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聚(ADP-核糖)聚合酶(PARP)抑制剂诱导肺癌细胞系凋亡。

Inhibition of poly(ADP-ribose) polymerase (PARP) induces apoptosis in lung cancer cell lines.

机构信息

Department of Cardiothoracic Surgery, University of Pittsburgh Cancer Institute, 15213, USA.

出版信息

Cancer Invest. 2011 Nov;29(9):608-16. doi: 10.3109/07357907.2011.621916.

Abstract

We have tested PJ34, a potent inhibitor of poly(ADP-ribose) polymerase (PARP), against various lung cancer cell lines (Calu-6, A549, and H460) and normal human bronchial epithelial cells (HBECs). While using WST1 dye assay, lung cancer cells exhibited LD(50) values of approximately 30 μM PJ34 (72-hr assay). Molecular data showed that the effect of PJ34-induced apoptosis on lung cancer cells occurs via a caspase-dependent pathway. The present study has clearly shown that (a) PARP inhibitor can independently kill tumor cells, (b) caspase-3 has modest influence on PARP-inhibitor-mediated cancer-specific toxicity, and (c) a pan-caspase inhibitor decreases the apoptotic effect of PJ34.

摘要

我们已经测试了 PJ34,一种有效的多聚(ADP-核糖)聚合酶(PARP)抑制剂,针对各种肺癌细胞系(Calu-6、A549 和 H460)和正常的人支气管上皮细胞(HBECs)。在使用 WST1 染料测定法时,肺癌细胞表现出 PJ34 的 LD(50)值约为 30 μM(72 小时测定)。分子数据表明,PJ34 诱导的细胞凋亡对肺癌细胞的影响是通过半胱天冬酶依赖性途径发生的。本研究清楚地表明:(a)PARP 抑制剂可以独立地杀死肿瘤细胞,(b)半胱天冬酶-3 对半胱天冬酶抑制剂介导的癌症特异性毒性的影响不大,(c)泛半胱天冬酶抑制剂降低 PJ34 的凋亡作用。

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