ArticleBMC cancer2019
JS-K, a nitric oxide donor, induces autophagy as a complementary mechanism inhibiting ovarian cancer.
Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 31 citations in OpenAlex.
- Overview of oxidative metabolism and autophagy under metal stress.Journal of experimental botany · 2026Review
- Nanomedicine-powered redox homeostasis modulation: Disrupting antioxidant systems and inducing oxidative stress for precision tumor therapy.Materials today. Bio · 2026Review
- JS-K induces autophagy-dependent ferroptosis in bladder cancer: a multimodal mechanistic and translational study.Precision clinical medicine · 2026Article
- Article
- 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
- S-Nitrosylated Proteins Involved in Autophagy inLife (Basel, Switzerland) · 2023Article
- Role of autophagy and its regulation by noncoding RNAs in ovarian cancer.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Gomisin A enhances the antitumor effect of paclitaxel by suppressing oxidative stress in ovarian cancer.Oncology reports · 2022Article
- Opportunities for Nitric Oxide in Potentiating Cancer Immunotherapy.Pharmacological reviews · 2022Review
- Gasotransmitters in the tumor microenvironment: Impacts on cancer chemotherapy (Review).Molecular medicine reports · 2022Review
- The Anti-Tumor Efficacy of Verbascoside on Ovarian CancerFrontiers in oncology · 2022Article
- Article
- Insight into the role of p62 in the cisplatin resistant mechanisms of ovarian cancer.Cancer cell international · 2020Review
- Nitric Oxide-Mediated Enhancement and Reversal of Resistance of Anticancer Therapies.Antioxidants (Basel, Switzerland) · 2019Review
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundOvarian cancer (OC) is the second most frequent gynecological cancer and is associated with a poor prognosis because OC progression is often asymptoma-tic and is detected at a late stage. There remains an urgent need for novel targeted therapies to improve clinical outcomes in ovarian cancer. As a nitric oxide prodrug, JS-K is reported highly cytotoxic to human cancer cells such as acute myeloid leukemia, multiple myeloma and breast cancer. This study is aim to investigate the influence of JS-K on proliferation and apoptosis in ovarian cancer cells and explored possible autophagy-related mechanisms, which will contribute to future ovarian cancer therapy and supply theory support that JS-K holds great promise as a novel therapeutic agent against ovarian cancer.
methodsThe cytotoxicity, extracellular ROS/RNS activity and apoptotic effect of JS-K and indicated inhibitors on ovarian cancer cells in vitro were evaluated by MTT assay, extracellular ROS/RNS assay, caspases activities assay and western blot. Further autophagy effect of JS-K and indicated inhibitors were examined by MTT assay, cell transfection, immunofluorescence analysis, transmission electron microscopy (TEM) analysis and western blot on ovarian cancer cells in vitro. In vivo, the BALB/c-nude female mice with SKOV3 ovarian cancer cells xenograft were used to examine the efficacy of JS-K treatment on tumor growth. PCNA and p62 proteins were analyzed by immunohistochemistry.
resultsIn vitro, JS-K inhibited the proliferation of ovarian cancer cells, induced apoptosis and cell nucleus shrinkage, enhanced the enzymatic activity of caspase-3/7/8/9, and significantly increased the production of ROS/RNS in ovarian cancer A2780 and SKOV3 cells, these effects were attenuated by inhibition of NAC. In addition, JS-K induced autophagy-related proteins and autophagosomes changes in ovarian cancer A2780 and SKOV3 cells. In vivo, JS-K inhibited tumor growth, decreased p62 protein expression and increased the expression levels of PCNA in xenograft models which were established using SKOV3 ovarian cancer cells.
conclusionTaken together, we demonstrated that ROS/RNS stress-mediated apoptosis and autophagy are mechanisms by which SKOV3 cells undergo cell death after treatment with JS-K in vitro. Moreover, JS-K inhibited SKOV3 tumor growth in vivo. An alternative therapeutic approach for triggering cell death in cancer cells could constitute a useful multimodal therapies for treating ovarian cancer, which is known for its resistance to apoptosis-inducing drugs.
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