ArticleThe Journal of biological chemistry2013
The natural compound cantharidin induces cancer cell death through inhibition of heat shock protein 70 (HSP70) and Bcl-2-associated athanogene domain 3 (BAG3) expression by blocking heat shock factor 1 (HSF1) binding to promoters.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.
- Bibliometric Analysis and Systemic Review of Cantharidin Research Worldwide.Current pharmaceutical biotechnology · 2024Pooled it
- Human DEAH-box helicase 8 regulates HSF1-mediated stress response and cancer-associated pre-mRNA splicing in tumour cells.NAR cancer · 2026Article
- Interaction between Maslinic acid and HSF1 enhances the ubiquitin degradation of HSF1, resulting in the inhibitory effect of pancreatic cancer.Discover oncology · 2025Article
- Novel drug research and therapeutic strategies targeting tumor metastasis and cancer stem cells.Frontiers in pharmacology · 2025Review
- Mylabris: a review of its biological characteristics, chemical composition, pharmacological, toxicology, pharmacokinetics, and marketed drugs.Frontiers in pharmacology · 2025Review
- HSF1 Activation Mechanisms, Disease Roles, and Small Molecule Therapeutics.International journal of biological sciences · 2025Review
- Review
- Gut microbial changes in a specialist blister beetle larvae and their nutritional metabolic characteristics.Ecology and evolution · 2024Article
- Heat Shock Factor 1 Inhibition: A Novel Anti-Cancer Strategy with Promise for Precision Oncology.Cancers · 2023Review
- Single-cell RNA sequencing to detect age-associated genes that identify senescent cells in the liver of aged mice.Scientific reports · 2023Article
- Proteomics identifies differentially expressed proteins in glioblastoma U87 cells treated with hederagenin.Proteome science · 2023Article
- An Undefined Interaction between Polyamines and Heat Shock Proteins Leads to Cellular Protection inMolecules (Basel, Switzerland) · 2023Review
- Efficacy and influencing factors of Insect Compound Particle combined with chemotherapy for mismatch repair-related locally advanced stage III CRC who had undergone surgery and achieved R0 resection: a multicenter, double-blind, randomized, placebo-controlled clinical trial protocol.Annals of translational medicine · 2023Article
- Targeting HSF1 for cancer treatment: mechanisms and inhibitor development.Theranostics · 2023Review
- Hepatotoxic mechanism of cantharidin: insights and strategies for therapeutic intervention.Frontiers in pharmacology · 2023Review
- Inhibition of MZF1/c-MYC Axis by Cantharidin Impairs Cell Proliferation in Glioblastoma.International journal of molecular sciences · 2022Article
- Therapeutic induction of Bcl2-associated athanogene 3-mediated autophagy in idiopathic pulmonary fibrosis.Clinical and translational medicine · 2022Article
- Cantharidin downregulates PSD1 expression and inhibits autophagic flux in yeast cells.FEBS open bio · 2022Article
- Chinese Herbal Medicine for Primary Liver Cancer Therapy: Perspectives and Challenges.Frontiers in pharmacology · 2022Review
- Advances in the study of HSP70 inhibitors to enhance the sensitivity of tumor cells to radiotherapy.Frontiers in cell and developmental biology · 2022Review
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4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heat shock factor 1 (HSF1) enhances the survival of cancer cells under various stresses. The knock-out of HSF1 impairs cancer formation and progression, suggesting that HSF1 is a promising therapeutic target. To identify inhibitors of HSF1 activity, we performed cell-based screening with a library of marketed and experimental drugs and identified cantharidin as an HSF1 inhibitor. Cantharidin is a potent antitumor agent from traditional Chinese medicine. Cantharidin inhibited heat shock-induced luciferase activity with an IC50 of 4.2 μm. In contrast, cantharidin did not inhibit NF-κB luciferase reporter activity, demonstrating that cantharidin is not a general transcription inhibitor. When the HCT-116 colorectal cancer cells were exposed to heat shock in the presence of cantharidin, the induction of HSF1 downstream target proteins, such as HSP70 and BAG3 (Bcl-2-associated athanogene domain 3), was suppressed. HSP70 and its co-chaperone BAG3 have been reported to protect cells from apoptosis by stabilizing anti-apoptotic Bcl-2 family proteins. As expected, treating HCT-116 cancer cells with cantharidin significantly decreased the amounts of BCL-2, BCL-xL, and MCL-1 protein and induced apoptotic cell death. Chromatin immunoprecipitation analysis showed that cantharidin inhibited the binding of HSF1 to the HSP70 promoter and subsequently blocked HSF1-dependent p-TEFb recruitment. Therefore, the p-TEFb-dependent phosphorylation of the C-terminal domain of RNA polymerase II was blocked, arresting transcription at the elongation step. Protein phosphatase 2A inhibition with PP2CA siRNA or okadaic acid did not block HSF1 activity, suggesting that cantharidin inhibits HSF1 in a protein phosphatase 2A-independent manner. We show for the first time that cantharidin inhibits HSF1 transcriptional activity.
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