INHIBITION OF DAPK3, PINPOINTED AS A KEY FACTOR IN THE DEVELOPMENT OF COLITIS-ASSOCIATED DYSPLASIA, INCREASES SEVERITY OF DSS-INDUCED COLITIS VIA HIPPO SIGNALING

Abstract

Ulcerative colitis (UC) is a progressive disorder that elevates the risk of cancer development through a colitis-dysplasia-carcinoma sequence. Recent evidence demonstrates the necessity of Hippo-YAP/TAZ signaling, interceded by cytoskeletal remodeling, for intestinal regeneration. Death-associated protein kinase 3 (DAPK3) is a regulator of actin-cytoskeleton reorganization that controls proliferation and apoptosis. We first identified DAPK3 as a candidate gene involved in UC progression, and then examined if inhibition of DAPK3 would increase the severity of colitis.