E-cadherin, catenin, cytoskeletal interactions and induced pluripotency

Abstract

Pluripotency is defined as the capability of cells to differentiate into cell types derived from each of the three embryonic germ layers (Kelly et al., 2011). Induced pluripotency defines a process of epigenetic reprogramming in which epigenetic changes implemented during differentiation are reversed to generate cells with a stem-like phenotype. Fibroblasts (Takahashi and Yamanaka, 2006; Sommer et al., 2009), human keratinocytes (Aasen et al., 2008) and nasal mucosal cells (Ono et al., 2012) can be reprogrammed to stem-like cells with introduction of four stem cell transcription factors Oct4, KLF4, Sox2 and c-Myc (OKSM). Previous studies have provided evidence that the adhesion and cellular signaling provided by a glycoprotein, known as E-cadherin, has essential functions in pluripotency. Induced pluripotency has potential medical application which the induced pluripotent stem cells (iPSCs) apply as clinical tools for modeling diseases, drug development, and to deliver cell-replacement therapy to support regenerative medicine (Goldthwaite, 2011).

The present review summarizes our current knowledge on the role of E-cadherin, its cellular signaling and cytoskeletal interactions in the induction and maintenance of pluripotent cells.