ArticleScientific reports2015
A reactive oxygen species activation mechanism contributes to JS-K-induced apoptosis in human bladder cancer cells.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 67 citations in OpenAlex.
- JS-K induces autophagy-dependent ferroptosis in bladder cancer: a multimodal mechanistic and translational study.Precision clinical medicine · 2026Article
- Capsular Polysaccharides Are Crucial for the Biosorption of Aqueous Pb(II) Ions by Limosilactobacillus fermentum B44 In Vitro.Biological trace element research · 2025Article
- JS-K induces ferroptosis in renal carcinoma cells by regulating the c-Myc-GSTP1 Axis.Scientific reports · 2025Article
- JS-K activates G2/M checkpoints through the DNA damage response and induces autophagy via CAMKKβ/AMPKα/mTOR pathway in bladder cancer cells.Journal of Cancer · 2024Article
- A Novel Quinazoline Derivative Prevents and Treats Arsenic-Induced Liver Injury by Regulating the Expression of RecQ Family Helicase.International journal of molecular sciences · 2023Article
- 6-Shogaol Overcomes Gefitinib Resistance via ER Stress in Ovarian Cancer Cells.International journal of molecular sciences · 2023Article
- Enhanced IRE1α Phosphorylation/Oligomerization-Triggered XBP1 Splicing Contributes to Parkin-Mediated Prevention of SH-SY5Y Cell Death under Nitrosative Stress.International journal of molecular sciences · 2023Article
- Article
- Cancer Metabolism and Ischemia-Reperfusion Injury: Two Sides of the Same Coin.Journal of clinical medicine · 2022Review
- Gasotransmitters in the tumor microenvironment: Impacts on cancer chemotherapy (Review).Molecular medicine reports · 2022Review
- Exogenous NO induces apoptosis of hepatocellular carcinoma cells via positive p38/JNK signaling pathway and negative ERK signaling pathways.Molecular and cellular biochemistry · 2021Article
- Betulinic Acid Restricts Human Bladder Cancer Cell Proliferation In Vitro by Inducing Caspase-Dependent Cell Death and Cell Cycle Arrest, and Decreasing Metastatic Potential.Molecules (Basel, Switzerland) · 2021Article
- Cinnamaldehyde induces endogenous apoptosis of the prostate cancer-associated fibroblasts via interfering the Glutathione-associated mitochondria function.Medical oncology (Northwood, London, England) · 2020Article
- Metformin in combination with JS-K inhibits growth of renal cell carcinoma cells via reactive oxygen species activation and inducing DNA breaks.Journal of Cancer · 2020Article
- Nitric Oxide-Mediated Enhancement and Reversal of Resistance of Anticancer Therapies.Antioxidants (Basel, Switzerland) · 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
- Mechanical, nanomorphological and biological reconstruction of early‑stage apoptosis in HeLa cells induced by cytochalasin B.Oncology reports · 2019Article
- JS-K enhances chemosensitivity of prostate cancer cells to Taxol via reactive oxygen species activation.Oncology letters · 2019Article
- Iso-pencillixanthone A from a marine-derived fungus reverses multidrug resistance in cervical cancer cells through down-regulating P-gp and re-activating apoptosis.RSC advances · 2018Article
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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) and cellular oxidant stress are regulators of cancer cells. The alteration of redox status, which is induced by increased generation of ROS, results in increased vulnerability to oxidative stress. The aim of this study is to investigate the influence of O2-(2,4-dinitrophenyl) 1-[(4-ethoxycarbonyl)piperazin-1-yl]diazen-1-ium-1,2-diolate (JS-K, C13H16N6O8) on proliferation and apoptosis in bladder cancer cells and explored possible ROS-related mechanisms. Our results indicated that JS-K could suppress bladder cancer cell proliferation in a concentration- and time-dependent manner and induce apoptosis and ROS accumulation in a concentration-dependent manner. With increasing concentrations of JS-K, expression of proteins that are involved in cell apoptosis increased in a concentration-dependent manner. Additionally, the antioxidant N-acetylcysteine (NAC) reversed JS-K-induced cell apoptosis; conversely, the prooxidant oxidized glutathione (GSSG) exacerbated JS-K-induced cell apoptosis. Furthermore, we found that nitrites, which were generated from the oxidation of JS-K-released NO, induced apoptosis in bladder cancer cells to a lower extent through the ROS-related pathway. In addition, JS-K was shown to enhance the chemo-sensitivity of doxorubicin in bladder cancer cells. Taken together, the data suggest that JS-K-released NO induces bladder cancer cell apoptosis by increasing ROS levels, and nitrites resulting from oxidation of NO have a continuous apoptosis-inducing effect.
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