Epithelial-mesenchymal transition (EMT) is a critical process in cancer cell metastasis, during which epithelial cells acquire mesenchymal characteristics, including enhanced cell motility and migration. During embryogenesis, primitive epithelial cells transition into motile mesenchymal cells through EMT, illustrating how embryogenesis produces mesenchymal cells essential for tissue development. EMT is also involved in the formation of secondary epithelial cells and can involve secondary epithelial cells during organogenesis and tissue repair. EMT is characterized 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 changes in epithelial and mesenchymal cell marker expression 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. The loss of epithelial cell adhesion molecules and changes in the epithelial cell phenotype are key features distinguishing normal epithelial cells from those undergoing EMT. Collectively, this results in epithelial cells losing apical-basal cell polarity, reorganizing their cytoskeleton, and reprogramming gene expression, which allows the development of an invasive phenotype in cancer metastasis.

EMT establishes epithelial cell plasticity and highlights the dynamic nature of epithelial-mesenchymal transitions, which are reversible through mesenchymal-epithelial transition (MET). Specialized squamous epithelial cells and neural crest cells are involved in developmental EMT processes, contributing to tissue patterning and morphogenesis. Tubular epithelial cells and kidney tubular epithelial cells are key models for studying EMT in tissue fibrosis and organ dysfunction. Primary mammalian epithelial cells are commonly used in EMT research due to their susceptibility to transition under experimental conditions. Through EMT, mesenchymal stem cells and vascular smooth muscle cells contribute to tissue remodeling and fibrosis. Regulation of the cell cycle is closely linked to EMT, influencing the behavior of migrating mesenchymal cells during development and cancer progression. Stem cells also play a significant role in EMT and tissue regeneration.

E-Cadherin

E-cadherin is a calcium-dependent adhesion protein found in epithelial tissues. Decreased E-cadherin expression is a fundamental event in EMT and cancer metastasis and has emerged as a molecular hallmark of carcinoma EMT. Also, it is considered the prototypical epithelial cell marker, serving as a key epithelial cell adhesion molecule whose loss is indicative of the epithelial to mesenchymal transition.

Figure 1. Immunocytochemistry/ Immunofluorescence - Anti-E Cadherin antibody [EP700Y] - Intercellular Junction Marker (ab40772).

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N-cadherin

N-cadherin, also known as CDH2, is a calcium-dependent adhesion molecule that plays a role in cell–cell interactions. During epithelial–mesenchymal transition (EMT), epithelial cells reduce E-cadherin expression and increase N-cadherin levels, supporting a shift toward a mesenchymal phenotype. This transition enhances cell motility and invasiveness, contributing to processes like embryonic development and cancer metastasis. N-cadherin is often studied as a biomarker for EMT and is linked to signaling pathways involving fibroblast growth factor receptors. Its expression is associated with changes in cellular behavior that support tissue remodeling and disease progression.

The loss of E-cadherin is typically associated with a gain of expression of the mesenchymal marker, N-cadherin, in many cancer types. It is thought to be necessary for tumor cells to gain invasive properties.

Figure 2. Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-N Cadherin antibody - Intercellular Junction Marker (ab18203).

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Vimentin

Vimentin is a type III intermediate filament protein commonly used as a biomarker for epithelial–mesenchymal transition (EMT). During EMT, epithelial cells adopt mesenchymal traits, including enhanced motility and structural flexibility. Vimentin supports these changes by reorganizing the cytoskeleton and influencing cell shape and migration. Its expression is often elevated in cancer cells undergoing EMT, linking it to tumor progression and metastasis. Researchers use vimentin to study dynamic cellular reprogramming in development, wound healing, and disease. Its role in EMT makes it a valuable target for investigating cell plasticity and therapeutic strategies in oncology and regenerative medicine.

Figure 3. Immunocytochemistry/ Immunofluorescence - Anti-Vimentin antibody [EPR3776] - Cytoskeleton Marker (ab92547).

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SNAIL

SNAIL is a zinc finger transcription factor that plays a role in regulating epithelial–mesenchymal transition (EMT). It represses epithelial markers like E-cadherin and promotes mesenchymal traits, supporting changes in cell adhesion, polarity, and mobility. These shifts are observed during embryonic development, tissue remodeling, and cancer progression. SNAIL influences chromatin structure by interacting with cofactors such as EZH2 and long non-coding RNAs, contributing to gene silencing. Its expression is often linked to increased invasiveness in carcinoma cells. Researchers study SNAIL to better understand cellular plasticity and the molecular mechanisms driving EMT in both physiological and pathological contexts.

Figure 4. Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-SNAIL + SLUG antibody (ab180714).

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References

1. Wells, A.  et al.  Clinical & Experimental Metastasis 25, 621–628 (2008).
2. Jia, W.  et al.  Anticancer Research 35, 2635–2643 (2015).
3. Vergara, D.  et al.  EuPA Open Proteomics 10, 31–41 (2016).
4. Lamouille, S., Xu, J. & Derynck, R. Nature Reviews Molecular Cell Biology 15, 178–196 (2014).