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. 2018 Sep 1;32(17-18):1175–1187. doi: 10.1101/gad.311852.118

Figure 2.

Figure 2.

STAT3 is required for the maintenance of differentiated cell identity in KRAS-induced PDAC. (A) Western blot analysis of nuclear and cytoplasmic extracts from control and STAT3 knockout KRASG12D p53 knockout pancreatic cells (left panel) and cells transduced with wild-type or mutant STAT3 alleles (middle and right panels). (B) FACS analysis of CD133 and SCA1 expression in KRASG12D p53 knockout pancreatic cells and their STAT3 mutant derivatives. (C) Growth and viability of KRASG12D p53 knockout pancreatic cells in two-dimensional (2D) monolayer (left panel) and three-dimensional (3D) nonadherent (right panel) cultures. The cells were cultured for 1 wk. Relative cumulative cell numbers are shown. Values correspond to average and SD. Asterisks indicate a statistically significant difference compared with wild-type controls. (D) Subcutaneous tumor formation in nude mice by KRASG12D p53 knockout pancreatic cells and their mutant STAT3 derivatives (104 cells per injection site). n ≥ 4 for each cell type. (E) H&E and IHC (KRT19 and SOX9) staining of tumors arising from KRASG12D p53 knockout cells shown in D. Representative images are shown. Bar, 200 µm.