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ABSTRACT: Background
Prostate cancer (PCa) bone metastasis can be markedly enhanced by increased receptor activator of NF kappa-B ligand (RANKL) expression in PCa cells. Molecular mechanisms that account for the increased predilection of PCa for bone include increased bone turnover, promotion of PCa cell growth and survival in the bone environment, and recruitment of bystander dormant cells to participate in bone metastasis. The current study tests the hypothesis that PCa cells acquire high adhesion to bone matrix proteins, which controls PCa bone colonization, under the RANKL/RANK and AR axes.Methods
We used a highly bone metastatic RANKL-overexpressing LNCaP PCa cell line, LNCaP(RANKL), as a model to pursue the molecular mechanisms underlying the increased adhesion of PCa cells to
SUBMITTER: Ziaee S
PROVIDER: S-EPMC4171564 | biostudies-literature | 2014 Sep
REPOSITORIES: biostudies-literature