ArticleOncology letters2017
Celastrol-induced apoptosis in human nasopharyngeal carcinoma is associated with the activation of the death receptor and the mitochondrial pathway.
Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 25 citations in OpenAlex.
- 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
- Recent Trends in anti-tumor mechanisms and molecular targets of celastrol.International journal of biological sciences · 2024Review
- Prospects of compounds of herbal plants as anticancer agents: a comprehensive review from molecular pathways.Frontiers in pharmacology · 2024Review
- Exploration of the effect of Celastrol on protein targets in nasopharyngeal carcinoma: Network pharmacology, molecular docking and experimental evaluations.Frontiers in pharmacology · 2022Article
- Targeting the signaling in Epstein-Barr virus-associated diseases: mechanism, regulation, and clinical study.Signal transduction and targeted therapy · 2021Review
- Review
- Arnicolide D, from the herbMolecules (Basel, Switzerland) · 2019Article
- Brevilin A Induces Cell Cycle Arrest and Apoptosis in Nasopharyngeal Carcinoma.Frontiers in pharmacology · 2019Article
- Euscaphic acid inhibits proliferation and promotes apoptosis of nasopharyngeal carcinoma cells by silencing the PI3K/AKT/mTOR signaling pathway.American journal of translational research · 2019Article
- Curcumol attenuates epithelial-mesenchymal transition of nasopharyngeal carcinoma cells via TGF-β1.Molecular medicine reports · 2018Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nasopharyngeal carcinoma (NPC) is a cancer that arises from the epithelium of the nasopharynx. Celastrol is a triterpene from traditional Chinese medicine, which demonstrates anti-proliferative activity in several cancer cell lines. However, the effect of celastrol on human NPC and the underlying mechanisms are not yet elucidated. The present study investigated whether celastrol induced apoptosis in human NPC cells, and the underlying molecular mechanisms were explored. Celastrol decreased the viability of HONE-1 and NPC-039 cells in a dose-dependent manner, and induced G1 and G2/M phase cell cycle arrest. The level of cleaved caspases-3, -8, and -9 and poly (ADP-ribose) polymerase 1 increased in cells treated with celastrol. There was an increase in active Bcl-2-like 11 isoform S, Bcl-2-associated X, Bcl-2 antagonist/killer and truncated BH3-interacting death antagonist, and the levels of the anti-apoptotic Bcl-2 and Bcl-2-like 1 decreased. Celastrol induced an increase in Fas, Fas-associated via death domain, TNF receptor superfamily members (TNRSF) 1A and 10B, and TNFRSF1A associated via death domain, and induced a dose-dependent reduction in mitochondrial membrane potential. Celastrol inhibited activation of mitogen-activated protein kinase (MAPK) 1/3 and 14, and induced MAPK 8/9 activation. The results indicated that celastrol induced apoptosis through the death receptor and the mitochondrial pathway in human NPC cells, and is a promising candidate in the development of drugs against NPC.
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