Kindlin-2 inhibited the growth and migration of colorectal cancer cells.

Activation of Wingless (Wnt)/beta-catenin signaling is a hallmark of colorectal carcinoma (CRC). It is very important to find out the molecular mechanism for the hyperactivation of Wnt/beta-catenin signaling and identify novel therapeutic targets. Kindlin-2, a regulator of integrins, recently has been found to be involved in the tumorigenesis. However, its expression profile and functions in the progression of CRC remain poorly understood. Here, we found that the expression of Kindlin-2 was downregulated in the CRC tissues. Moreover, overexpression of Kindlin-2 in CRC cells and normal colon epithelial cells inhibited cell proliferation and migration, while downregulation of Kindlin-2 promoted the tumorigenecity of CRC cells in vitro and in vivo. Mechanistically, Kindlin-2 decreased the phosphorylation of Ser9 in glycogen synthase kinase (GSK) 3beta and promoted the ubiquitination of beta-catenin. Taken together, our study suggests the suppressive roles of Kindlin-2 in the pathogenesis of CRC.