Figure 1 from Bcl-xL Is a Key Mediator of Apoptosis Following KRASG12C Inhibition in KRASG12C-mutant Colorectal Cancer

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Response to AZ’1569 in KRASG12C MT colorectal cancer cells. A,KRASG12CMT colorectal cancer cells were treated with increasing concentrations of AZ’1569 for 120 hours and cell viability determined using CTG assay. IC50 values were calculated using Prism software package. Dashed line indicates 50% cell viability. Representative of three independent experiments is shown. B, Colorectal cancer cells were treated with AZ’1569 for 48 hours. PARP, cleaved C3, and KRAS were determined by WB (top), caspase-3/7 activity levels were measured with values presented as a percentage of their respective controls. Significance was analyzed using an unpaired t test (bottom). (Cl = cleaved). C, Signaling analysis upon AZ’1569 treatment. KRASG12C MT colorectal cancer cell lines were treated with 1 μmol/L AZ’1569 for the indicated times, and protein lysates were used for WB analysis for the KRAS downstream effectors. Densitometry on WB images was quantified using ImageJ software and normalized to the respective untreated control. Dashed lines on the graphs represent a value of 1.

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