ArticleAmerican journal of translational research2023
Celastrol enhances tamoxifen sensitivity in the treatment of triple negative breast cancer via mitochondria mediated apoptosis pathway.
Article in American journal of translational research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- The Antitumor Potential of Celastrol: Research Progress on Antitumor Mechanisms and Strategies for Toxicity Reduction with Efficacy Enhancement.Biomolecules · 2026Review
- ML385 increases ferroptosis via inhibiting Nrf2/HO-1 pathway to enhances the sensitivity of MCF-7 TAMR to tamoxifen.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Emerging Target Discovery Strategies Drive the Decoding of Therapeutic Power of Natural Products and Further Drug Development: A Case Study of Celastrol.Exploration (Beijing, China) · 2025Review
- 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
- Oxidative Stress Inducers in Cancer Therapy: Preclinical and Clinical Evidence.Antioxidants (Basel, Switzerland) · 2023Review
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Authors and funding
8 authors.
Funding
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Abstract
objectiveTo investigate the enhancement of chemosensitivity of tamoxifen (TAM) in triple negative breast cancer (TNBC) by celastrol (CEL) through mitochondrial mediated pathway.
methodsHuman TNBC MDA-MB-231 cells were divided to the control group (medium treatment), TAM-L group (low concentration TAM treatment, 0.5 μM TAM treatment), TAM-H group (1 μM TAM treatment), CEL-L group (low concentration CEL treatment, 1 μM CEL), CEL-H group (high concentration CEL treatment, 3 μM CEL), CEL-L+TAM group (low concentration CEL and TAM co-treatment) and CEL-H+TAM group (high concentration of CEL co-treated with TAM). The proliferation and invasion of cells in each cell group were detected by MTT assay and Transwell assay, respectively. Changes in mitochondrial membrane potential were determined by JC-1 staining. 2'-7'-dichlorofluorescein diacetate (DCFH-DA) fluorescence probe combined with flow cytometry was used to measure the levels of reactive oxygen species (ROS) in cells. The GSH/(GSSG+GSH) level in the cells was detected with glutathione (GSH)/oxidized glutathione (GSSG) enzyme-linked immunosorbent assay (ELISA) kit. The expression levels of the apoptosis-related proteins B lymphocytoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), sheared cysteine-containing aspartate protein hydrolase 3 (Cleaved Caspase-3), and cytochrome C (Cytc) in each group were measured by Western blot. The tumor model of subcutaneous transplantation of TNBC cells in nude mice was established. After administration, the volume and mass of tumors in each group were measured, and the tumor inhibition rate was calculated.
resultsCompared with the Control group, cell proliferation inhibition rate (24 h, 48 h), apoptosis rate, ROS level, Bax, cleaved caspase-3 and Cytc protein expression were conspicuously increased in the TAM, CEL-L, CEL-H, CEL-L+TAM and CEL-H+TAM groups (all P < 0.05), and cell migration and invasion, mitochondrial membrane potential, GSH level, and Bcl-2 protein expression were conspicuously decreased (all P < 0.05). Compared with the TAM group, the cell proliferation inhibition rate (24 h, 48 h), apoptosis rate, ROS level, Bax, cleaved caspase-3 and Cytc protein expression were increased in the CEL-H+TAM group (all P < 0.05), and cell migration rate, cell invasion number, mitochondrial membrane potential, GSH level and Bcl-2 protein expression were decreased in the CEL-H+TAM group (all P < 0.05). Compared with the CEL-L group, the cell proliferation inhibition rate (24 h, 48 h), apoptosis rate, ROS level, Bax, cleaved caspase-3 and Cytc protein expression were significantly increased in the CEL-H group (all P < 0.05), and cell migration rate, cell invasion number, mitochondrial membrane potential, GSH level and Bcl-2 protein expression were decreased in the CEL-H group (all P < 0.05). Compared with the model group, the tumor volume of TAM group, CEL-H group, CEL-L+TAM group and CEL-H+TAM group decreased (all P < 0.05). Compared with TAM group, the tumor volume in CEL-H+TAM group decreased significantly (P < 0.05).
conclusionCEL can promote apoptosis and enhance the TAM sensitivity in TNBC treatment through a mitochondria-mediated pathway.
Indexed as
Identifiers
37193187PMC10182490What OpenQuestion holds
Registered trials
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