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. Author manuscript; available in PMC: 2011 Oct 30.
Published in final edited form as: Mol Cancer Ther. 2008 Feb;7(2):297–313. doi: 10.1158/1535-7163.MCT-07-2166

Table 1.

GST-MDA-7 causes a caspase-9-dependent induction of primary human glioma cell death

Treatment: caspase inhibitor GBM5 GST GBM5 GST-MDA-7 GBM6 GST GBMG GST-MDA-7 GBM12 GST GBM12 GST-MDA-7
Vehicle 2.2 ± 0.6 34.0 ± 2.1 4.4 ± 0.6 45.2 ± 2.3 2.1 ± 0.8 20.3 ± 0.8
z-VAD 2.9 ± 1.0 7.7 ± 0.6* 6.4 ± 0.4 11.7 ± 1.5* 4.0 ± 1.2 9.1 ± 1.5*
IETD 3.4 ± 1.0 34.4 ± 2.9 4.8 ± 0.2 45.0 ± 7.2 3.5 ± 1.4 20.7 ± 2.7
LEHD 3.6 ± 7.5 8.9 ± 1.7* 3.3 ± 2.3 12.0 ± 1.5* 4.7 ± 1.8 11.0 ± 0.6*

NOTE: Primary human glioma cells (GBM5, GBM6, and GBM12) were treated 24 h after plating with vehicle (DMSO), a pan-caspase inhibitor (z-VAD), a caspase-8 specific inhibitor (IETD), or a caspase-9 specific inhibitor (LEHD; all at 50 μmol/L) followed 30 min later by treatment of cells with 20 nmol/L GST-MDA-7 or GST. Cell viability was determined 96 h after GST-MDA-7 treatment by trypan blue exclusion assays in triplicate using a hemacytometer (±SE; n = 5).

*

P < 0.05, lower amount of cell killing than vehicle-treated cells.