Urocortin's inhibition of tumor growth and angiogenesis in hepatocellular carcinoma via corticotrophin-releasing factor receptor 2
Urocortin's inhibition of tumor growth and angiogenesis in hepatocellular carcinoma via corticotrophin-releasing factor receptor 2
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DOI：
10.1080/07357900701788106
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发表时间：
2008-01-01
影响因子：
2.4
通讯作者：
Li, Shengnan
中科院分区：
文献类型：
--
作者：
Wang, Juejin;Xu, Youhua;Li, Shengnan
尿皮质素 (UCN) 通过促肾上腺皮质激素释放因子受体 (CRFR)、CRFR1 2 发挥作用。据报道，CRFR2 是血管形成的强直抑制因子，这意味着它在肿瘤血管生成中的作用。在这里，我们发现UCN可以抑制裸鼠肝细胞癌（HCC）的生长并降低肿瘤微血管密度。肝癌细胞不表达CRFR，而血管表达CRFR，主要是CRFR2。体外三维培养测定显示UCN抑制血管生成，这种作用被CRFR2拮抗剂抗sauvagine-30消除，证明了CRFR2的参与。此外，UCN在体内通过CRFR2抑制内皮细胞增殖并促进内皮细胞凋亡并下调VEGF表达。
Urocortin (UCN) functions via corticotrophin-releasing factor receptors (CRFRs), CRFR1 2. CRFR2 is reported to be a tonic suppressor of vascularization, implying its role in tumor angiogenesis. Here, it was found that UCN inhibited the growth of hepatocellular carcinoma (HCC) and reduced tumor microvessel density in nude mice. Hepatoma cells didn't express CRFRs whereas vessels expressed CRFRs, mainly CRFR2. In vitro three-dimensional culture assay showed UCN inhibited angiogenesis, this effect was abolished by CRFR2 antagonist, anti-sauvagine-30, demonstrating involvement of CRFR2. Furthermore, UCN inhibited the proliferation and promoted the apoptosis of endothelial cells and down-regulated VEGF expression in vivo via CRFR2.