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    題名: 5 ' Cytosine-phospho-guanine island methylation is responsible for p14ARF inactivation and inversely correlates with p53 overexpression in resected non-small cell lung cancer
    作者: Hsu, HS;Wang, YC;Tseng, RC;Chang, JW;Chen, JT;Shih, CM;Chen, CY;Wang, YC
    貢獻者: 附設醫院內科部呼吸治療科;Natl Taiwan Normal Univ, Dept Life Sci, Taipei 116, Taiwan;Natl Yang Ming Univ, Sch Med, Div Thorac Surg, Vet Gen Hosp, Taipei 112, Taiwan;Taichung Vet Gen Hosp, Dept Pathol, Taichung, Taiwan;Taichung Vet Gen Hosp, Div Thorac Surg, Taichung, Taiwan;China Med Coll Hosp, Div Pulm & Crit Care Med, Dept Internal Med, Taichung, Taiwan;Chung Shan Med Univ, Inst Med, Taichung, Taiwan
    日期: 2004
    上傳時間: 2010-09-24 14:20:20 (UTC+8)
    出版者: AMER ASSOC CANCER RESEARCH
    摘要: Arylamine N-acetyltransferase (NAT) plays an important role in the metabolism of 2-aminofluorene (AF) and some types of arylamine drugs and carcinogens. Our previous studies have demonstrated that paclitaxel decreases NAT activity in human bladder, blood, colon and lung cancer cells. In this study, paclitaxel was selected to test the inhibition of NAT activity (N-acetylation of AF) and NAT gene expression in a human bladder cancer cell line (T24). The NAT activity was determined by high performance liquid chromatography for measuring the levels of N-acetylation of AF. The data showed that a 24-hour paclitaxel treatment decreased the amount of N-acetylation of AF in T24 cells. The NAT enzymes were stained and analyzed by Western blotting and flow cytometry. The tests indicated that paclitaxel decreased the levels of NAT in T24 cells. The expression of the NAT gene (mRNA T NAT) was determined by polymerase chain reaction (PCR) and cDNA microarray and it was found that paclitaxel induced the down-regulation of mRNA NAT expression in T24 cells.
    關聯: CLINICAL CANCER RESEARCH 10(14):4734-4741
    顯示於類別:[台中附設醫院] 期刊論文

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