PDTC可在II型滤泡性淋巴瘤细胞中激活I型TRAIL信号通路。

PDTC enables type I TRAIL signaling in type II follicular lymphoma cells.

作者信息

Nuutinen Ulla, Simelius Niina, Ropponen Antti, Eeva Jonna, Mättö Mikko, Eray Mine, Pellinen Riikka, Wahlfors Jarmo, Pelkonen Jukka

机构信息

Department of Clinical Microbiology, Institute of Clinical Medicine, University of Kuopio, Kuopio, Finland.

出版信息

Leuk Res. 2009 Jun;33(6):829-36. doi: 10.1016/j.leukres.2008.09.025. Epub 2008 Nov 1.

DOI:10.1016/j.leukres.2008.09.025

PMID:18977530

Abstract

Based on Bcl-X(L) overexpression studies we identified type I and type II follicular lymphoma cell lines in response to TRAIL. We demonstrate here that either amount of caspase-8 activation or Bid cleavage could not define the dependence on mitochondria. Furthermore, an inhibitor of NF-kappaB, PDTC, enabled TRAIL to activate type I apoptotic pathway in type II cells. However, an inhibitor of IKK did not switch apoptosis to type I pathway in type II cells, indicating that NF-kappaB might not be responsible for the switch.

摘要

基于Bcl-X(L)过表达研究，我们鉴定出了对TRAIL有反应的I型和II型滤泡性淋巴瘤细胞系。我们在此证明，半胱天冬酶-8激活量或Bid裂解量均无法确定对线粒体的依赖性。此外，NF-κB抑制剂PDTC可使TRAIL在II型细胞中激活I型凋亡途径。然而，IKK抑制剂并未使II型细胞的凋亡转换为I型途径，这表明NF-κB可能与这种转换无关。