Integrins contribute to essential components of tumor progression such as survival, proliferation, and cell motility1. Specifically, integrin α6β4 is a known driver of tumor cell invasion2, which in turn promotes metastasis3. In cancer cells, integrin α6β4 signaling is activated upon binding to laminin extracellular matrix proteins and in cooperation with growth factor receptors such as EGFR, RON, and c-MET4–6. Activation of integrin α6β4 results in stimulation of downstream signaling pathways including PI3K, MAPK, Src family kinases, Rho family small GTPases, and the Nuclear Factor of Activated T-cells (NFAT)7–9 that contribute to invasion, angiogenesis, anoikis-resistance, cell survival, and proliferation10. Integrin α6β4 enhances these properties in part through transcriptional upregulation of pro-tumorigenic genes including S100A4 in breast cancer11, 12 and the EGFR ligands AREG and EREG in pancreatic carcinomas13.