Abstract
Epithelial-Mesenchymal Transition (EMT) and its reverse process, Mesenchymal-to-Epithelial Transition (MET) are well-studied processes involved in cell differentiation during development and organ formation, as well as in its reverse process in somatic cell reprogramming. In addition, involvement of a deregulated form of the EMT in tumor progression has long been known. Understanding the molecular and cellular mechanisms for cancer development, progression, and metastasis is a fundamental challenge toward advancing and improving therapeutic strategies. In this mini-review, by considering the distinct phenotypes of available Dido mutations in mice, for the first time we connect Dido gene function and participation with EMT and MET in the areas of cell differentiation, reprogramming, and cancer development.
Keywords
Epithelial-mesenchymal transition, Cell differentiation, Somatic cell reprogramming, Gene expression, Tumor formation, metastasis, Dido gene