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癌症化疗中克服MDR1介导的多药耐药性的最新进展。

An update on overcoming MDR1-mediated multidrug resistance in cancer chemotherapy.

作者信息

Takara Kohji, Sakaeda Toshiyuki, Okumura Katsuhiko

机构信息

Department of Hospital Pharmacy, School of Medicine, Kobe University, 7-5-2 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.

出版信息

Curr Pharm Des. 2006;12(3):273-86. doi: 10.2174/138161206775201965.

Abstract

The intrinsic or acquired resistance to anticancer drugs remains one of the most significant factors impeding the progress of cancer chemotherapy. This phenomenon often involves simultaneous resistance to other anticancer drugs that differ in their chemical structure and mode of action and are not even used in chemotherapy. This phenotype has been called multidrug resistance (MDR). Although the cellular basis underlying MDR is not fully understood, several factors mediating therapy resistance in tumors have been proposed. One of the mechanisms leading to chemoresistance of tumor cells is the increased activity of transporter proteins. The best-characterized transporter protein is MDR1/P-glycoprotein, and a number of clinical investigations have suggested that its intrinsic or acquired overexpression resulted in a poor clinical outcome of chemotherapy. Various types of compounds and techniques for the reversal of MDR1/P-glycoprotein-mediated MDR have been developed, and efforts have concentrated on the inhibition of function and suppression of expression. This review summarizes the current state of knowledge of MDR1/P-glycoprotein and the modulation of MDR by targeting MDR1/P-glycoprotein.

摘要

对抗癌药物的内在或获得性耐药性仍然是阻碍癌症化疗进展的最重要因素之一。这种现象通常涉及对其他抗癌药物的同时耐药,这些药物在化学结构和作用方式上不同,甚至未用于化疗。这种表型被称为多药耐药性(MDR)。尽管尚未完全了解MDR的细胞基础,但已经提出了几种介导肿瘤治疗耐药性的因素。导致肿瘤细胞化疗耐药的机制之一是转运蛋白活性增加。最具特征的转运蛋白是MDR1/P-糖蛋白,许多临床研究表明,其内在或获得性过表达导致化疗临床结果不佳。已经开发了各种类型的化合物和技术来逆转MDR1/P-糖蛋白介导的MDR,并且努力集中在功能抑制和表达抑制上。本综述总结了MDR1/P-糖蛋白的当前知识状态以及通过靶向MDR1/P-糖蛋白对MDR的调节。

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