ArticleJournal of Cancer2024
JS-K activates G2/M checkpoints through the DNA damage response and induces autophagy via CAMKKβ/AMPKα/mTOR pathway in bladder cancer cells.
Article in Journal of Cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- JS-K induces autophagy-dependent ferroptosis in bladder cancer: a multimodal mechanistic and translational study.Precision clinical medicine · 2026Article
- An integrated analysis identified mitochondrial ribosomal protein MRPL3 as a potential prognostic biomarker and therapeutic target in pancreatic cancer.Journal of Cancer · 2025Article
- The role of AMPKα subunit in Alzheimer's disease: In-depth analysis and future prospects.Heliyon · 2024Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to investigate the effects of JS-K, a nitric oxide donor prodrug, on DNA damage and autophagy in bladder cancer (BCa) cells and to explore the potential related mechanisms. Through detecting proliferation viability, cell morphology observation and colony formation assay low concentrations of JS-K significantly inhibited BCa growth while having no effect on normal cells. JS-K induced an increase in the level of DNA damage protein γH2AX and a decrease in the level of DNA damage repair-related proteins PCNA and RAD51 in BCa cells, indicating that JS-K can induce DNA damage in BCa cells and inhibit DNA damage repair. JS-K induced G2/M phase block and calcium overload using flow cytometry analysis. Moreover, we also investigated the levels of cell G2/M cycle checkpoint-related protein and autophagy-associated protein by western blot. The results of our study demonstrated that JS-K induced BCa cells G2/M phase arrest due to upregulating proteins related to DNA damage-related G2/M checkpoint activation (p-ATM, p-ATR, p-Chk1, p-Chk2, and p-Cdc2) and down-regulation of Cyclin B1 protein. In addition, our study demonstrated that JS-K-induced autophagy in BCa cells was related to the CAMKKβ/AMPKα/mTOR pathway.
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Registered trials
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