Functional antagonism between STAT3 and SMAD4 regulates EMT

Oncogenic mutations in KRAS are among the most common in cancer. Classical
models suggest that loss of epithelial characteristics and the acquisition
of mesenchymal traits are associated with cancer aggressiveness and
therapy resistance. We identify STAT3 as a genetic modifier of
TGF-beta-induced epithelial to mesenchymal transition in mutant KRAS
tumors. RNA sequencing was performed with murine cells expressing mutant
KRAS either overexpressing hyperactive STAT3Y640, or CRISPR-mediated
knockout of STAT3, SMAD4, or KRAS. Excel files of differential expression
compared to control mutant RAS cells or fpkm files are provided.