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Fig. 6 | BMC Cancer

Fig. 6

From: Rac inhibition as a novel therapeutic strategy for EGFR/HER2 targeted therapy resistant breast cancer

Fig. 6

Inhibition of upregulated Rac in therapy resistant variants. a Rac activation was determined by a pulldown assay using the p21-binding domain of p21-activated kinase (PAK) from lysates of therapy sensitive or resistant SKBR3 cells. Representative western blots for active Rac.GTP, total Rac, and actin are shown. b SKBR3 gefitinb and lapatinib sensitive and resistant cells were subjected to a MTT assay for cell viability following 24 h in the Rac inhibitor EHop-016 at 0, 5, or 10 μM. c SKBR3 lapatinib resistant cells were subjected to a MTT assay for cell viability following 24 h in vehicle (0), 0.1 μM lapatinib, 250 nM MBQ-167, or a combination of 0.1 μM lapatinib and 250 nM MBQ-167. d SKBR3 lapatinib resistant cells were subjected to a caspase3/7 assay for apoptosis following 24 h in vehicle (0), 0.1 μM lapatinib, 250 nM MBQ-167, or a combination of 0.1 μM lapatinib and 250 nM MBQ-167. e MDA-MB-435 laptinib resistant HER2+ cells were treated with 0.1 μM lapatinib, 250 nM MBQ-167, or a combination of 0.1 μM lapatinib and 250 nM MBQ-167 for 48 h and cell viability quantified by a MTT assay; fold change in cell viability relative to vehicle is shown. f MDA-MB-435 trastuzumab resistant HER2+ cells were treated with 5 or 10 μg/ml trastuzumab, 250 nM MBQ-167, or a combination of 5 μg/ml trastuzumab and 250 nM MBQ-167 for 48 h and cell viability quantified by a MTT assay; fold change in cell viability relative to vehicle is shown. N = 3 ± SEM * = p ≤ 0.05, ** = p ≤ 0.01**** = p ≤ 0.001

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