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頁籤選單縮合
題名 | 作用於DNA拓樸異構酶之抗癌藥物= |
---|---|
作者 | 商惠芳; 陳作琳; 林嘉伯; 黃昭蓮; |
期刊 | 藥物食品分析 |
出版日期 | 19950900 |
卷期 | 3:3 1995.09[民84.09] |
頁次 | 頁145-153 |
分類號 | 418.31 |
語文 | chi |
關鍵詞 | DNA拓樸異構酶; 抗癌藥物; DNA topoisomerase poison; DNA topoisomerase I; DNA topoisomerase II; |
英文摘要 | Eukaryotic DNA topoisomerases are ubiquitous nuclear enzymes that alter DNA topology by breaking and rejoining DNA strands. There are two classes of DNA topoisomerases; DNA topoisomerase I introduces a transient single-strand DNA break, while topoisomerase II introduces transient double-strand DNA breaks for each catalytic reaction. Both are important for solving topological problems arising during DNA replication, transcription, recombinaion and other cellular functions. Recently, scientists have realized the importance of topoisomerases as new therapeuic targets for antibacterial, antifungal, antiparastitic, antiviral and anticancer drugs. The present review focuses on anticancer drugs targeting mammalian DNA topoisomerases, which are named DNA topoisomerase poison. Camptothecin and VM26 (teniposide) are representative DNA topoisomerase poisons that target DNA topoisomerase I and topoisomerase II, respectively. These drugs alter the breakage-reunion reactions of DNA topoisomerases by trapping topoisomerase-DNA cleavable complexes in both the purified system and cultured cells. However, resistance to various DNA topoisomerase poisons has been documented in cancer cells with repect to MDRI overexpression, reduced topoisomerase levels, drug-resistant mutant topoisomerase, lengthened cell cycle time and altered DNA repair function. A better understanding of the molecular targets for anticancer drugs and the various drug-resistance mechanisms may help us to discover and tailor new drugs for particular drug-resistant tumors. |
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