Figure 5.

MMP11 promotes tumor cellular endoplasmic reticulum (ER) stress response (UPR^ER) and alters mitochondrial UPR (UPR^mt) in mammary gland tumors. (A) (a) Confocal images of tumor sections were stained using an anti-phosphorylated α subunit of eukaryotic translation initiation factor 2 (eIF2α) (p-eIF2α) antibody, from 12-week-old PyMT^Tg; MMP11^Tg and control age-matched mice; (b) Confocal images of tumor sections stained with anti-p-eIF2α from 14-week-old PyMT^Tg; MMP11^KO and control; a control staining without primary antibody is shown below; (a,b) relative image quantification are presented as histograms in the right; (B) (a) RT-qPCR analysis of genes implicated in UPR^ER in tumors from 6-week-old PyMT^Tg; MMP11^Tg mice compared to tumors from control mice; (b) and in tumors from PyMT^Tg; MMP11^KO mice compared to controls; (C) (a–c) Expression profile of genes implicated in the three arms of the UPR^mt in tumor samples from 6-week-old PyMT^Tg; MMP11^Tg mice compared to controls; (d–f) Expression profile of genes implicated in the three arms of the UPR^mt in tumor samples from 10-week-old PyMT^Tg; MMP11^KO mice compared to controls; (D) Western blot analysis of phosphorylated AMP-activated kinase (AMPK) (pAMPK^T172) in tumors from (a) 6-week-old PyMT^Tg; MMP11^Tg and (b) 10-week-old PyMT^Tg; MMP11^KO mice, respectively, as compared to their controls. Quantification of the ratios of pAMPK/AMPK is presented below the blots, normalized to GAPDH expression. Data are presented as fold changes. N = 6–8 mice/group, data are presented as mean ± SEM, * p < 0.05, ** p < 0.01, *** p < 0.001 (unpaired t-test).