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. Author manuscript; available in PMC: 2011 May 16.

Published in final edited form as: Lung Cancer. 2010 Jul 31;71(3):271–282. doi: 10.1016/j.lungcan.2010.06.002

Fig. 2 — Expression of p53, p21, caspase 3, cleaved caspase 3, PARP, cleaved PARP, Bax, Bcl₂, survivin in H460 (A) and A549 (B) tumor cell lysates by western blotting and (C) quantitation of apoptotic protein expression. H460 cells were treated with Cis (0.8 μM), Nos (30 μM), and Cis (0.8 μM) + Nos (30 μM) and A549 cells were treated with Cis (2.5 μM), Nos (40 μM), and Cis (2.58 μM) + Nos (40 μM) for 72 h and whole-cell lysates were analyzed by western blotting for protein expression. Protein expression levels (relative to β-actin) were determined. Mean ± SE for three replicate determinations. One-way ANOVA followed by post-Tukey test was used for statistical analysis. P < 0.01 (*significantly different from untreated controls; **significantly different from Nos and Cis single treatments).

Fig. 2 — Expression of p53, p21, caspase 3, cleaved caspase 3, PARP, cleaved PARP, Bax, Bcl₂, survivin in H460 (A) and A549 (B) tumor cell lysates by western blotting and (C) quantitation of apoptotic protein expression. H460 cells were treated with Cis (0.8 μM), Nos (30 μM), and Cis (0.8 μM) + Nos (30 μM) and A549 cells were treated with Cis (2.5 μM), Nos (40 μM), and Cis (2.58 μM) + Nos (40 μM) for 72 h and whole-cell lysates were analyzed by western blotting for protein expression. Protein expression levels (relative to β-actin) were determined. Mean ± SE for three replicate determinations. One-way ANOVA followed by post-Tukey test was used for statistical analysis. P < 0.01 (*significantly different from untreated controls; **significantly different from Nos and Cis single treatments).