紫杉醇耐药机理研究进展

肿瘤细胞对紫杉醇的耐药性是限制紫杉醇临床应用的一个重要因素,本文就其耐药机理加以综述。研究认为P-糖蛋白（P-glycoprotein,P-gp)表达的升高,微管β亚基和α亚基的改变,凋亡途径中PKC、bcl-2、p53、ErbB2的表达改变均与其耐药性有关。临床上逆转紫杉醇耐药主要是利用一些紫杉醇类似物降低P-gp的表达或抑制它的活性,或者应用抗体、免疫毒素、反义寡核苷酸、脂质体逆转耐药,另外,将紫杉醇与其它药物联合应用也可能是一种有前景的联合化疗方案。

Development of research for drug-resistance mechanism of taxol

The resistant problem is the main restriction factor for clinical usage of taxol. The main mechanism of its resistance includes the high expression of P-gp, beta- and alpha-tubulin isotypes, the alteration expression of PKC, Bcl-2, p53, and ErbB2. The reversing method includes the use of analogues of taxol to reduce the expression of P-gp, or the use of antibody, immunotoxin, antisence oligonucleotide, and liposomes. The combination with other drugs can also be a method to reverse the resistance of taxol.