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Figure 3 | BMC Cancer

Figure 3

From: Differential modulation of nicotine-induced gemcitabine resistance by GABA receptor agonists in pancreatic cancer cell xenografts and in vitro

Figure 3

A: Levels of cleaved caspase-3 in xenograft tissues. Cleaved caspase-3 was measured in xenograft tissues by ELISA assay. The differences among treatment groups were significant (P < 0.001 by Kruskal-Wallis ANOVA). Gemcitabine significantly increased cleaved caspase-3 levels, a response enhanced by GABA but significantly reduced by baclofen or nicotine. GABA restored these anti-apoptotic effects of gemcitabine in nicotine treated mice while also significantly increasing cleaved caspase-3 levels when given as a single agent. Baclofen significantly reduced the apoptosis-inducing effect of gemcitabine while failing to reverse the adverse effects of nicotine. *Significantly ( p < 0.01 by Mann–Whitney test) different from controls.Significantly (p < 0.01 by Mann–Whitney test) different from gemcitabine alone. Significantly (p < 0.01 by Mann–Whitney test) different from treatment with gemcitabine plus nicotine. B: Levels of p-AKT in xenograft tissues (ELISA assays). Variation in p-AKT levels among treatment groups was significant (p < 0.001 by Krsukal-Wallis ANOVA). Gemcitabine and GABA each significantly reduced p-AKT levels whereas baclofen significantly increased p-AKT levels above those observed in control mice. Nicotine and baclofen each significantly diminished the inhibitory effects of gemcitabine on p-AKT. All data are mean values and standard deviations from five randomly selected xenografts per treatment group. Significantly ( p < 0.01 by Mann–Whitney test) different from controls. Significantly (p < 0.01 by Mann–Whitney test) different from gemcitabine alone. Significantly (p < 0.01 by Mann–Whitney test) different from treatment with gemcitabine plus nicotine.

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