Biomarkers for epithelial-mesenchymal transitions

Abstract

Somatic cells that change from one mature phenotype to another exhibit the property of plasticity. It is increasingly clear that epithelial and endothelial cells enjoy some of this plasticity, which is easily demonstrated by studying the process of epithelial-mesenchymal transition (EMT). Published reports from the literature typically rely on ad hoc criteria for determining EMT events; consequently, there is some uncertainty as to whether the same process occurs under different experimental conditions. As we discuss in this Personal Perspective, we believe that context and various changes in plasticity biomarkers can help identify at least three types of EMT and that using a collection of criteria for EMT increases the likelihood that everyone is studying the same phenomenon -namely, the transition of epithelial and endothelial cells to a motile phenotype.

Epithelial–mesenchymal transition in malignant mesothelioma

“…[36][37][38] This crucial passage coincided with an increased expression of Slug, Twist, ZEB1, and ZEB2, a set of wellknown nuclear factors that inhibit E-cadherin gene transcription by binding to its promoter. 5,7,19,21,22 E-cadherin has recently been found to be regulated at protein level by mechanisms implicating miRNAs, a class of small non-coding RNAs that modulate gene expression post-transcriptionally. [19][20][21][22] Indeed, it has been demonstrated in vitro that miR-205 controls ZEB1 and ZEB2 levels by targeting their messenger RNA, thus enhancing E-cadherin expression and maintaining the epithelial phenotype.…”

“…2 Commonly used molecular markers of epithelial-mesenchymal transition include a reduced expression of E-cadherin, cytokeratins (CK), and b-catenin (in the membrane), and an increased expression of Snail, Slug, Twist, ZEB1, ZEB2, N-cadherin, vimentin, a-smooth muscle actin (aSMA), S100A4, and matrix metalloproteinases (MMP). 5,7 In particular, activation of the transcriptional regulators Snail, Slug, Twist, ZEB1, and ZEB2 enables the changes in gene expression patterns underlying epithelial-mesenchymal transition to be regulated. [8][9][10][11][12] These molecular markers repress the gene expression of E-cadherin, a marker of the epithelial phenotype.…”

“…[8][9][10][11][12] These molecular markers repress the gene expression of E-cadherin, a marker of the epithelial phenotype. [7][8][9][13][14][15][16] MicroRNAs (or miRNAs) are a class of short noncoding RNAs that regulate gene expression in several physiological and pathological cellular processes. 17,18 Recently, miR-205 has been identified as a key regulator of epithelial-mesenchymal transition enforcing the epithelial phenotype.…”

FSP1+ Fibroblasts Promote Skin Carcinogenesis by Maintaining MCP-1-Mediated Macrophage Infiltration and Chronic Inflammation

“…Remarkably, FSP1 is also a prototypical marker for cells after epithelial-mesenchymal transition (EMT) during cancer development and fibrogenesis. 34 During tissue repair and inflammatory injury, most epithelial cells undergoing type 2 EMT express FSP1 early in transition to fibroblasts. 34 By double-staining of E-cadherin and FSP1, a few FSP1 ϩ epithelial cells were indeed detected after repeated applications of TPA (data not shown).…”

“…34 During tissue repair and inflammatory injury, most epithelial cells undergoing type 2 EMT express FSP1 early in transition to fibroblasts. 34 By double-staining of E-cadherin and FSP1, a few FSP1 ϩ epithelial cells were indeed detected after repeated applications of TPA (data not shown). Because no evidence showed cancer development when GCV was applied to deplete proliferating fibroblasts in the promotion stage, type 2 EMT may be one source of FSP1 ϩ fibroblasts in this process.…”