https://scholars.lib.ntu.edu.tw/handle/123456789/533356
標題: | Tryptanthrin inhibits MDR1 and reverses doxorubicin resistance in breast cancer cells | 作者: | Yu S.-T. Chen T.-M. Tseng S.-Y. YEN-HUI CHEN |
關鍵字: | Breast cancer; Doxorubicin; MCF-7; MDR reversal; MDR1; Multidrug resistance; p53; Tryptanthrin | 公開日期: | 2007 | 卷: | 358 | 期: | 1 | 起(迄)頁: | 79-84 | 來源出版物: | Biochemical and Biophysical Research Communications | 摘要: | Development of agents to overcome multidrug resistance (MDR) is important in cancer chemotherapy. Up to date, few chemicals have been reported to down-regulate MDR1 gene expression. We evaluated the effect of tryptanthrin on P-glycoprotein (P-gp)-mediated MDR in a breast cancer cell line MCF-7. Tryptanthrin could depress overexpression of MDR1 gene. We observed reduction of P-gp protein in parallel with decreases in mRNA in MCF-7/adr cells treated with tryptanthrin. Tryptanthrin suppressed the activity of MDR1 gene promoter. Tryptanthrin also enhanced interaction of the nuclear proteins with the negatively regulatory CAAT region of MDR1 gene promoter in MCF-7/adr. It might result in suppression of MDR1 gene. In addition, tryptanthrin decreased the amount of mutant p53 protein with decreasing mutant p53 protein stability. It might contribute to negative regulation of MDR1 gene. In conclusion, tryptanthrin exhibited MDR reversing effect by down-regulation of MDR1 gene and might be a new adjuvant agent for chemotherapy. ? 2007 Elsevier Inc. All rights reserved. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-34248186686&doi=10.1016%2fj.bbrc.2007.04.107&partnerID=40&md5=c374c83f576d26ac03dc20315222fa18 https://scholars.lib.ntu.edu.tw/handle/123456789/533356 |
ISSN: | 0006291X | DOI: | 10.1016/j.bbrc.2007.04.107 | SDG/關鍵字: | doxorubicin; glycoprotein P; messenger RNA; multidrug resistance protein 1; protein p53; quinazoline derivative; tryptanthrin; unclassified drug; article; breast cancer; cancer cell; cell strain MCF 7; controlled study; gene amplification; gene expression; gene repression; human; human cell; priority journal; protein stability; Antineoplastic Agents; Breast Neoplasms; Cell Line, Tumor; Doxorubicin; Drug Resistance, Multiple; Drug Resistance, Neoplasm; Female; Gene Expression Regulation, Neoplastic; Humans; Mutation; P-Glycoprotein; Promoter Regions (Genetics); Quinazolines; Tumor Suppressor Protein p53 |
顯示於: | 臨床藥學研究所 |
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