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. 2018 Jun 13;12:1727–1742. doi: 10.2147/DDDT.S158518

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© 2018 Bourn and Cekanova. This work is published and licensed by Dove Medical Press Limited

The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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Axitinib activates caspase-3/7 and cleavage of caspase-3 in TCC cells. h-5637 and K9TCC#1Lillie cells were treated with 0, 1, 5, and 10 μM axitinib or AB1010 for 24 hours. (A) Relative activities of caspase-3/7 were detected from cell lysates using the Caspase-Glo 3/7 luminescence assay. Both RTKIs treatments increased the caspase-3/7 activities in h-5637 cells, but not in K9TCC#1Lillie. Relative caspase-3/7 activities were normalized to control and values represent mean ± SE of two replicates of three independent experiments. Student’s t-test, **p<0.01. (B) Axitinib treatment significantly increased the expression of cPARP (specific band labeled with arrow) in h-5637 cells and cCaspase-3 in both h-5637 and K9TCC#1Lillie cells as detected by WB analysis. The treatment of 10 μM AB1010 significantly increased cCaspase-3 expression in K9TCC#1Lillie cells. Actin was used as a loading control. (C) Densitometry analyses of cCaspase-3 and cPARP protein levels from WB analysis were performed using VisionWorks analysis software. Values represent the mean ± SE of the measured densitometry of each protein band from three independent experiments. Paired Student’s t-test was used to compare axitinib and AB1010 treatments to control groups (*p<0.05, **p<0.01, ***p<0.001).

Abbreviations: RTKI, receptor tyrosine kinase inhibitor; WB, Western blot; MW, molecular weight; TCC, transitional cell carcinoma; cPARP, cleaved poly (ADP-ribose) polymerase; cCaspase-3, cleaved caspase-3.

Axitinib activates caspase-3/7 and cleavage of caspase-3 in TCC cells. h-5637 and K9TCC#1Lillie cells were treated with 0, 1, 5, and 10 μM axitinib or AB1010 for 24 hours. (A) Relative activities of caspase-3/7 were detected from cell lysates using the Caspase-Glo 3/7 luminescence assay. Both RTKIs treatments increased the caspase-3/7 activities in h-5637 cells, but not in K9TCC#1Lillie. Relative caspase-3/7 activities were normalized to control and values represent mean ± SE of two replicates of three independent experiments. Student’s t-test, **p<0.01. (B) Axitinib treatment significantly increased the expression of cPARP (specific band labeled with arrow) in h-5637 cells and cCaspase-3 in both h-5637 and K9TCC#1Lillie cells as detected by WB analysis. The treatment of 10 μM AB1010 significantly increased cCaspase-3 expression in K9TCC#1Lillie cells. Actin was used as a loading control. (C) Densitometry analyses of cCaspase-3 and cPARP protein levels from WB analysis were performed using VisionWorks analysis software. Values represent the mean ± SE of the measured densitometry of each protein band from three independent experiments. Paired Student’s t-test was used to compare axitinib and AB1010 treatments to control groups (*p<0.05, **p<0.01, ***p<0.001).

Abbreviations: RTKI, receptor tyrosine kinase inhibitor; WB, Western blot; MW, molecular weight; TCC, transitional cell carcinoma; cPARP, cleaved poly (ADP-ribose) polymerase; cCaspase-3, cleaved caspase-3.