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. 2014 Oct 21;19(2):340–350. doi: 10.1111/jcmm.12444

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© 2015 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Fig 2 — Activation of PARP, caspases and other apoptosis mediators during HSP27-dependent gemcitabine-induced apoptosis. (A and B) Immunoblotting showing cleavage of PARP, CASPASE 3, CASPASE 8 and CASPASE 9 upon gemcitabine treatment in HSP27-overexpressing PL5/hu18 but not parental control cells in a dose-dependent (A) and time-dependent (B) manner. (C) Proliferation assays displaying abrogation of HSP27-dependent gemcitabine sensitivity through pre-incubation with the pan-caspase inhibitor Z-VAD-FMK at 20 μM for 3 hrs. Error bars represent SEM of at least three independent experiments. (D) Immunoblotting assessing expression changes of the indicated pro- or anti-apoptotic molecules in parental PL5 and PL5/hu18 cells upon treatment with gemcitabine at 25 nM at the indicated time-points. ß-ACTIN served as loading control. (E) Immunoblotting displaying time-dependent BIM expression changes in PL5/hu18 cells treated with gemcitabine at 25 nM. (F) Immunoblotting assessing expression changes of CHOP and GRP78 in parental PL5 and PL5/hu18 cells upon treatment with gemcitabine at 25 nM at the indicated time-points. ß-ACTIN served as loading control. Confirmatory HSP27 overexpression in PL5/hu18 cells is additionally depicted.