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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >GPR56, an atypical G protein-coupled receptor, binds tissue transglutaminase, TG2, and inhibits melanoma tumor growth and metastasis
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GPR56, an atypical G protein-coupled receptor, binds tissue transglutaminase, TG2, and inhibits melanoma tumor growth and metastasis

机译：GPR56是一种非典型的G蛋白偶联受体，与组织转谷氨酰胺酶TG2结合，并抑制黑素瘤肿瘤的生长和转移

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The survival and growth of tumor cells in a foreign environment is considered a rate-limiting step during metastasis. To identify genes that may be essential for this process, we isolated highly metastatic variants from a poorly metastatic human melanoma cell line and performed expression analyses of metastases and primary tumors from these cells. GPR56 is among the genes markedly down-regulated in the metastatic variants. We show that overexpression of GPR56 suppresses tumor growth and metastasis, whereas reduced expression of GPR56 enhances tumor progression. Levels of GPR56 do not correlate with growth rate in vitro, suggesting that GPR56 may mediate growth suppression by interaction with a component in the tumor microenvironment in vivo. We show that GPR56 binds specifically to tissue transglutaminase, TG2, a widespread component of tissue and tumor stroma previously implicated as an inhibitor of tumor progression. We discuss the mechanisms whereby GPR56-TG2 interactions may suppress tumor growth and metastasis.
机译：肿瘤细胞在外来环境中的存活和生长被认为是转移过程中的限速步骤。为了鉴定对该过程可能必不可少的基因，我们从转移不良的人黑素瘤细胞系中分离了高度转移的变体，并从这些细胞中进行了转移和原发肿瘤的表达分析。 GPR56是转移性变体中明显下调的基因之一。我们表明，GPR56的过表达抑制肿瘤的生长和转移，而减少的GPR56的表达增强了肿瘤的进展。 GPR56的水平与体外生长速率无关，表明GPR56可能通过与体内肿瘤微环境中的组分相互作用而介导生长抑制。我们显示GPR56特异性结合组织转谷氨酰胺酶TG2，组织和肿瘤基质的广泛组成部分，以前被认为是肿瘤进展的抑制剂。我们讨论了GPR56-TG2相互作用可能抑制肿瘤生长和转移的机制。

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