Prostate cancer metastasis: Role of the host microenvironment in promoting epithelial to mesenchymal transition and increased bone and adrenal gland metastasis
Article first published online: 10 AUG 2006
Copyright © 2006 Wiley-Liss, Inc.
Volume 66, Issue 15, pages 1664–1673, November 2006
How to Cite
Xu, J., Wang, R., Xie, Z. H., Odero-Marah, V., Pathak, S., Multani, A., Chung, L. W.K. and Zhau, H. E. (2006), Prostate cancer metastasis: Role of the host microenvironment in promoting epithelial to mesenchymal transition and increased bone and adrenal gland metastasis. Prostate, 66: 1664–1673. doi: 10.1002/pros.20488
- Issue published online: 20 SEP 2006
- Article first published online: 10 AUG 2006
- Manuscript Accepted: 16 MAY 2006
- Manuscript Received: 17 FEB 2006
- organ-specific tropism;
- clonal interaction;
- cancer cell heterogeneity;
- animal model;
- cancer progression
The ARCaP cell line was established from the ascites fluid of a patient with metastatic prostate cancer. This study characterized the host microenvironmental role in cancer progression, epithelial to mesenchymal transition (EMT), and bone and adrenal metastasis in parental ARCaP and its derived cell subclones.
Cytogenetic profiles, growth, migration, invasion, cellular interaction, drug sensitivities, and gene expression of ARCaP cell subclones were compared. In vivo gene expression, behavior, and metastasis of ARCaP subclones were analyzed by serial intracardiac injections into SCID mice.
ARCaPE cells, with cobblestone morphology, underwent EMT through cellular interaction with host bone and adrenal gland. Lineage-derived ARCaPM cells, with spindle-shape fibroblastic morphology, exhibited decreased cell adhesion and increased metastasis to bone and adrenal gland. Cytogenetic analyses of parental and ARCaP subclones confirmed their clonality.
ARCaP uniquely models the molecular basis of prostate cancer bone and adrenal metastases and epithelial to mesenchymal transition. Prostate 66: 1664–1673, 2006. © 2006 Wiley-Liss, Inc.