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首页> 外文期刊>Cellular Signalling >Dickkopf-1 (DKK-1) interrupts FAK/PI3K/mTOR pathway by interaction of carbonic anhydrase IX (CA9) in tumorigenesis
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Dickkopf-1 (DKK-1) interrupts FAK/PI3K/mTOR pathway by interaction of carbonic anhydrase IX (CA9) in tumorigenesis

机译：Dickkopf-1（DKK-1）通过碳酸酐酶IX（CA9）在肿瘤发生中的相互作用中断FAK / PI3K / mTOR途径

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摘要

Recently, we found that carbonic anhydrase IX (CA9) modulates tumor-associated cell migration and invasion, and then identified dickkopf-1 (DKK-1) as a novel CA9-interacting protein. In this study, we have determined the binding regions that are required for interaction between CA9 and DKK-1 through in vitro and in vivo. The N-terminal domain of CA9 is participated to interact with the Val ~(60)-Tyr ~(168) site of DKK-1. We also observed that DKK-1 inhibits endothelial cell angiogenesis of CA9 in tumorigenesis. Furthermore, induction of CA9-mediated mTOR phosphorylation and angiogenesis was significantly inhibited by over-expression of DKK-1. Taken together, these findings identify DKK-1 as a potential factor in the regulation of CA9 cellular homeostasis and also suggest a new possible role for DKK1-1 in tumorigenesis.
机译：最近，我们发现碳酸酐酶IX（CA9）调节肿瘤相关的细胞迁移和侵袭，然后确定dickkopf-1（DKK-1）作为一种新型的CA9相互作用蛋白。在这项研究中，我们确定了CA9和DKK-1之间通过体外和体内相互作用所需的结合区。参与CA9的N末端域与DKK-1的Val〜（60）-Tyr〜（168）位点相互作用。我们还观察到DKK-1在肿瘤发生中抑制CA9的内皮细胞血管生成。此外，DKK-1的过表达显着抑制了CA9介导的mTOR磷酸化和血管生成的诱导。综上所述，这些发现确定DKK-1是调节CA9细胞稳态的潜在因素，并且还暗示DKK1-1在肿瘤发生中可能具有新的作用。

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