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首页> 外文期刊>Nature >G-protein-coupled receptor of Kaposi's sarcoma-associated herpesvirus is a viral oncogene and angiogenesis activator (see comments) (published erratum appears in Nature 1998 Mar 12;392(6672):210)
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G-protein-coupled receptor of Kaposi's sarcoma-associated herpesvirus is a viral oncogene and angiogenesis activator (see comments) (published erratum appears in Nature 1998 Mar 12;392(6672):210)

机译：卡波济氏肉瘤相关疱疹病毒的G蛋白偶联受体是一种病​​毒致癌基因和血管生成激活剂（见评论）（发表的勘误发表于Nature 1998 Mar 12; 392（6672）：210）

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摘要

The Kaposi's sarcoma-associated herpesvirus (KSHV/HHV8) is a gamma-2 herpesvirus that is implicated in the pathogenesis of Kaposi's sarcoma and of primary effusion B-cell lymphomas (PELs). KSHV infects malignant and progenitor cells of Kaposi's sarcoma and PEL, it encodes putative oncogenes and genes that may cause Kaposi's sarcoma pathogenesis by stimulating angiogenesis. The G-protein-coupled receptor encoded by an open reading frame (ORF 74) of KSHV is expressed in Kaposi's sarcoma lesions and in PEL and stimulates signalling pathways linked to cell proliferation in a constitutive (agonist-independent) way. Here we show that signalling by this KSHV G-protein-coupled receptor leads to cell transformation and tumorigenicity, and induces a switch to an angiogenic phenotype mediated by vascular endothelial growth factor, an angiogenesis and Kaposi's-spindle-cell growth factor. We find that this receptor can activate two protein kinases, JNK/SAPK and p38MAPK, by triggering signalling cascades like those induced by inflammatory cytokines that are angiogenesis activators and mitogens for Kaposi's sarcoma cells and B cells. We conclude that the KSHV G-protein-coupled receptor is a viral oncogene that can exploit cell signalling pathways to induce transformation and angiogenesis in KSHV-mediated oncogenesis.
机译：卡波西氏肉瘤相关疱疹病毒（KSHV / HHV8）是一种伽马2疱疹病毒，与卡波西氏肉瘤和原发性B细胞淋巴瘤（PEL）的发病机制有关。 KSHV感染卡波西氏肉瘤和PEL的恶性和祖细胞，它编码推定的癌基因和可能通过刺激血管生成而引起卡波西氏肉瘤发病的基因。由KSHV的开放阅读框（ORF 74）编码的G蛋白偶联受体在卡波西氏肉瘤病变和PEL中表达，并以本构性（独立于激动剂的方式）刺激与细胞增殖有关的信号通路。在这里，我们显示由这种KSHV G蛋白偶联受体引起的信号传导导致细胞转化和致瘤性，并诱导切换到由血管内皮生长因子，血管生成和卡波西氏纺锤体细胞生长因子介导的血管生成表型。我们发现该受体可以通过触发信号级联反应来激活两个蛋白激酶，即JNK / SAPK和p38MAPK，这些信号级联反应是由炎症性细胞因子诱导的，这些炎症性细胞因子是卡波西氏肉瘤细胞和B细胞的血管生成激活剂和有丝分裂原。我们得出的结论是，KSHV的G蛋白偶联受体是一种病​​毒致癌基因，可以利用细胞信号通路在KSHV介导的肿瘤发生中诱导转化和血管生成。

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