雌酮和17β-雌二醇逆转乳腺癌耐药蛋白介导的多药耐药。
Estrone and 17beta-estradiol reverse breast cancer resistance protein-mediated multidrug resistance.
作者信息
Imai Yasuo, Tsukahara Satomi, Ishikawa Etsuko, Tsuruo Takashi, Sugimoto Yoshikazu
机构信息
Division of Molecular Biotherapy, Cancer Chemotherapy Center, Japanese Foundation for Cancer Research,Toshima-ku, Tokyo 170-8455, Japan.
出版信息
Jpn J Cancer Res. 2002 Mar;93(3):231-5. doi: 10.1111/j.1349-7006.2002.tb02162.x.
Abstract
Breast cancer resistance protein (BCRP), an adenosine triphosphate-binding cassette transporter, confers resistance to a series of anticancer reagents, including mitoxantrone, SN-38 and topotecan. In the present study, we found that estrone and 17beta-estradiol potentiated the cytotoxicity of mitoxantrone, SN-38 and topotecan in BCRP-transduced K562 cells (K562 / BCRP). These estrogens showed only a marginal effect, or none, in parental K562 cells. Estrone and 17beta-estradiol increased the cellular accumulation of topotecan in K562 / BCRP cells, but not in K562 cells, suggesting that these estrogens inhibit the BCRP-mediated drug efflux and overcome drug resistance.
摘要
乳腺癌耐药蛋白（BCRP）是一种三磷酸腺苷结合盒转运蛋白，可赋予对一系列抗癌试剂的耐药性，包括米托蒽醌、SN-38和拓扑替康。在本研究中，我们发现雌酮和17β-雌二醇增强了米托蒽醌、SN-38和拓扑替康在转导了BCRP的K562细胞（K562 / BCRP）中的细胞毒性。这些雌激素在亲本K562细胞中仅显示出微小作用或无作用。雌酮和17β-雌二醇增加了拓扑替康在K562 / BCRP细胞中的细胞蓄积，但在K562细胞中未增加，这表明这些雌激素抑制BCRP介导的药物外排并克服耐药性。
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