ArticleMolecules (Basel, Switzerland)2012
10-acetylirciformonin B, a sponge furanoterpenoid, induces DNA damage and apoptosis in leukemia cells.
Article in Molecules (Basel, Switzerland), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Article
- A Review on Genotoxic and Genoprotective Effects of Biologically Active Compounds of Animal Origin.Toxins · 2023Review
- Review
- Physapruin A Enhances DNA Damage and Inhibits DNA Repair to Suppress Oral Cancer Cell Proliferation.International journal of molecular sciences · 2022Article
- New Drugs from the Sea: Pro-Apoptotic Activity of Sponges and Algae Derived Compounds.Marine drugs · 2019Review
- Apoptosis induction on human breast cancer T47D cell line by extracts ofF1000Research · 2019Article
- Cytotoxic Compounds Derived from Marine Sponges. A Review (2010-2012).Molecules (Basel, Switzerland) · 2017Review
- A Survey of Marine Natural Compounds and Their Derivatives with Anti-cancer Activity Reported in 2012.Molecules (Basel, Switzerland) · 2015Review
- Reactive oxygen species and autophagy modulation in non-marine drugs and marine drugs.Marine drugs · 2014Review
- Cracking the cytotoxicity code: apoptotic induction of 10-acetylirciformonin B is mediated through ROS generation and mitochondrial dysfunction.Marine drugs · 2014Article
- A survey of marine natural compounds and their derivatives with anti-cancer activity reported in 2011.Molecules (Basel, Switzerland) · 2013Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
10-Acetylirciformonin B, a furanoterpenoid derived from irciformonin B found in a marine sponge, has been reported to possess potent cytotoxic activity against several cancer cell lines. However, the mechanism of its apoptotic activity against human leukemia cells has never been reported. The purpose of this study was to investigate the cytotoxic effects of 10-acetylirciformonin B and its possible mechanism of action against leukemia HL 60 cells. We found that 10-acetylirciformonin B decreased cell viability through the inhibition of cell growth as well as the induction of DNA damage and apoptosis in a dose-dependent manner. The induction of DNA damage was mediated by the increase of p-CHK2 and γ-H2A.X, which was suggested from the increase of tail movement in the neutral Comet assay. Induction of apoptosis was mediated with the increase in caspases 8, 9 and 3 activation as well as PARP cleavage. In summary, our resultsindicate that 10-acetylirciformonin B treatment causes apoptosis in leukaemia cells; probably through a caspase-dependent regulatory pathway.
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Registered trials
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.