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 Lettjournal_title
FEBS lettersauthors
Lu YY,Chen TS,Wang XP,Qu JL,Chen Mdoi
10.1016/j.febslet.2010.08.014subject
Has Abstractpub_date
2010-09-24 00:00:00pages
4019-26issue
18eissn
0014-5793issn
1873-3468pii
S0014-5793(10)00670-8journal_volume
584pub_type
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