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Title 

Failure to activate caspase 3 in phorbol ester-resistant leukemia cells is associated with resistance to apoptotic cell death

Authors 

Y J ChoiJ W ParkJ H WooY H KimSang-Han LeeJ M LeeT K Kwon

Publisher 

Elsevier

Issue Date 

2002

Citation 

Cancer Letters, vol. 182, no. 2, pp. 183-191

Keywords 

Aktapoptosiscaspase 3cell cycleprotein kinase C inhibitor2 [1 (3 amidinothiopropyl) 1h indol 3 yl] 3 (1 methyl 1h indol 3 yl)maleimidecaspase inhibitorphorbol 13 acetate 12 myristatecancer cell culturehuman cell

Abstract 

The protein kinase C (PKC)-specific inhibitor, Ro-31-8220, has been shown to induce anti-proliferation and apoptosis of human cancer cell lines. In the present study, we determined the molecular pathways that lead to apoptosis after treatment of cells with the PKC-specific inhibitor RO-31-8220. For this, we used the U937 human leukemia cell line and a phorbolmyristate acetate (PMA)-resistant derivative cell line, R-U937. Ro-31-8220 treatment of U937 cells leads to apoptosis, which is accompanied by activation of caspase 3 (as measured by decreased levels of the 32kDa inactive form and increased proteolytic cleavage of phospholipase C (PLC)-γ1). The broad-range caspase inhibitor z-VAD-fmk inhibits this induction of apoptosis, supporting a direct link between caspase activation and Ro-31-8220 induction of apoptosis. This activation of apoptosis is also accompanied by release of cytochrome c, but not by altered expression of Bcl-2 family protein or IAP family proteins. In R-U937 cells, Ro-31-8220 fails to cause release of cytochrome c, activation of caspase 3, or apoptosis. Activation of Akt occurs to a greater extent in the R-U937 cells than the U937 cells and thus might be related to protection from Ro-31-8220-induced apoptosis.

ISSN 

0304-3835

Link 

http://dx.doi.org/10.1016/S0304-3835(02)00082-4

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


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