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. Author manuscript; available in PMC: 2016 Jan 1.
Published in final edited form as: Mol Cancer Ther. 2014 Nov 19;14(1):183–192. doi: 10.1158/1535-7163.MCT-14-0584

Figure 2.

Figure 2

The viability of MDA-MB-231 cells treated with SRT1720 is decreased due to necrosis but not apoptosis. A, Apoptosis/necrosis measurement by annexin V/propidium iodide analysis of MDA-MB-231 cells treated with 5 µmol/L of SRT1720 for 8 hours. There was a 1 % increase in early apoptosis and a 12% increase in late apoptosis/necrotic cells (P < 0.01, **). B, Propidium iodide positive MDA-MB-231 cells treated with SRT1720 for 8 hours as a measurement for necrosis. There was a significant increase in necrosis with 5 (13%) and 10 (24%) µmol/L of SRT1720 treatment (P < 0.001, ***). C, Viability of MDA-MB-231 cells treated with SRT1720 and 20 µmol/L of the pan-caspase inhibitor ZVAD for 24 hours. SRT1720 caused a 74% reduction in cell viability (P < 0.001, ***). There was no significant difference between SRT1720 treatment alone and in combination with ZVAD. D, Expression of active caspase-3 in MDA-MB-231 cells treated with either 5 or 10 µmol/L SRT1720 or 10 µmol/L of the proteosome inhibitor bortezomib as a control for caspase-3 activation. There was increased caspase 3 cleavage with bortezomib but not SRT1720 (upper band on immunoblot).