Effects of JS-K, a novel anti-cancer nitric oxide prodrug, on gene expression in human hepatoma Hep3B cells
| العنوان: | Effects of JS-K, a novel anti-cancer nitric oxide prodrug, on gene expression in human hepatoma Hep3B cells |
|---|---|
| المؤلفون: | Huan Wang, Ray Dong, Jie Liu, Joseph E. Saavedra, Xueqian Wang, Zhengyun Liu |
| المصدر: | Biomedicine & Pharmacotherapy. 88:367-373 |
| بيانات النشر: | Elsevier BV, 2017. |
| سنة النشر: | 2017 |
| مصطلحات موضوعية: | 0301 basic medicine, Carcinoma, Hepatocellular, CD14, Antineoplastic Agents, Biology, Nitric Oxide, Piperazines, 03 medical and health sciences, 0302 clinical medicine, Cell Line, Tumor, Humans, Cytotoxic T cell, Prodrugs, Cytotoxicity, Glutathione Transferase, Pharmacology, Tissue Inhibitor of Metalloproteinase-1, Cell Death, Neovascularization, Pathologic, Caspase 3, Liver Neoplasms, General Medicine, Prodrug, Molecular biology, Matrix Metalloproteinases, digestive system diseases, Gene Expression Regulation, Neoplastic, Isoenzymes, 030104 developmental biology, Apoptosis, 030220 oncology & carcinogenesis, Cancer cell, Tumor necrosis factor alpha, Thrombospondins, Azo Compounds, Immunostaining, Acute-Phase Proteins |
| الوصف: | JS-K is a novel anticancer nitric oxide (NO) prodrug effective against a variety of cancer cells, including the inhibition of AM-1 hepatoma cell growth in rats. To further evaluate anticancer effects of JS-K, human hepatoma Hep3B cells were treated with JS-K and the compound control JS-43-126 at various concentrations (0–100 μM) for 24 h, and cytotoxicity was determined by the MTS assay. The compound control JS-43-126 was not cytotoxic to Hep3B cells at concentrations up to 100 μM, while the LC 50 for JS-K was about 10 μM. To examine the molecular mechanisms of antitumor effects of JS-K, Hep3B cells were treated with 1–10 μM of JS-K for 24 h, and then subjected to gene expression analysis via real time RT-PCR and protein immunostain via confocal images. JS-K is a GST-α targeting NO prodrug, and decreased immunostaining for GST-α was associated with JS-K treatment. JS-K activated apoptosis pathways in Hep3B cells, including induction of caspase-3, caspase-9 , Bax , TNF-α , and IL-1β , and immunostaining for caspase-3 was intensified. The expressions of thrombospondin-1 (TSP-1) and the tissue inhibitors of metalloproteinase-1 (TIMP-1) were increased by JS-K at both transcript and protein levels. JS-K treatment also increased the expression of differentiation-related genes CD14 and CD11b , and depressed the expression of c-myc in Hep3B cells. Thus, multiple molecular events appear to be associated with anticancer effects of JS-K in human hepatoma Hep3B cells, including activation of genes related to apoptosis and induction of genes involved in antiangiogenesis and tumor cell migration. |
| تدمد: | 0753-3322 |
| DOI: | 10.1016/j.biopha.2017.01.080 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1c386e8cf4485b51fd328aa821afc63a https://doi.org/10.1016/j.biopha.2017.01.080 |
| Rights: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....1c386e8cf4485b51fd328aa821afc63a |
| قاعدة البيانات: | OpenAIRE |
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