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Fig. 7 | BMC Cancer

Fig. 7

From: Differential cytotoxicity induced by the Titanium(IV)Salan complex Tc52 in G2-phase independent of DNA damage

Fig. 7

Activation of p38 stress-kinase, caspase7 and PARP1 cleavage by Tc52 in U2OS and HEK293. Treatment regimen was as described for Fig. 4. Ctr: solvent treated samples, +: positive control. Shown below each incubation time (2 h, 6 h, 30 h) are the different Tc52 concentrations used, i.e., 2 μM, 5 μM, and 10 μM. For statistical analysis, ratio of ECL signals of target protein compared to the respective loading control was calculated. Significant changes compared to solvent-control were analyzed by two-way ANOVA with Dunnett's Multiple Comparison Test, p < 0.05 = *; p < 0.01 = **; p < 0.001 = ***. a: Respective western blot panel for U2OS cells, displaying levels of phosphorylated p38 (p-p38) stress kinase, total p38 (p38), α-tubulin, cleaved caspase7, GAPDH, PARP1 and 85-kDa apoptotic fragment (arrow), and β-actin. b: Respective western blot panel for HEK293 cells, displaying levels of phosphorylated p38 (p-p38) stress kinase, total p38 (p38), α-tubulin, cleaved caspase7, GAPDH, PARP1 and 85-kDa apoptotic fragment (arrow), and β-actin. c: Evaluation of stress-response in U2OS cells from at least three independent experiments. Panels display ratios of p-p38/p38, cleaved caspase7/GAPDH and PARP1 85 kDa/total, which all increase significantly in a time- and dose-dependent manner. d: Evaluation of stress-response in HEK293 from at least three independent experiments. Panels display ratios of p-p38/p38, cleaved caspase7/GAPDH and PARP1 85 kDa/total. Only p38-dependent stress response increases significantly in a time- and dose-dependent manner without any signs of apoptotic alterations (cleavage of caspase7 or PARP1)

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