肿瘤多药耐药的细胞生物学机制
Cell biological mechanisms of multidrug resistance in tumors.
作者信息
Simon S M, Schindler M
机构信息
Laboratory of Cellular Biophysics, Rockefeller University, New York, NY 10021.
出版信息
Proc Natl Acad Sci U S A. 1994 Apr 26;91(9):3497-504. doi: 10.1073/pnas.91.9.3497.
Abstract
Multidrug resistance (MDR) is a generic term for the variety of strategies tumor cells use to evade the cytotoxic effects of anticancer drugs. MDR is characterized by a decreased sensitivity of tumor cells not only to the drug employed for chemotherapy but also to a broad spectrum of drugs with neither obvious structural homology nor common targets. This pleiotropic resistance is one of the major obstacles to the successful treatment of tumors. MDR may result from structural or functional changes at the plasma membrane or within the cytoplasm, cellular compartments, or nucleus. Molecular mechanisms of MDR are discussed in terms of modifications in detoxification and DNA repair pathways, changes in cellular sites of drug sequestration, decreases in drug-target affinity, synthesis of specific drug inhibitors within cells, altered or inappropriate targeting of proteins, and accelerated removal or secretion of drugs.
摘要
多药耐药性（MDR）是一个通用术语，用于描述肿瘤细胞用来逃避抗癌药物细胞毒性作用的多种策略。MDR的特征在于肿瘤细胞不仅对用于化疗的药物敏感性降低，而且对一系列既无明显结构同源性也无共同靶点的药物敏感性降低。这种多效性耐药是肿瘤成功治疗的主要障碍之一。MDR可能源于质膜、细胞质、细胞区室或细胞核内的结构或功能变化。从解毒和DNA修复途径的改变、药物隔离细胞位点的变化、药物-靶点亲和力的降低、细胞内特定药物抑制剂的合成、蛋白质靶向改变或不当以及药物的加速清除或分泌等方面讨论了MDR的分子机制。
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