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Intra-Cardiac Injection of Human Prostate Cancer Cells to Create a Bone Metastasis Xenograft Mouse Model
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Cellular Plasticity in Prostate Cancer Bone Metastasis
Dima Y Jadaan1, Mutaz M Jadaan2, John P McCabe2
1University College Dublin, Belfield, Dublin, Ireland.
Prostate Cancer
|July 7, 2015
Summary
Cellular plasticity, the ability of tumor cells to switch between epithelial and mesenchymal states (EMT and MET), plays a role in prostate cancer bone metastasis. Targeting both states is crucial for effective treatment.
Area of Science:
- Oncology
- Cell Biology
- Cancer Metastasis
Background:
- Tumor cells exhibit cellular plasticity, reversibly transitioning between epithelial-mesenchymal states (EMT and MET).
- Prostate cancer (PC) bone metastasis is a significant clinical challenge.
- Understanding cellular plasticity in PC bone metastasis is crucial for developing targeted therapies.
Purpose of the Study:
- To review and appraise the clinical evidence for cellular plasticity in prostate cancer bone metastasis.
- To examine the expression of epithelial, mesenchymal, and stem cell markers in PC bone metastasis.
Main Methods:
- Systematic electronic literature search using PubMed.
- Inclusion of studies analyzing marker expression in human PC bone metastasis tissues.
- Review of nineteen relevant studies with varying sample sizes and heterogeneity.
Main Results:
- Most stem cell markers (except CXCR4) were positively expressed in bone metastasis tissues.
- Expression of EMT and MET markers was heterogeneous across and within samples.
- Key EMT and stemness markers involved in osteomimicry (Notch, Met, Wnt/β) were highly expressed.
Conclusions:
- Clinical evidence supports the role of cellular plasticity in prostate cancer bone metastasis.
- Targeting PC bone metastasis requires considering both epithelial and mesenchymal states.
- Clinical detection of cellular plasticity faces several challenges.
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