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Prostate cancer metastasis: Role of the host microenvironment in promoting epithelial to mesenchymal transition and increased bone and adrenal gland metastasis
Author(s) -
Xu Jianchun,
Wang Ruoxiang,
Xie Zhi Hui,
OderoMarah Valerie,
Pathak Sen,
Multani Asha,
Chung Leland W.K.,
Zhau Haiyen E.
Publication year - 2006
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.20488
Subject(s) - metastasis , epithelial–mesenchymal transition , prostate cancer , pathology , bone metastasis , biology , cancer research , prostate , mesenchymal stem cell , cancer , medicine , genetics
BACKGROUND 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. METHODS 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. RESULTS ARCaP E cells, with cobblestone morphology, underwent EMT through cellular interaction with host bone and adrenal gland. Lineage‐derived ARCaP M 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. CONCLUSIONS 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.