ArticleOncology letters2017
JS-K promotes apoptosis by inducing ROS production in human prostate cancer cells.
Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- Design, Synthesis and Antitumor Activity Evaluation in Vitro of Novel 1,6-Naphthyridine Derivatives.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026Article
- JS-K induces ferroptosis in renal carcinoma cells by regulating the c-Myc-GSTP1 Axis.Scientific reports · 2025Article
- Formononetin inhibits osteosarcoma cell proliferation and promotes apoptosis by regulating the miR-214-3p/phosphatase and tensin homolog pathway.Translational cancer research · 2020Article
- The evolving landscape for cellular nitric oxide and hydrogen sulfide delivery systems: A new era of customized medications.Biochemical pharmacology · 2020Review
- A review of the relatively complex mechanism of JS-K induced apoptosis in cancer cells.Translational cancer research · 2019Review
- JS-K, a nitric oxide donor, induces autophagy as a complementary mechanism inhibiting ovarian cancer.BMC cancer · 2019Article
- JS-K induces reactive oxygen species-dependent anti-cancer effects by targeting mitochondria respiratory chain complexes in gastric cancer.Journal of cellular and molecular medicine · 2019Article
- Antibacterial activity and mechanism of silver nanoparticles against multidrug-resistantInternational journal of nanomedicine · 2019Article
- JS-K enhances chemosensitivity of prostate cancer cells to Taxol via reactive oxygen species activation.Oncology letters · 2019Article
- Emodin Induces Apoptosis of Colon Cancer Cells via Induction of Autophagy in a ROS-Dependent Manner.Oncology research · 2018Article
- Quinalizarin Induces Apoptosis through Reactive Oxygen Species (ROS)-Mediated Mitogen-Activated Protein Kinase (MAPK) and Signal Transducer and Activator of Transcription 3 (STAT3) Signaling Pathways in Colorectal Cancer Cells.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Microenvironment-Cell Nucleus Relationship in the Context of Oxidative Stress.Frontiers in cell and developmental biology · 2018Review
- A Mini-Review of Reactive Oxygen Species in Urological Cancer: Correlation with NADPH Oxidases, Angiogenesis, and Apoptosis.International journal of molecular sciences · 2017Review
- [Sanggenon C induces apoptosis of prostate cancer PC3 cells by activating caspase 3 and caspase 9 pathways].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS) are chemical species that alter redox status, and are responsible for inducing carcinogenesis. The purpose of the present study was to assess the effects of the glutathione S transferase-activated nitric oxide donor prodrug, JS-K, on ROS accumulation and on proliferation and apoptosis in human prostate cancer cells. Cell proliferation and apoptosis, ROS accumulation and the activation of the mitochondrial signaling pathway were measured. The results demonstrated that JS-K may inhibit prostate cancer cell growth in a dose- and time-dependent manner, and induce ROS accumulation and apoptosis in a dose-dependent manner. With increasing concentrations of JS-K, expression of pro-apoptotic proteins increased, but Bcl-2 expression decreased. Additionally, the antioxidant N-acetylcysteine reversed JS-K-induced cell apoptosis; conversely, the pro-oxidant glutathione disulfide exacerbated JS-K-induced apoptosis. In conclusion, the data suggest that JS-K induces prostate cancer cell apoptosis by increasing ROS levels.
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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.