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Updated: Jun 5, 2026
11:42
Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
Published on: April 7, 2017
Epithelial and mesenchymal phenotypic switchings modulate cell motility in metastasis
Alan Wells1, Yvonne L Chao, Jelena Grahovac
1Department of Pathology, Pittsburgh VAMC and University of Pittsburgh, Pittsburgh, PA 15213, USA. wellsa@upmc.edu
Frontiers in Bioscience (Landmark Edition)
|January 4, 2011
Summary
Cancer cell plasticity drives metastasis by enabling cells to switch between epithelial and mesenchymal phenotypes. Understanding these changes is key to developing new cancer therapies.
Area of Science:
- Oncology
- Cell Biology
- Cancer Research
Background:
- Metastasis, the spread of cancer cells, is a major cause of cancer-related deaths.
- Current therapies are often ineffective against metastatic tumors.
- Understanding the mechanisms of cancer cell motility is crucial for developing new treatments.
Purpose of the Study:
- To review the role of carcinoma cell phenotypic plasticity in metastasis.
- To discuss how environmental signals modulate cancer cell behavior.
- To introduce a novel method for analyzing epithelial-mesenchymal transitions.
Main Methods:
- Literature review on cancer cell plasticity and metastasis.
- Analysis of signaling pathways involved in epithelial-mesenchymal transition.
- Discussion of extracellular matrix components and their roles.
Main Results:
- Carcinoma cells exhibit phenotypic plasticity, reversibly switching between epithelial and mesenchymal states.
- Intercellular adhesions and extracellular signals regulate these phenotypic switches.
- Specific extracellular matrix components (matrikines, matricryptines) influence cell behavior.
Conclusions:
- Phenotypic plasticity is a critical factor in cancer cell motility and metastasis.
- Environmental cues significantly impact cancer cell behavior and progression.
- Further research into these mechanisms may lead to improved cancer therapies.
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