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

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© 2018 D'Amico et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 5. — STAT3 and TP63 cooperatively regulate expression of epithelial-specific genes. (A) Quantitative RT–PCR of SOCS3 and ΔNP63 mRNA levels in control, STAT3 knockout, and STAT3 Y640F transduced KRAS^G12D p53 knockout lung epithelial cells. Relative expression levels are shown normalized to GAPDH. (B) Gene ontology analysis of control, STAT3 knockout-expressing, and STAT3 Y640F-expressing tumors derived from transcriptome analysis of KRAS^G12D p53 knockout lung epithelial cells. (C) Heat map of RNA sequencing (RNA-seq) data representing a subset of differentially expressed genes specifically involved in EMT and epithelial identity in control, STAT3 knockout-expressing, and STAT3 Y640F-expressing tumors derived from KRAS^G12D p53 knockout lung epithelial cells. (D) Heat maps of RPPA data representing differentially expressed proteins in KRAS^G12D p53 knockout lung epithelial cells and their STAT3 derivatives. (E) Signaling perturbations in KRAS-related pathways derived from RPPA analysis by loss or gain of STAT3 function in KRAS^G12D p53 knockout lung epithelial cells. (F) H&E and IHC (ΔNP63) of tumors derived from fully formed murine lung ADC tumor cells following their culture and modification to express STAT3 knockout or ectopic wild-type STAT3. (G) Histological features of tumors arising from KRAS^G12D lung epithelial cells with STAT3, TP63, and TGFBR2 genotypes. (*) Mixed epithelial–mesenchymal tumor phenotype consisting of ≤10% mesenchymal component. (**) Mixed epithelial–mesenchymal tumor phenotype consisting of ≤10% epithelial component. (H) Model representing the mechanism by which STAT3 and TP63 regulate epithelial cell commitment and differentiation in KRAS-driven carcinogenesis.