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The JNK inhibitor SP600125 enhances dihydroartemisinin-induced apoptosis by accelerating Bax translocation into mitochondria in human lung adenocarcinoma cells |
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| Authors: | Ying-Ying Lu Xiao-Ping Wang Min Chen |
| Institution: | a MOE Key Laboratory of Laser Life Science and Institute of Laser Life Science, South China Normal University, Guangzhou 510631, China b Department of Anesthesiology, The First Affiliated Hospital of Jinan University, Guangzhou 510632, China c Institute of Optoelectronics, Shenzhen University, Key Laboratory of Optoelectronic Devices and Systems of Ministry of Education and Guangdong Province, Shenzhen 518060, China |
| 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. |
| Keywords: | DHA dihydroartemisinin STS staurosporine ROS reactive oxygen species JNK c-Jun N-terminal Kinase CCK-8 cell counting kit FCM Flow cytometry FRAP fluorescence recovery after photobleaching ΔΨm mitochondrial membrane potential Rho123 rhodamine123 GFP-Cyt c GFP-cytochrome c |
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