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首页> 美国卫生研究院文献>Cancer Science >Altered Expression of γ‐Glutamylcysteine Synthetase Metallothionein and Topoisomerase I or II during Acquisition of Drug Resistance to Cisplatin in Human Ovarian Cancer Cells
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Altered Expression of γ‐Glutamylcysteine Synthetase Metallothionein and Topoisomerase I or II during Acquisition of Drug Resistance to Cisplatin in Human Ovarian Cancer Cells

机译：人卵巢癌细胞对顺铂耐药性获得过程中γ-谷氨酰半胱氨酸合成酶金属硫蛋白和拓扑异构酶I或II表达的改变

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This study was designed to elucidate the mechanisms of cisplatin (CDDP) resistance using two human ovarian cancer cell lines, KF and TYK, and two CDDP‐resistant lines, KFr and TYK/R, derived from the former lines. KFr and TYK/R showed about 3‐fold higher resistance to the cytotoxic effects of CDDP than their parental lines. They also showed a significant increase in sensitivity to not only etoposide, but also (+)‐(4S)‐4, ll‐diethyl‐4‐hydroxy‐9‐[(4‐piperidino‐piperidino)carbonyloxy]‐lH‐pyrano[3′,4′:6,7]inodolizino[l,2‐b]quinoline‐3,14(4H, 12H)‐dione hydrochloride trihydrate (CPT‐11). Cellular CDDP accumulation levels in KFr and TYK/R were decreased from those of the parental cells. By contrast, the cellular glutathione (GSH) content in KFr cells was 1.7‐fold higher than that in KF, whereas TYK/R cells had a 40% lower content than TYK cells. Cellular mRNA levels of drug‐resistance‐related genes, such as DNA topoisomerase (topo) I and topo II, glutathione S‐transferase‐π (GST‐π;), γ‐glutamylcysteine synthetase (.γ‐GCS), and metallothionein (hMT) genes, were compared between drug‐sensitive KF or TYK and KFr or TYK/R. KFr cells had 8.5‐ and 24.7‐fold higher mRNA levels of γ‐GCS and topo II genes than KF cells while KFr had only a slight increase in GST‐π mRNA level as compared with KF. By contrast, TYK/R cells had 2.9‐ and 1.7‐fold higher hMT and topo I mRNA levels than TYK cells. Acquisition of CDDP resistance in human ovarian cancer cells thus appeared to be related mainly to expression of γ‐GCS, topo II and hMT genes, and partly to that of topo I and GST‐π genes, in addition to a decrease in CDDP accumulation
机译：这项研究旨在阐明使用两个人类卵巢癌细胞系KF和TYK以及两个源自前者系的CDDP耐药系KFr和TYK / R来阐明顺铂（CDDP）耐药的机制。 KFr和TYK / R对CDDP的细胞毒性作用的抵抗力比其亲本高约3倍。他们不仅对依托泊苷，而且对（+）-（4S）-4，ll-二乙基-4-羟基-9-[（4-哌啶子基-哌啶子基）羰氧基] -1H-吡喃基[]的敏感性也显着提高。 3'，4'：6,7] inodolizino [1,2-b] quinoline-3,14（4H，12H）-dione hydrochloride trihydrochloride（CPT-11）。与亲代细胞相比，KFr和TYK / R中的细胞CDDP积累水平降低了。相比之下，KFr细胞中的细胞谷胱甘肽（GSH）含量是KF中的1.7倍，而TYK / R细胞的含量却比TYK细胞低40％。耐药相关基因的细胞mRNA水平，例如DNA拓扑异构酶（topo）I和topo II，谷胱甘肽S-转移酶-π（GST-π;），γ-谷氨酰半胱氨酸合成酶（.γ-GCS）和金属硫蛋白（在药物敏感性KF或TYK与KFr或TYK / R之间比较了hMT）基因。 KFr细胞的γ-GCS和topo II基因的mRNA水平比KF细胞高8.5和24.7倍，而KFr的GST-πmRNA水平仅比KF略有增加。相比之下，TYK / R细胞的hMT和topo I mRNA水平比TYK细胞高2.9和1.7倍。因此，人类卵巢癌细胞对CDDP抗性的获得似乎主要与γ-GCS，topo II和hMT基因的表达有关，部分与topo I和GST-π基因的表达有关，此外还减少了CDDP的积累

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