MOESM1 of Autophagy inhibition improves the cytotoxic effects of receptor tyrosine kinase inhibitors

Additional file 1: Figure S1. Caspase-3 and PI measurement upon treatments. A) Apoptosis activation was evaluated by measuring the intensity of PARP cleavage (89 kDa proteolytic PARP fragment), and by evaluating a decrease in the pro-Caspase-3 (35 kDa protein) level. Active Caspase-3 forms are observed as cleaved proteins with molecular weight below 20 kDa. GAPDH served as a loading control protein. D = DMSO; Af—Afatinib (8 μM); Sor—Sorafenib (14 μM); TP—TP-0903 (0.15 μM). B) Percentage of PI positive cells with respect to total cell number was presented as mean ± SD out of triplicates. D—DMSO; Af—Afatinib; Sor—Sorafenib; TP—TP-0903. p value is marked as **p < 0.01; n.s.—non-significant. C) Changes in the proliferation rate upon treatment with the three RTKi were determined by means of PCNA expression. The numbers indicate relative expression (densitometry) obtained after normalization to GAPDH protein level, which was used a loading control, and with respect to DMSO control (DMSO = 1)