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核因子κB在肿瘤坏死因子相关凋亡诱导配体抵抗中起作用吗?

Is there a role for nuclear factor kappaB in tumor necrosis factor-related apoptosis-inducing ligand resistance?

作者信息

Plantivaux Amandine, Szegezdi Eva, Samali Afshin, Egan Laurence

机构信息

Department of Pharmacology and Therapeutics, National University of Ireland, Galway, Ireland.

出版信息

Ann N Y Acad Sci. 2009 Aug;1171:38-49. doi: 10.1111/j.1749-6632.2009.04725.x.

Abstract

One strategy for cancer management consists of promoting selective apoptosis of cancer cells. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), a proapoptotic cytokine, is a promising anticancer agent because of its ability to selectively induce apoptosis in established tumor cell lines but not in nontransformed cells. However, many tumors have developed mechanisms of resistance against killing by TRAIL. Whether or not the transcription factor nuclear factor (kappaB) is involved in TRAIL resistance is uncertain, and this short review aims to summarize currently available data on this question.

摘要

癌症治疗的一种策略是促进癌细胞的选择性凋亡。肿瘤坏死因子相关凋亡诱导配体(TRAIL)是一种促凋亡细胞因子,因其能够在已建立的肿瘤细胞系中选择性诱导凋亡,而在未转化细胞中则不能,所以它是一种很有前景的抗癌药物。然而,许多肿瘤已经形成了对TRAIL杀伤的耐药机制。转录因子核因子κB是否参与TRAIL耐药尚不确定,本简短综述旨在总结关于这个问题的现有数据。

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