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EMT, MET, Plasticity, and Tumor Metastasis
Basil Bakir1, Anna M Chiarella2, Jason R Pitarresi1
1Abramson Cancer Center, University of Pennsylvania, Philadelphia, PA 19104, USA.
Trends in Cell Biology
|August 18, 2020
Summary
Cancer cell plasticity, involving epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET), is crucial for tumor metastasis. The roles of EMT, MET, and partial EMT (pEMT) depend on tumor type and metastatic stage.
Area of Science:
- Oncology
- Cancer Biology
- Cellular Plasticity
Background:
- Cancer cell identity and plasticity are critical for tumor initiation, progression, and metastasis.
- Epithelial-mesenchymal transition (EMT), mesenchymal-epithelial transition (MET), and partial EMT (pEMT) represent key cellular states driving these processes.
- The specific functions of these transitions can differ based on tumor type, dissemination status, and metastatic colonization.
Purpose of the Study:
- To review the roles of EMT, MET, pEMT, and cellular plasticity in the context of tumor metastasis.
- To highlight the context-dependent nature of these transitions in cancer progression.
Main Methods:
- Literature review of studies on EMT, MET, pEMT, and cancer metastasis.
- Synthesis of current understanding regarding the functional significance of these transitions.
Main Results:
- EMT, MET, and pEMT are fundamental to cancer cell plasticity and metastasis.
- The impact of these transitions is highly variable, influenced by specific tumor characteristics and the metastatic cascade.
- Understanding these states is essential for deciphering metastatic mechanisms.
Conclusions:
- Cellular plasticity, mediated by EMT, MET, and pEMT, is a key driver of tumor metastasis.
- The functional outcomes of these transitions are context-specific, necessitating tailored therapeutic strategies.
- Further research into these dynamic cellular states is crucial for effective cancer treatment.
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