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Updated: Jun 22, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
EMT: when epithelial cells decide to become mesenchymal-like cells
1Division of Matrix Biology, Beth Israel Deaconess Medical Center, and Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02215, USA. rkalluri@bidmc.harvard.edu
Epithelial-mesenchymal transition (EMT) is vital for embryonic development and reactivated in adults for wound healing, regeneration, fibrosis, and cancer. Inflammation influences adult EMT, unlike in embryos.
Area of Science:
- Cell biology
- Developmental biology
- Cancer biology
Background:
- Epithelial-mesenchymal transition (EMT) is a fundamental biological process essential for embryonic development.
- In adults, EMT is implicated in wound healing, tissue regeneration, organ fibrosis, and cancer progression.
- Inflammation plays a significant role in adult EMT, a factor absent during embryonic development.
Purpose of the Study:
- To review the multifaceted roles of EMT in embryonic development and adult physiological and pathological processes.
- To explore the involvement of inflammation in adult EMT.
- To discuss proposed classifications of EMT into subtypes with distinct functional outcomes.
Main Methods:
- Literature review of studies on EMT in embryonic development, wound healing, regeneration, fibrosis, and cancer.
- Analysis of the role of inflammation in adult EMT.
- Discussion of proposed EMT classification systems.
Main Results:
- EMT is a conserved mechanism for cell dispersal in embryos.
- In adults, EMT contributes to fibroblast formation in injured tissues and metastasis of epithelial cancer cells.
- Inflammation is a key driver of EMT in adult tissues.
Conclusions:
- EMT is a critical process with distinct roles in embryonic development and adult tissue dynamics.
- Understanding EMT subtypes and the influence of inflammation is crucial for addressing diseases like fibrosis and cancer.
- EMT represents a fundamental mechanism for cell plasticity with implications across multiple biological contexts.
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