ArticleNeurosurgery2012
JS-K, a glutathione S-transferase-activated nitric oxide donor with antineoplastic activity in malignant gliomas.
Article in Neurosurgery, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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.
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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.
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Who cites it
27 citing papers in PubMed, 45 citations in OpenAlex.
- Vericiguat as an adjunct to temozolomide therapy improves behavioral and tumor outcomes in experimental glioblastoma.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Fifty Years of Diazeniumdiolate Research: A Tribute to Dr. Larry K. Keefer.Critical reviews in oncogenesis · 2023Article
- Glutathione-Biomolecules · 2022Article
- Nanosensitizers for sonodynamic therapy for glioblastoma multiforme: current progress and future perspectives.Military Medical Research · 2022Review
- Current understanding of the human microbiome in glioma.Frontiers in oncology · 2022Review
- The evolving landscape for cellular nitric oxide and hydrogen sulfide delivery systems: A new era of customized medications.Biochemical pharmacology · 2020Review
- Article
- Cyclooxygenase (COX) Inhibition by Acetyl Salicylic Acid (ASA) Enhances Antitumor Effects of Nitric Oxide in Glioblastoma In Vitro.Molecular neurobiology · 2019Article
- 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
- GlutathioneDrug design, development and therapy · 2018Review
- NOS Expression and NO Function in Glioma and Implications for Patient Therapies.Antioxidants & redox signaling · 2017Review
- JS-K, a nitric oxide pro-drug, regulates growth and apoptosis through the ubiquitin-proteasome pathway in prostate cancer cells.BMC cancer · 2017Article
- ATF3 reduces migration capacity by regulation of matrix metalloproteinases via NFCell death discovery · 2017Article
- Nitric oxide released from JS-K induces cell death by mitotic catastrophe as part of necrosis in glioblastoma multiforme.Cell death & disease · 2016Article
- Nitric oxide: Friend or Foe in Cancer Chemotherapy and Drug Resistance: A Perspective.Journal of cancer science & therapy · 2016Article
- N-(2-Hydroxypropyl)methacrylamide Copolymer-Drug Conjugates for Combination Chemotherapy of Acute Myeloid Leukemia.Macromolecular bioscience · 2016Article
- Nitric oxide-mediated sensitization of resistant tumor cells to apoptosis by chemo-immunotherapeutics.Redox biology · 2015Review
- A reactive oxygen species activation mechanism contributes to JS-K-induced apoptosis in human bladder cancer cells.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundGlutathione S-transferases (GSTs) control multidrug resistance and are upregulated in many cancers, including malignant gliomas. The diazeniumdiolate JS-K generates nitric oxide (NO) on enzymatic activation by glutathione and GST, showing promising NO-based anticancer efficacy.
objectiveTo evaluate the role of NO-based antitumor therapy with JS-K in U87 gliomas in vitro and in vivo.
methodsU87 glioma cells and primary glioblastoma cell lines were exposed to JS-K and a variety of inhibitors to study cell death by necrosis, apoptosis, and other mechanisms. GST expression was evaluated by immunocytochemistry, polymerase chain reaction, and Western blot, and NO release from JS-K was studied with a NO assay. The growth-inhibitory effect of JS-K was studied in a U87 xenograft model in vivo.
resultsDose-dependent inhibition of cell proliferation was observed in human U87 glioma cells and primary glioblastoma cells in vitro. Cell death was partially induced by caspase-dependent apoptosis, which could be blocked by Z-VAD-FMK and Q-VD-OPH. Inhibition of GST by sulfasalazine, cGMP inhibition by ODQ, and MEK1/2 inhibition by UO126 attenuated the antiproliferative effect of JS-K, suggesting the involvement of various intracellular death signaling pathways. Response to JS-K correlated with mRNA and protein expression of GST and the amount of NO released by the glioma cells. Growth of U87 xenografts was reduced significantly, with immunohistochemical evidence for increased necrosis and apoptosis and reduced proliferation.
conclusionOur data show for the first time the potent antiproliferative effect of JS-K in gliomas in vitro and in vivo. These findings warrant further investigation of this novel NO-releasing prodrug in gliomas.
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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.