinese herb Tripterygium wilfordii, has been shown to have multiple bioactivities. Although among these activities, its anti-cancer effects have attracted the most attention, the effect of celastrol on gefitinib-resistant non-small cell lung cancer (NSCLC) cells is not clearly known. Here, we examined the potency of celastrol in three different NSCLC cell lines. We explored its treatment mechanism in two gefitinib-resistant NSCLC cell lines (H1650 and H1975). Our data demonstrated that celastrol exerted its apoptotic effect in a dose- and time-dependent manner. Also, the mitochondria membrane potential was gradually lost and the ratio of Bax/Bcl-2 increased after the treatment of celastrol, both of which are indicators of mitochondria membrane integrity. Although the caspases were activated, the treatment with pan-caspase inhibitor could partially inhibit the level of apoptosis. Moreover, the protein level of Hsp90 client proteins, EGFR and AKT, was measured. Interestingly, both client proteins were remarkably down-regulated after the treatment of celastrol. Taken together, our data showed that celastrol may be developed as a promising agent for treating gefitinib-resistant NSCLCs by inducing apoptosis through caspase-dependent pathways and Hsp90 client protein degradation.
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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.