Differentiation Therapy Targeting the β-Catenin/CBP Interaction in Pancreatic Cancer

Abstract

We report for the first time that <i>K-Ras</i> activation increases the CBP/β-catenin interaction in pancreatic cancer; and that ICG-001 specific antagonism of the CBP/β-catenin interaction sensitizes pancreatic cancer cells and tumors to gemcitabine treatment. These effects were associated with increases in the expression of let-7a microRNA; suppression of <i>K-Ras</i> and survivin; and the elimination of drug-resistant cancer stem/tumor-initiating cells.