Fig. 7
From: Epigenetic silencing of AATK in acinar to ductal metaplasia in murine model of pancreatic cancer
Transient AATK expression in ADM guided cytokeratin 19 intermediate filament and apical-basal polarity. a H&E and multiplex immunofluorescence (AATK/CK19/HNF1A/P63/Ki67/DAPI) staining of (a) non-invasive pancreatic tissue sections from KrasG12D/+; Pdx1-Cre mice and invasive ductal sections from KrasG12D/+; Trp53fl/+; Pdx1-Cre mice. Individual colour channels and merged composite pictures are shown with arrows indicating polarized ADM ductal cells, arrowheads indicating proliferating p63-positive ductal cells, and asterisks indicating HNF1α+ acinar cells. b Higher magnitude visualization of the cellular localization of AATK, CK19, and HNF1A in the KC mice. c VAV1 targeted the cell cycle pathway gene network and cytokeratin 6B expression in Panc-04.03 cells. * AATK mRNA and VAV1 mRNA were positively co-expressed. Kaplan-Meier estimates of the overall survival and disease-free/progression-free survival of patients in the cBioPortal. d Relative mRNA expression fold changes in two stable cell lines expressing the AATK shRNA -A5 and -B5 in Mia Paca-2 cells by qPCR. Top upregulated genes were highlighted in red. The mRNA expression were calculated by ∆∆Ct method using GAPDH (circle) as the internal control. Each of the four lentiviral transduced cell pools shAATK-A5, shAATK_B5, Scramble control, and Empty-vector controls were selected by puromycin for 25 days prior to the total RNA isolation. The DNAse digestion, cDNA preparation, and qPCR procedures were conducted with standard protocols