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Beta-adrenergic signaling promotes tumor angiogenesis and prostate cancer progression through HDAC2-mediated suppression of thrombospondin-1
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Beta-adrenergic signaling promotes tumor angiogenesis and prostate cancer progression through HDAC2-mediated suppression of thrombospondin-1
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Journal Article
Beta-adrenergic signaling promotes tumor angiogenesis and prostate cancer progression through HDAC2-mediated suppression of thrombospondin-1
2017
Overview
Chronic behavioral stress and beta-adrenergic signaling have been shown to promote cancer progression, whose underlying mechanisms are largely unclear, especially the involvement of epigenetic regulation. Histone deacetylase-2 (HDAC2), an epigenetic regulator, is critical for stress-induced cardiac hypertrophy. It is unknown whether it is necessary for beta-adrenergic signaling-promoted cancer progression. Using xenograft models, we showed that chronic behavioral stress and beta-adrenergic signaling promote angiogenesis and prostate cancer progression. HDAC2 was induced by beta-adrenergic signaling
in vitro
and in mouse xenografts. We next uncovered that HDAC2 is a direct target of cAMP response element-binding protein (CREB) that is activated by beta-adrenergic signaling. Notably, HDAC2 is necessary for beta-adrenergic signaling to induce angiogenesis. We further demonstrated that, upon CREB activation, HDAC2 represses thrombospondin-1 (TSP1), a potent angiogenesis inhibitor, through epigenetic regulation. Together, these data establish a novel pathway that HDAC2 and TSP1 act downstream of CREB activation in beta-adrenergic signaling to promote cancer progression.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 38/44
/ 38/77
/ 59/5
/ 64/60
/ 82/29
/ 96/1
/ 96/95
/ Adrenergic beta-Agonists - pharmacology
/ Animals
/ Cellular signal transduction
/ Cyclic AMP response element-binding protein
/ Cyclic AMP Response Element-Binding Protein - metabolism
/ Enzymes
/ Gene Expression Regulation, Neoplastic
/ Histone Deacetylase 2 - metabolism
/ Humans
/ Kinases
/ Male
/ Medicine
/ Mice
/ Neovascularization, Pathologic - metabolism
/ Oncology
/ Prostatic Neoplasms - genetics
/ Prostatic Neoplasms - metabolism
/ Prostatic Neoplasms - pathology
/ Signal Transduction - drug effects
/ Thrombospondin 1 - metabolism
/ Tumors
