ArticleJournal of translational medicine2013
Hirsutanol A, a novel sesquiterpene compound from fungus Chondrostereum sp., induces apoptosis and inhibits tumor growth through mitochondrial-independent ROS production: hirsutanol A inhibits tumor growth through ROS production.
Article in Journal of translational medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 32 citations in OpenAlex.
- Advancements in the therapeutic potential of sesquiterpenoids for the treatment of hepatocellular carcinoma (Review).International journal of oncology · 2025Review
- Pro-Health and Anti-Cancer Activity of Fungal Fractions Isolated from Milk-Supplemented Cultures ofBiomolecules · 2021Article
- Hirsutanol A inhibits T-acute lymphocytic leukemia Jurkat cell viability through cell cycle arrest and p53-dependent induction of apoptosis.Experimental and therapeutic medicine · 2021Article
- Encapsulating Halofuginone Hydrobromide in TPGS Polymeric Micelles Enhances Efficacy Against Triple-Negative Breast Cancer Cells.International journal of nanomedicine · 2021Article
- Monarubins A-C from the Marine Shellfish-Associated FungusMarine drugs · 2020Article
- Cytotoxic alkaloids from the marine shellfish-associated fungusRSC advances · 2020Article
- Article
- Linear Triquinane Sesquiterpenoids: Their Isolation, Structures, Biological Activities, and Chemical Synthesis.Molecules (Basel, Switzerland) · 2018Review
- Mitochondrial and caspase pathways are involved in the induction of apoptosis by nardosinen in MCF-7 breast cancer cell line.Research in pharmaceutical sciences · 2018Article
- Additional New Cytotoxic Triquinane-Type Sesquiterpenoids Chondrosterins K-M from the Marine Fungus Chondrostereum sp.Marine drugs · 2016Article
- Blue-Print Autophagy: Potential for Cancer Treatment.Marine drugs · 2016Review
- Can Some Marine-Derived Fungal Metabolites Become Actual Anticancer Agents?Marine drugs · 2015Review
- Reactive oxygen species and autophagy modulation in non-marine drugs and marine drugs.Marine drugs · 2014Review
- Induced marine fungus Chondrostereum sp. as a means of producing new sesquiterpenoids chondrosterins I and J by using glycerol as the carbon source.Marine drugs · 2014Article
- REACTIVE OXYGEN SPECIES AND COLORECTAL CANCER.Current colorectal cancer reports · 2013Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHirsutanol A is a novel sesquiterpene compound purified from fungus Chondrostereum sp. in Sarcophyton tortuosum. Our previous studies had demonstrated that hirsutanol A exhibited potent cytotoxic effect on many kinds of cancer cell lines. In the current study, the antitumor activity of hirsutanol A and its molecular mechanisms were investigated.
methodsHirsutanol A induced growth inhibition and apoptotic cell death of human colon cancer SW620 cells and human breast cancer MDA-MB-231cells were determined using MTT assay and flow cytometry assay, respectively. The effect of hirsutanol A on intrinsic ROS level and change in mitochondrial membrane potential (△ψm) of different cell lines were also measured by flow cytometry assay. The function of JNK was compromised by JNK siRNA or JNK inhibitor SP600125. The expression of cytochrome c, p-JNK, p-c-Jun after treatment with hirsutanol A were detected by Western blot analysis. Finally, the in vivo anti-tumor effect of hirsutanol A was examined in human cancer cell SW620 xenograft model.
resultsThe results showed that hirsutanol A significantly induced apoptosis, mitochondrial-independent increase of Reactive Oxygen Species (ROS) level, change of mitochondrial membrane potential, release of cytochrome c in human cancer cells. Preventing increase of ROS level using the potent antioxidant N-acetyl-L-cysteine (NAC) markedly decreased hirsutanol A-induced apoptosis. In addition, JNK signaling pathway was activated by hirsutanol A through elevating ROS level. Blockade of JNK signaling pathway by JNK specific inhibitor SP600125 enhanced apoptosis and hirsutanol A-induced ROS accumulation. Also, hirsutanol A exhibited antitumor activity in human cancer cell SW620 xenograft model.
conclusionThese data suggested that hirsutanol A inhibited tumor growth through triggering ROS production and apoptosis.
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