Cellular Plasticity in Prostate Cancer Bone Metastasis
Purpose. Experimental data suggest that tumour cells can reversibly transition between epithelial and mesenchymal states (EMT and MET), a phenomenon known as cellular plasticity. The aim of this review was to appraise the clinical evidence for the role of cellular plasticity in prostate cancer (PC)...
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| Format: | Article |
| Language: | English |
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Wiley
2015-01-01
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| Series: | Prostate Cancer |
| Online Access: | http://dx.doi.org/10.1155/2015/651580 |
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| author | Dima Y. Jadaan Mutaz M. Jadaan John P. McCabe |
| author_facet | Dima Y. Jadaan Mutaz M. Jadaan John P. McCabe |
| author_sort | Dima Y. Jadaan |
| collection | DOAJ |
| description | Purpose. Experimental data suggest that tumour cells can reversibly transition between epithelial and mesenchymal states (EMT and MET), a phenomenon known as cellular plasticity. The aim of this review was to appraise the clinical evidence for the role of cellular plasticity in prostate cancer (PC) bone metastasis. Methods. An electronic search was performed using PubMed for studies that have examined the differential expression of epithelial, mesenchymal, and stem cell markers in human PC bone metastasis tissues. Results. The review included nineteen studies. More than 60% of the studies used ≤20 bone metastasis samples, and there were several sources of heterogeneity between studies. Overall, most stem cell markers analysed, except for CXCR4, were positively expressed in bone metastasis tissues, while the expression of EMT and MET markers was heterogeneous between and within samples. Several EMT and stemness markers that are involved in osteomimicry, such as Notch, Met receptor, and Wnt/β pathway, were highly expressed in bone metastases. Conclusions. Clinical findings support the role of cellular plasticity in PC bone metastasis and suggest that epithelial and mesenchymal states cannot be taken in isolation when targeting PC bone metastasis. The paper also highlights several challenges in the clinical detection of cellular plasticity. |
| format | Article |
| id | doaj-art-b2f510d89a474ae883f264a98a8b8d04 |
| institution | Kabale University |
| issn | 2090-3111 2090-312X |
| language | English |
| publishDate | 2015-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Prostate Cancer |
| spelling | doaj-art-b2f510d89a474ae883f264a98a8b8d042025-02-03T01:00:21ZengWileyProstate Cancer2090-31112090-312X2015-01-01201510.1155/2015/651580651580Cellular Plasticity in Prostate Cancer Bone MetastasisDima Y. Jadaan0Mutaz M. Jadaan1John P. McCabe2University College Dublin, Belfield, Dublin, IrelandDepartment of Orthopaedic Surgery, Galway University Hospitals, Galway, IrelandDepartment of Orthopaedic Surgery, Galway University Hospitals, Galway, IrelandPurpose. Experimental data suggest that tumour cells can reversibly transition between epithelial and mesenchymal states (EMT and MET), a phenomenon known as cellular plasticity. The aim of this review was to appraise the clinical evidence for the role of cellular plasticity in prostate cancer (PC) bone metastasis. Methods. An electronic search was performed using PubMed for studies that have examined the differential expression of epithelial, mesenchymal, and stem cell markers in human PC bone metastasis tissues. Results. The review included nineteen studies. More than 60% of the studies used ≤20 bone metastasis samples, and there were several sources of heterogeneity between studies. Overall, most stem cell markers analysed, except for CXCR4, were positively expressed in bone metastasis tissues, while the expression of EMT and MET markers was heterogeneous between and within samples. Several EMT and stemness markers that are involved in osteomimicry, such as Notch, Met receptor, and Wnt/β pathway, were highly expressed in bone metastases. Conclusions. Clinical findings support the role of cellular plasticity in PC bone metastasis and suggest that epithelial and mesenchymal states cannot be taken in isolation when targeting PC bone metastasis. The paper also highlights several challenges in the clinical detection of cellular plasticity.http://dx.doi.org/10.1155/2015/651580 |
| spellingShingle | Dima Y. Jadaan Mutaz M. Jadaan John P. McCabe Cellular Plasticity in Prostate Cancer Bone Metastasis Prostate Cancer |
| title | Cellular Plasticity in Prostate Cancer Bone Metastasis |
| title_full | Cellular Plasticity in Prostate Cancer Bone Metastasis |
| title_fullStr | Cellular Plasticity in Prostate Cancer Bone Metastasis |
| title_full_unstemmed | Cellular Plasticity in Prostate Cancer Bone Metastasis |
| title_short | Cellular Plasticity in Prostate Cancer Bone Metastasis |
| title_sort | cellular plasticity in prostate cancer bone metastasis |
| url | http://dx.doi.org/10.1155/2015/651580 |
| work_keys_str_mv | AT dimayjadaan cellularplasticityinprostatecancerbonemetastasis AT mutazmjadaan cellularplasticityinprostatecancerbonemetastasis AT johnpmccabe cellularplasticityinprostatecancerbonemetastasis |