Description
The conversion of an epithelial cell to a mesenchymal cell is critical to vertebrate embryogenesis and a defining structural feature of organ development, such as forming fibroblasts in injured tissues, or in initiating metastases in epithelial cancer. From a general perspective, EMT is about disaggregating epithelial units and reshaping epithelia for movement. This phenotypic conversion requires the molecular reprogramming of epithelia with new biochemical instructions. It is known that commonly used molecular markers for EMT include increased expression of N-cadherin and vimentin, nuclear localization of beta-catenin, and increased production of the transcription factors such as Snail, Twist, and SIP1/ZEB2. Much of this conversion, however, has been studied during experiments that expose new transduction and signaling pathways in epithelia, and more recently in fibrogenic tissues. It is not yet clear whether the fibroblast transition of EMT is an expected middle phase of transdifferentiating epithelia, or whether EMT producing fibroblasts is an arrested form of transdifferentiation. EMT is easily engaged by a combination of cytokines associated with proteolytic digestion of basement membranes upon which epithelia reside. We analyzed PCA and hierarchical clustering method of the gene expression pattern of the renal tubular cells and mammary gland cells. We then identified the genes which discriminate between the renal tubular and the mammary gland epithelial cells (PC1), or EMT-induced and non-induced cells (PC3). Undergoing EMT identifies the genes that discriminate between the renal tubular and the mammary gland epithelial cells(PC1), or EMT-induced and non-induced cells (PC3).