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Updated: Jun 10, 2026
11:42
Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
Published on: April 7, 2017
Epithelial plasticity, cancer stem cells and bone metastasis formation
1Leiden University Medical Center, Department of Urology J3-100, Albinusdreef 2, 2333 ZA Leiden, The Netherlands. G.van_der_Pluijm@lumc.nl
Bone
|July 31, 2010
Summary
Cancer cells acquire an invasive phenotype through epithelial-to-mesenchymal transition (EMT) for bone metastasis. This plasticity is crucial for cancer stem cell properties and therapy resistance.
Area of Science:
- Oncology
- Cancer Biology
- Metastasis Research
Background:
- Bone metastasis predominantly arises from epithelial cancers like breast and prostate.
- Cancer cells undergo epithelial-to-mesenchymal transition (EMT) to gain motility and invasiveness.
- Epithelial plasticity, including EMT and mesenchymal-to-epithelial transition (MET), is key in cancer cell dissemination and colonization.
Purpose of the Study:
- To review the role of epithelial plasticity in bone metastasis.
- To explore the connection between EMT, cancer stem cells, and therapy resistance.
- To discuss implications for novel targeted drug therapies.
Main Methods:
- Review of current literature on epithelial plasticity in cancer metastasis.
- Analysis of studies investigating EMT and MET in bone metastasis.
- Synthesis of data linking EMT to cancer stem cell properties and treatment resistance.
Main Results:
- EMT enables cancer cell invasion, dissemination, and colonization of bone.
- Bone microenvironment facilitates MET, allowing tumor cells to form glandular structures.
- EMT confers stem cell-like properties, promoting immune evasion, apoptosis resistance, and therapy resistance.
Conclusions:
- Epithelial plasticity is a critical driver of bone metastasis and minimal residual disease.
- EMT-induced cancer stem cells present significant challenges in treatment and relapse.
- Understanding EMT is vital for developing effective targeted therapies against bone metastasis.
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