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- W2184197034 abstract "The antitumor effects of pharmacologic inhibitors of angiogenesis are hampered in patients by the rapid development of tumor resistance, notably through increased invasiveness and accelerated metastasis. Here, we reevaluatedtheroleoftheendogenousantiangiogenicthrombospondin1(TSP1)inprostatecarcinomasinwhich angiogenesisisanactiveprocess.Inxenograftedtumors,weobservedthatTSP1altogetherinhibitedangiogenesis and fostered tumor development. Our results show that TSP1 is a potent stimulator of prostate tumor cell migration. This effect required CD36, whichalso mediates TSP1 antiangiogenic activity, and was mimicked by an antiangiogenic TSP1-derived peptide. As suspected for pharmacologic inhibitors of angiogenesis, the TSP1 capacities to increase hypoxia and to trigger cell migration are thus inherently linked. Importantly, although antiangiogenicTSP1increaseshypoxiainvivo,ourdatashowthat,inturn,hypoxiainducedTSP1,thusgenerating a vicious circle in prostate tumors. In radical prostatectomy specimens, we found TSP1 expression significantly associatedwithinvasivetumorsandwithtumorswhicheventuallyrecurred.TSP1maythushelpselectpatientsat risk of prostate-specific antigen relapse. Together, the data suggest that intratumor disruption of the hypoxic cycle through TSP1 silencing will limit tumor invasion. Cancer Res; 71(24); 7649–58. � 2011 AACR." @default.
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- W2184197034 date "2011-01-01" @default.
- W2184197034 modified "2023-09-24" @default.
- W2184197034 title "Thrombospondin-1TriggersCellMigrationandDevelopment of Advanced Prostate Tumors" @default.
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