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. Author manuscript; available in PMC: 2009 Oct 1.
Published in final edited form as: Cancer Res. 2008 Oct 1;68(19):7985–7994. doi: 10.1158/0008-5472.CAN-08-1418

Figure 1.

Figure 1

Figure 1

BCL-2 protects against paclitaxel-induced apoptosis and ABT-737 might overcome BCL-2-mediated paclitaxel resistance. A, MCF-7 cells were stably transfected with control vector (MCF-7 Mock) or pCI.Neo.FlagBCL-2 (MCF-7 BCL-2). The expression of FLAG-BCL-2 in transfected cells were verified by immunoblotting with anti-BCL-2 or anti-FLAG antibody. β-Actin was probed as a loading control. B, cells were treated with treated with paclitaxel (100 nM), ABT-737 (100 nM), combination of paclitaxel (100 nM) and ABT-737 (100 nM), enantiomer of ABT-737 (100 nM) or combination of enantiomer of ABT-737 (100 nM) and paclitaxel (100 nM) for 48 h. The percent apoptotic response was evaluated by Annexin V staining. Columns, mean of three independent experiments; bars, SE. **, P < 0.01, paclitaxel plus ABT-737 treated with respect to paclitaxel-only treated. C, T47-D cells were stably transfected with control vector (T47D Mock) or pCI.Neo.FlagBCL-2 (T47D BCL-2). The expression of FLAG-BCL-2 in transfected cells were verified by immunoblotting with anti-BCL-2 or anti-FLAG antibody. β-Actin was probed as a loading control. D, cells were treated with treated with paclitaxel (100 nM), ABT-737 (100 nM), combination of paclitaxel (100 nM) and ABT-737 (100 nM), enantiomer of ABT-737 (100 nM) or combination of enantiomer of ABT-737 (100 nM) and paclitaxel (100 nM) for 48 h. The percent apoptotic response was evaluated by Annexin V staining. Columns, mean of three independent experiments; bars, SE. **, P < 0.01, paclitaxel plus ABT-737 treated with respect to paclitaxel-only treated.