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. 2016 Jan 7;7(5):5924–5942. doi: 10.18632/oncotarget.6827

Figure 2. C12 induces tumor apoptotic cell death independent of anti-apoptotic Bcl-2 proteins.

Figure 2

(A) Retrovirally overexpressed Bcl-2 in A549 cells was examined by western blot. (B) Cell viability was measured 48 hours after C12 or actinomycin D (ActD) exposure. (C) Caspase-3/7 activities were determined following 2 hour exposure to C12 and 24 hour exposure to actinomycin D. (D) C12's effect on mitochondrial membrane potential is independent of Bcl-2. A549-vector and A549-Bcl-2-overexpressing cells were loaded with JC1, and its fluorescence was measured using imaging microscopy during the treatment with 100 μM C12 and 5 μM FCCP. Typical results from three independent experiments are shown. (E) C12 caused equivalent depolarization of mitochondrial potential in vector and Bcl-2-overexpressing A549 cells. All data are shown as mean ± standard deviation of three independent experiments. Asterisks indicate P < 0.05 (*); ns, no significant by student's unpaired t test.