Fig. 6
From: PERK induces resistance to cell death elicited by endoplasmic reticulum stress and chemotherapy
The role of PERK in chemosensitivity in vivo. a. Tumor growth of HT29 and HT29/MDR, inducibly silenced for PERK, untreated (Ctrl) or treated with oxaliplatin (oPt), as indicated in Methods. Data are mean ± SD (15 mice/group). *p < 0.01 for HT29 oPt vs. HT29 Ctrl group; °p < 0.005 for HT29/MDR Ctrl – doxy vs. HT29 Ctrl, HT29/MDR oPt – doxy vs. HT29 oPt group; # p < 0.005 for HT29/MDR Ctrl + doxy vs. HT29/MDR Ctrl – doxy, HT29/MDR oPt + doxy vs. HT29/MDR oPt – doxy. b. Photographs of representative tumors of each group. c Sections of tumors from each group of animals stained with hematoxylin and eosin (HE) or with the indicated antibodies. Nuclei were counter-stained with hematoxylin. Bar = 10 μm. The photographs are representative of sections from 5 tumors. d. Immunostaining quantification. Percentage of PERK, MRP1 and cleaved caspase 3-positive cells was determined in sections from 5 animals of each group (91–109 cells/field), using Photoshop program. *p < 0.002 for HT29/MDR Ctrl – doxy vs HT29 Ctrl, HT29/MDR oPt – doxy vs HT29 oPt, °p < 0.02 for HT29/MDR Ctrl + doxy vs HT29/MDR Ctrl – doxy, HT29/MDR oPt + doxy vs HT29/MDR oPt – doxy