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• W2048392784 abstract "Abstract Recent evidence has suggested that bone marrow-derived mesenchymal stem cells (MSCs) may be effective cellular vehicles for delivering anti-cancer agents, as they have shown to home to tumor sites. However, the signals required for homing and recruitment of MSCs to tumor sites are not well understood. In this communication, we characterized the biomediators and the possible downstream signaling pathways that responsible for the migration of MSCs toward RCC. Our in vitro migration assay demonstrated that RCC attracted MSCs much more efficient than normal human renal epithelial cells (HRE) did. Systemic administration of MSCs into RCC-bearing mice also caused rapid recruitment of MSCs at the site of tumor xenografts as well as distant metastases. To identify RCC-derived soluble factor(s) involved in MSC migration, we used antibody-based cytokine arrays to screened conditioned media (CM) from RCC cells and normal HRE cells. Among 180 cytokines we tested, solely one cytokine, PDGF-AA, was significantly up-regulated in RCC cells with a 10 fold-increased expression to HRE. On the other hand, MSC expressed high level of PDGF receptor-α in both RNA and protein level, as determined by qRT-PCR and Western blotting analysis, respectively. Functional blockage of PDGF-AA in RCC cells using either neutralizing antibody or targeting siRNA abrogated RCC-CM induced MSC migration. Pretreatment of MSCs with inhibitory antibodies against PDGF receptor-α or PDGF receptor kinase inhibitor also reduced MSC migration toward either rPDGF-AA or RCC-CM, indicating that increased MSC migration by RCC is dependent on PDGF-AA signaling through the PDGF receptor-α. We also found that RCC-CM but not HRE-CM elicited a time-dependent phosphorylation of Akt and downstream GSK3, and sustained accumulation of β-catenin protein in MSCs. These effects were abolished when MSC were pretreated with kinase inhibitor for PDGF receptor-α. Collectively, our data demonstrate that RCC tumor cells specifically recruit MSCs, which is mediated by PDGF-AA through activation of PDGF receptor signaling and AKT/GSK-3 pathways. These findings may expose new targets for diagnostic and therapeutic strategies and reduce the morbidity and mortality from metastatic disease. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 410. doi:10.1158/1538-7445.AM2011-410" @default.
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• W2048392784 date "2011-04-01" @default.
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• W2048392784 title "Abstract 410: Platelet derived growth factor AA mediated the tropism of human mesenchymal stem cells for renal cell carcinoma" @default.
• W2048392784 doi "https://doi.org/10.1158/1538-7445.am2011-410" @default.
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