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Your guide to EMT markers in cancer.
Activation of epithelial to mesenchymal transition (EMT) is a key process in cancer cell metastasis, during which epithelial cells acquire mesenchymal characteristics with an enhancement of cell motility and migration.
EMT is characterised by a loss of epithelial cell markers, such as cytokeratins and E-cadherin, followed by an upregulation in the expression of mesenchymal cell markers, such as N-cadherin, vimentin, and fibronectin.
These epithelial and mesenchymal cell marker expression changes lead to a reduction in adhesion between the transitioning cell and adjacent epithelial cells, and an increase in the secretion of enzymes that degrade the extracellular matrix.1 Collectively, this results in epithelial cells losing apical-basal cell polarity, reorganizing their cytoskeleton, and reprogramming gene expression; enabling the development of an invasive phenotype in cancer metastasis.2
Decreased E-cadherin expression is a fundamental event in EMT and cancer metastasis and has emerged as a molecular hallmark of the carcinoma EMT.3
The loss of E-cadherin is typically associated with a gain of expression of the mesenchymal marker, N-cadherin, in many cancer types and is thought to be necessary for tumor cells to gain invasive properties.4
We recommend Anti-N Cadherin antibody (ab18203)
Image (above): Immunohistochemistry (formalin/PFA-fixed paraffin-embedded sections) of human liver cancer tissue stained with Anti-N Cadherin antibody (ab18203).
We recommend Recombinant Anti-Vimentin antibody [EPR3776] (ab92547).
The change in the epithelial and mesenchymal gene expression that occurs during EMT is regulated by multiple transcription factor families that include SNAI1/Snail, ZEB1/ZEB2, and basic helix-loop-helix transcription factors (bHLH).2
We recommend Anti-SNAIL + SLUG antibody (ab180714).
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