The JNK inhibitor SP600125 enhances dihydroartemisinin-induced apoptosis by accelerating Bax translocation into mitochondria in human lung adenocarcinoma cells.

Abstract:

:The C-Jun N-terminal Kinase (JNK) inhibitor SP600125 is widely used to inhibit the JNK-mediated Bax activation and cell apoptosis. However, this report demonstrates that SP600125 synergistically enhances the dihydroartemisinin (DHA)-induced human lung adenocarcinoma cell apoptosis by accelerating Bax translocation and subsequent intrinsic apoptotic pathway involving mitochondrial membrane depolarization, cytochrome c release, caspase-9 and caspase-3 activation. The dynamical analysis of GFP-Bax mobility inside single living cells using fluorescence recovery after photobleaching revealed that SP600125 aggravated the DHA-induced decrease of Bax mobility and Bax translocation. These results for the first time present a novel pro-apoptotic action of SP600125 in DHA-induced apoptosis.

journal_name

FEBS Lett

journal_title

FEBS letters

authors

Lu YY,Chen TS,Wang XP,Qu JL,Chen M

doi

10.1016/j.febslet.2010.08.014

subject

Has Abstract

pub_date

2010-09-24 00:00:00

pages

4019-26

issue

18

eissn

0014-5793

issn

1873-3468

pii

S0014-5793(10)00670-8

journal_volume

584

pub_type

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