Epithelial-Mesenchymal Transition (EMT) in Immunofluorescence Research
Epithelial-Mesenchymal Transition (EMT)  IF
Epithelial-mesenchymal transition (EMT) is an essential process during development whereby epithelial cells acquire mesenchymal, fibroblast-like properties and display reduced intracellular adhesion and increased motility. This is a critical feature of normal embryonic development, which is also utilized by malignant epithelial tumors to spread beyond their origin.
EMT Overview
This tightly regulated process is associated with a number of cellular and molecular events. EMT depends on a reduction in expression of cell adhesion molecules. Cadherins mediate calcium-dependent cell-cell adhesion and play critical roles in normal tissue development.

E-cadherin is considered an active suppressor of invasion and growth of many epithelial cancers. Recent studies indicate that cancer cells have upregulated N-cadherin in addition to loss of E-cadherin. This change in cadherin expression is called the "cadherin switch" and downregulation of E-cadherin is one of the hallmarks of EMT.

Molecular Mechanisms of EMT
Cell Junctions and Polarity
Tight junctions, or zonula occludens, form a continuous barrier to fluids across the epithelium and endothelium. They function in regulation of paracellular permeability and in the maintenance of cell polarity, blocking the movement of transmembrane proteins between the apical and the basolateral cell surfaces.
Tight junctions are composed of claudin and occludin proteins, which join the junctions to the cytoskeleton. Zona occludens (ZO) proteins (e.g., ZO-1) are peripheral membrane adaptor proteins that link junctional transmembrane proteins such as occludin and claudin to the actin cytoskeleton.
Key Transcription Factors
Slug (SNAI2) is a widely expressed transcriptional repressor and member of the Snail family of zinc finger transcription factors. Similar to the related Snail protein, Slug binds to the E-cadherin promoter region to repress transcription during development.
ZEB family proteins (e.g., ZEB1) are zinc finger and homeobox domain containing transcription factors, whose targets of regulation include E-cadherin. TWIST1 is a basic helix-loop-helix (b-HLH) transcription factor that functions as a master regulator of embryonic morphogenesis, and plays essential roles in mesenchymal differentiation.
TWIST is upregulated in various human tumors and has been suggested to be a driver of EMT and metastasis.
Structural Proteins

Vimentin is an intermediate filament of mesenchymal origin and is present at early developmental stages. Vimentin's dynamic structural changes and spatial re-organization in response to extracellular stimuli helps to coordinate various signaling pathways.

EMT Regulation Network Diagram

EMT is regulated by a complex network involving transcriptional regulation, post-translational modifications, epigenetic modifications, non-coding RNAs, and signaling pathways.


Relevant Antibodies
Catalog#Product NameApplicationReactivity
AMRe21480Claudin 1 Rabbit Monoclonal antibodyWB,IHC,IF,IP,ELISAHuman,Mouse,Rat
AMRe01411E Cadherin Rabbit Monoclonal AntibodyWB,IHC-F,IHC-P,ICC/IF,IPHuman
AMRe21484N Cadherin Rabbit Monoclonal antibodyWB,IHC,IF,IP,ELISAHuman,Mouse,Rat
AMM81417SNAI2 Mouse Monoclonal AntibodyWB,IHC,ICC,FC,ELISAHuman
AMM81225TWIST1 Mouse Monoclonal AntibodyWB,IHC,ICC,FC,ELISAHuman,Mouse,Rat,Rabbit
AMRe21330Vimentin Rabbit Monoclonal antibodyWB,IHC,IF,IP,ELISAHuman,Mouse,Rat
AMRe21526AREB6 Rabbit Monoclonal antibodyWB,IHC,IF,IP,ELISAHuman,Rat
AMRe21195ZO1 Rabbit Monoclonal antibodyWB,IHC,IF,IP,ELISAHuman,Mouse,Rat
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References
  • Aigner, K. et al. (2007) Oncogene 26, 6979-88.
  • Peinado, H. et al. (2007) Nat Rev Cancer 7, 415-28.
  • Moreno-Bueno, G. et al. (2008) Oncogene 27, 6958-69.
  • Wheelock, M.J. and Johnson, K.R. (2003) Annu Rev Cell Dev Biol 19, 207-35.
  • Christofori, G. (2003) EMBO J 22, 2318-23.
  • Hazan, R.B. et al. (2004) Ann N Y Acad Sci 1014, 155-63.
  • Shin, K. et al. (2006) Annu Rev Cell Dev Biol 22, 207-35.
  • Oliveira, S.S. and Morgado-Díaz, J.A. (2007) Cell Mol Life Sci 64, 17-28.
  • Matter, K. and Balda, M.S. (2007) J Cell Sci 120, 1505-11.
  • Hernandez, S. et al. (2007) Exp Cell Res 313, 1533-47.
  • Umeda, K. et al. (2006) Cell 126, 741-54.
  • Reichert, M. et al. (2000) J Biol Chem 275, 9492-500.
  • Helfand, B.T. et al. (2004) J Cell Sci 117, 133-41.
  • Inukai, T. et al. (1999) Mol Cell 4, 343-52.
  • Barrallo-Gimeno, A. and Nieto, M.A. (2005) Development 132, 3151-61.
  • Bolós, V. et al. (2003) J Cell Sci 116, 499-511.
  • Turner, F.E. et al. (2006) J Biol Chem 281, 21321-31.
  • Lee, M.S. et al. (1999) J Cell Biochem 75, 566-77.
  • Chen, Z.F. and Behringer, R.R. (1995) Genes Dev 9, 686-99.
  • Yang, J. et al. (2004) Cell 117, 927-39.
  • Watanabe, O. et al. (2005) Anticancer Res 24, 3851-6.

Voisey 

Voisey is a technical support specialist at EnkiLife, proficient in immunology and cell biology. She is committed to providing customers with professional and efficient technical support. Additionally, she  is involved in research on customers' fields of study and designs highly cost-effective solutions for them.

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