ArticleJournal of cancer research and clinical oncology2009
Role of reactive oxygen species in proapoptotic ability of oncogenic H-Ras to increase human bladder cancer cell susceptibility to histone deacetylase inhibitor for caspase induction.
Article in Journal of cancer research and clinical oncology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Redox System and Oxidative Stress-Targeted Therapeutic Approaches in Bladder Cancer.Antioxidants (Basel, Switzerland) · 2024Review
- A triple combination gemcitabine + romidepsin + cisplatin to effectively control triple-negative breast cancer tumor development, recurrence, and metastasis.Cancer chemotherapy and pharmacology · 2021Article
- Oxidative stress in bladder cancer: an ally or an enemy?Molecular biology reports · 2021Review
- Article
- Current updates on the role of reactive oxygen species in bladder cancer pathogenesis and therapeutics.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020Review
- Compensatory combination of romidepsin with gemcitabine and cisplatin to effectively and safely control urothelial carcinoma.British journal of cancer · 2020Article
- Histone deacetylase inhibitor MPT0B291 suppresses Glioma GrowthInternational journal of biological sciences · 2020Article
- Revisiting Histone Deacetylases in Human Tumorigenesis: The Paradigm of Urothelial Bladder Cancer.International journal of molecular sciences · 2019Review
- Romidepsin enhances the cytotoxicity of fludarabine, clofarabine and busulfan combination in malignant T-cells.Leukemia research · 2016Article
- Romidepsin targets multiple survival signaling pathways in malignant T cells.Blood cancer journal · 2015Article
- Targeting Histone Deacetylases in Diseases: Where Are We?Antioxidants & redox signaling · 2015Review
- Differential effects of ethanol on bid, tBid, and Bax:tBid interactions in postnatal day 4 and postnatal day 7 rat cerebellum.Alcoholism, clinical and experimental research · 2015Article
- The Interplay between ROS and Ras GTPases: Physiological and Pathological Implications.Journal of signal transduction · 2012Article
- Reactive oxygen species-mediated therapeutic control of bladder cancer.Nature reviews. Urology · 2011Review
- Differential induction of reactive oxygen species through Erk1/2 and Nox-1 by FK228 for selective apoptosis of oncogenic H-Ras-expressing human urinary bladder cancer J82 cells.Journal of cancer research and clinical oncology · 2011Article
- Autophagic survival in resistance to histone deacetylase inhibitors: novel strategies to treat malignant peripheral nerve sheath tumors.Cancer research · 2011Article
- Romidepsin (FK228), a potent histone deacetylase inhibitor, induces apoptosis through the generation of hydrogen peroxide.Cancer science · 2010Article
- Molecular genesis of non-muscle-invasive urothelial carcinoma (NMIUC).Expert reviews in molecular medicine · 2010Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeReveal mechanisms for the novel proapoptotic ability of oncogenic H-Ras to increase cell susceptibility to a histone deacetylase inhibitor (HDACI) FR901228 for inducing caspase activation and selective apoptosis.
methodsHuman urinary bladder cancer J82 and oncogenic H-Ras-expressing J82 cells were used to reveal differential induction of intracellular reactive oxygen species (ROS), caspase activation, and apoptosis by HDACI FR901228. ROS levels and caspase-8, -9, and -3/7 activities were measured by flow cytometry and luminescence assays, respectively. Specific inhibitors were used to suppress caspases and ROS. Western blot analysis determined modulators of caspase pathways.
resultsROS, caspase activity, and cell death was differentially increased by FR901228 in oncogenic H-Ras-expressing J82 versus parental cells. Blocking ROS resulted in reduced FR901228-induced cell death and caspase activation. Suppression of caspase-8 resulted in reduced FR901228-activated caspase-9 and -3/7. Suppression of caspase-9 resulted in reduced FR901228-activated caspase-3/7. Although FR901228 induced an ROS-dependent increase of FasL, FasL failed to induce caspase activation and cell death.
conclusionIncreased ROS played an important role in the activation of the extrinsic and intrinsic caspase pathways to cooperatively induce executioner caspase-3/7 through a novel FasL-independent pathway in FR901228-induced selective apoptosis of oncogenic H-Ras-expressing J82 versus parental cells.
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