國家衛生研究院 NHRI:Item 3990099045/4703
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    题名: Induction of cell death by a novel selenophene derivative, D-501036, in human cancer cell lines
    作者: Shiah, HS;Lee, WS;Juang, SH;Chang, CJ;Chang, JY
    贡献者: National Institute of Cancer Research
    摘要: D-501036, 2,5-bis(5-hydroxymethyl-2-selenienyl)-3-hydroxymethyl-N-methylpyrrol,a novel selenophene derivative, is a highly potent antitumor agent with a broadspectrum antitumor activity against various experimental tumors cells with the IC50 innanomolar range. This compound has previously shown to exert effectively antitumoractivity against A498 xenografted human renal carcinoma cells in vivo. Treatmentof D-501036 causes cells arrest in S-phase followed by sub-G1 accumulation. Inthis study, we explored the D-501036-induced apoptotic pathway in human oraland hepatic cancer cell lines, KB and HepG2, respectively. The 50% inhibition ofgrowth of D-501036 (IC50) for KB and HepG2 cells was 470 and 2.0 nM, respectively.In Annexin-V assay, we found that the percentage of apoptotic cells induced byD-501036 was increased in a concentration- and time-dependent manner. There aretwo canonical pathways of initiation caspases, caspase 8 and 9, which are mediatedby death receptor-mediated pathway and stress-induced mitochondrial pathway.The results showed that the protein levels of procaspase 9 and 3 were decreasedand the activity of caspase 9 and 3 was increased in a dose-dependent manner.No alteration of either the amount or activity of Fas/Fas-L and procaspase 8 wasnoted in D-501036-treated cells. We further investigated that mitochondria-relatedpro-apoptotic and anti-apoptotic proteins. We found that Bax was translocated fromcytosol to mitochondria and Bcl-2 level was decreased. In addition, the mitochondrialmembrane potential permeability ( Grm) and cytochrome c release to cytosol werealso increased in cells treated with different concentrations of D-501036. We furtherdemonstrated that the levels of phosphorylated p53 at Ser15 and total p53 wasincreased in a dose- and time-dependent manner. In addition, the p53-regulatedpro-apoptotic proteins, NOXA and PUMA, were induced in the D-501036-treatedcells. In conclusion, these results demonstrated that D-501036 induced cell deaththrough p53-related mitochondrial pathway.
    日期: 2005-12
    關聯: Clinical Cancer Research. 2005 Dec;11(24):9101S.
    Link to: http://www.aacr.org/Uploads/DocumentRepository/pdf_files/2005MTCT/MT05_abstracts_C.pdf
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1078-0432&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000234382701130
    显示于类别:[張俊彥] 會議論文/會議摘要
    [夏和雄(1996-2012)] 會議論文/會議摘要

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