Defective Bax activation in Hodgkin B-cell lines confers resistance to staurosporine-induced apoptosis
Defective Bax activation in Hodgkin B-cell lines confers resistance to staurosporine-induced apoptosis
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DOI：
10.1038/sj.cdd.4401024
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发表时间：
2002-07-01
影响因子：
12.4
通讯作者：
Jürgensmeier, JM
中科院分区：
文献类型：
--
作者：
Kashkar, H;Krönke, M;Jürgensmeier, JM
Deregulated apoptosis represents an important hallmark of tumor cells. Here we investigated the induction of cell death signaling pathways in cell lines previously established from patients with Hodgkin's disease. Our data show that Hodgkin's disease derived B-cell lines uniformly proved resistant to staurosporine, a protein kinase C inhibitor that preferentially stimulates the mitochondrial apoptotic pathway. Contrary to control cell lines, staurosporine failed to induce cytochrome c release from mitochondria in Hodgkin derived B-cells. Correspondingly, activation of caspases was not observed in these cells. In staurosporine-treated Hodgkin cells Bax remained in its inactive state, indicating that these cell lines have a defect in this crucial step in apoptotic signaling upstream of the mitochondria. Our results suggest that the failure to activate Bax might represent a common defect of Hodgkin tumor cells of the B-cell lineage.
