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Epithelial to Mesenchymal Transition (EMT) – Cellular Plasticity, Cancer Progression and Biomarker Analysis

What is the Epithelial to Mesenchymal Transition (EMT)?

Epithelial to mesenchymal transition (EMT) is a dynamic and reversible biological process in which epithelial cells lose polarity and cell–cell adhesion while acquiring mesenchymal traits such as enhanced motility, invasiveness, and resistance to apoptosis.

EMT plays essential roles in:

  • Embryonic development
  • Tissue regeneration and wound healing
  • Organ fibrosis
  • Cancer progression and metastasis

Rather than a binary switch, EMT represents a spectrum of intermediate hybrid states, where cells display both epithelial and mesenchymal characteristics. This plasticity is critical in tumor evolution and therapeutic resistance.

AnyGenes qPCR array for studying epithelial to mesenchymal transition (EMT) in cancer progression, fibrosis, and tissue regeneration.

EMT activity can be efficiently assessed by measuring gene expression of EMT transcription factors, epithelial markers, mesenchymal markers, and pathway-specific biomarker signatures.

Epithelial-to-Mesenchymal-Transition-markers
(B) EMT is induced mainly by a set of transcription factors (EMT‐TFs) like ZEB1, ZEB2, SNAIL, SLUG and TWIST that differ in protein structure, size, and individual functions. All of them are repressors of epithelial factors like E‐cadherin and activate mesenchymal markers like Vimentin, Fibronectin or N‐cadherin. Epithelial cells displaying apical–basal polarity are held together by tight junctions, adherens junctions, and desmosomes and are anchored to the underlying basement membrane by hemidesmosomes. They express three different polarity complexes that together with the junctional molecules maintain epithelial cell polarity.
In the classical EMT, expression of EMT‐TFs leads to inhibition of major components of these epithelial structures and concomitantly activates the expression of genes associated with the mesenchymal state. Cells gain front–rear polarity, display actin stress fibers, become motile and acquire invasive capacities. Notably, tumor cells very rarely switch to a completely mesenchymal phenotype, but fluently convert between various intermediate states displaying certain mesenchymal features but keeping partial sets of epithelial characteristics. Further, EMT is a reversible process. Mesenchymal cells can revert to the epithelial state undergoing MET. An important role in the execution of MET is played by microRNAs of the miR‐200 and mir‐34 families that are regulated in double‐negative feedback loops with the EMT‐TFs ZEB1/2 and SNAIL, respectively, that serve to reinforce either the epithelial or the mesenchymal state.

Key takeaways

  • Central regulator of cellular plasticity
  • Drives migration, invasion and metastasis
  • Controlled by EMT transcription factors (SNAIL, ZEB, TWIST)
  • Activated by TGF-β, Wnt, Notch and PI3K-AKT signaling
  • Major biomarker source in oncology and fibrosis research

Types of epithelial to mesenchymal transition

Type 1 EMT

Embryonic development and organogenesis.

Type 2 EMT

Wound healing and fibrosis.

Type 3 EMT

Cancer-associated EMT promoting invasion and metastasis

Core molecular mechanisms of EMT

EMT transcription factors (EMT-TFs)

EMT is orchestrated by master regulators that repress epithelial genes and activate mesenchymal programs:

  • SNAIL1 / SNAIL2 (SLUG)
  • ZEB1 / ZEB2
  • TWIST1 / TWIST2

These transcription factors:

  • Repress E-cadherin (CDH1)
  • Induce Vimentin (VIM)
  • Promote N-cadherin (CDH2)
  • Activate extracellular matrix remodeling genes

Loss of epithelial characteristics

During EMT:

  • Tight junctions and adherens junctions are disrupted
  • Apico-basal polarity is lost
  • Basement membrane attachment weakens

Epithelial markers decrease:

  • E-cadherin
  • Claudins
  • Occludins

Acquisition of mesenchymal traits

Cells gain:

  • Front–rear polarity
  • Actin stress fibers
  • Enhanced migration
  • Invasive capacity

Mesenchymal markers increase:

  • Vimentin
  • Fibronectin
  • N-cadherin

Reversibility: MET

EMT is reversible through mesenchymal-to-epithelial transition (MET).

MicroRNAs such as:

  • miR-200 family
  • miR-34 family

Form double-negative feedback loops with ZEB and SNAIL, stabilizing epithelial or mesenchymal states.

Signaling pathways driving EMT

EMT integrates extracellular signals via multiple pathways:

Pathway crosstalk creates complex regulatory networks that sustain plasticity.

Epithelial to mesenchymal transition in cancer progression

In oncology, EMT enables:

  • Tumor cell dissemination
  • Metastatic colonization
  • Immune evasion
  • Resistance to chemotherapy and radiotherapy
  • Acquisition of cancer stem cell traits

Importantly, most tumor cells adopt partial EMT states, contributing to heterogeneity and therapy resistance.

High EMT marker expression often correlates with poor prognosis.

EMT in fibrosis and tissue remodeling

Persistent EMT contributes to:

  • Liver fibrosis
  • Pulmonary fibrosis
  • Renal fibrosis

Excessive mesenchymal activation promotes extracellular matrix deposition and organ dysfunction.

Therapeutic relevance

Targeting EMT represents a major strategy in:

  • Anti-metastatic therapies
  • Anti-fibrotic interventions
  • Cancer stem cell targeting
  • Combination therapies with TGF-β or Wnt inhibitors

Accurate EMT biomarker profiling is essential for patient stratification and therapeutic monitoring.

Why study EMT with AnyGenes®?

At AnyGenes®, we provide high-performance qPCR arrays and customizable SignArrays® dedicated to EMT pathway analysis.

Our solutions enable researchers to:

  • Quantify EMT transcription factor signatures
  • Analyze epithelial and mesenchymal marker balance
  • Study pathway cross-talk (TGF-β, Wnt, Notch, PI3K-AKT)
  • Investigate hybrid EMT states
  • Generate robust, publication-ready data

Epithelial to mesenchymal transition biomarker analysis with AnyGenes®

What can be analyzed?

  • SNAIL, SLUG, ZEB1, ZEB2, TWIST
  • CDH1 (E-cadherin), CDH2 (N-cadherin)
  • VIM, FN1
  • TGF-β pathway components
  • Wnt/β-catenin regulators
  • EMT-related microRNAs

Customize your own signaling pathways (SignArrays®) with the factors of your choice!
Simply download and complete our Personalized SignArrays® information file and send it at [email protected] to get started on your project.

Frequently asked questions

EMT is a reversible biological process in which epithelial cells lose polarity and adhesion and acquire mesenchymal properties, increasing motility and invasiveness.

EMT is triggered by signaling pathways such as TGF-β, Wnt/β-catenin, Notch, PI3K-AKT and inflammatory signals.

EMT promotes metastasis, tumor plasticity, immune evasion and resistance to therapy.

Yes. Mesenchymal cells can revert to epithelial states through mesenchymal-to-epithelial transition (MET).

EMT activity can be assessed by measuring gene expression of transcription factors, epithelial markers, mesenchymal markers, and downstream signaling targets using targeted gene expression tools such as qPCR arrays.

  1. Manfioletti G, Fedele M. Epithelial–Mesenchymal Transition (EMT) 2021. Int J Mol Sci. (2022);23(10):5848.
  2. Lachat C, et al. Epithelial to Mesenchymal Transition History: From Embryonic Development to Cancers. Biomolecules. (2021);11(6):782.
  3. Dudas J, et al. Epithelial to Mesenchymal Transition: A Mechanism that Fuels Cancer Radio/Chemoresistance. Cells. (2020);9(2):428.
  4. Marconi GD, et al. Epithelial-Mesenchymal Transition (EMT): The Type-2 EMT in Wound Healing, Tissue Regeneration and Organ Fibrosis. Cells. (2021);10(7):1587.
  5. Brabletz S, et al. Dynamic EMT: a multi‐tool for tumor progression. EMBO J. (2021);40(18):e108647.

Epithelial to mesenchymal transition biomarker list

You can check the biomarker list included in this pathway, see below:

Species : Homo sapiens (human)

Human Signaling pathway

Signaling PathwaysProduct refInformations

Epithelial To Mesenchymal Transition

EMT1H1

List infos


Species : Mus musculus (mouse)

Mouse signaling pathway

Signaling PathwaysProduct refInformations

Epithelial To Mesenchymal Transition

EMT1M1

List infos


Species : Rattus norvegicus (rat)

Rat signaling pathway

Signaling PathwaysProduct refInformations

Epithelial To Mesenchymal Transition

*******

List In progress...


Species : Sus Scrofa (Pig)

Pig signaling pathway

Signaling PathwaysProduct refInformations

Epithelial To Mesenchymal Transition

*******

List In progress...


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[email protected]