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• W2130133905 abstract "Abstract As tumor development relies on a coordination of angiogenesis and tumor growth, an efficient antitumor strategy should target both the tumor and its associated vessels. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces apoptosis in a tumor-selective manner. Additionally, thrombospondin-1, a naturally occurring inhibitor of angiogenesis, and a recombinant protein containing functional domains of thrombospondin-1, 3TSR, have been shown to be necessary and sufficient to inhibit tumor angiogenesis. Here, we show that a combination of a TRAIL receptor 2 agonist antibody, Lexatumumab, and 3TSR results in a significantly enhanced and durable tumor inhibition. We further observed that 3TSR induces apoptosis in primary endothelial cells by up-regulating the expression of TRAIL receptors 1 and 2 in a CD36 and Jun NH2-terminal kinase-dependent manner leading to the activation of both intrinsic and extrinsic apoptotic machineries. The modulation of these pathways is critical for 3TSR-induced apoptosis as disrupting either via specific inhibitors reduced apoptosis. Moreover, 3TSR attenuates the Akt survival pathway. These studies indicate that 3TSR plays a critical role in regulating the proapoptotic signaling pathways that control growth and death in endothelial cells and that a combination of TRAIL and 3TSR acts as a double hit against tumor and tumor-associated vessels. [Cancer Res 2009;69(9):3856–65]" @default.
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• W2130133905 date "2009-04-30" @default.
• W2130133905 modified "2023-10-16" @default.
• W2130133905 title "A Double Hit to Kill Tumor and Endothelial Cells by TRAIL and Antiangiogenic 3TSR" @default.
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• W2130133905 doi "https://doi.org/10.1158/0008-5472.can-08-2940" @default.
• W2130133905 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2981788" @default.
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• W2130133905 hasPublicationYear "2009" @default.
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