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首页> 美国卫生研究院文献>EBioMedicine >Hydroxylase Activity of ASPH Promotes Hepatocellular Carcinoma Metastasis Through Epithelial-to-Mesenchymal Transition Pathway
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Hydroxylase Activity of ASPH Promotes Hepatocellular Carcinoma Metastasis Through Epithelial-to-Mesenchymal Transition Pathway

机译：ASPH的羟化酶活性通过上皮-间充质转化途径促进肝癌转移

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摘要

Over-expression of aspartyl (asparagynal)-β-hydroxylase (ASPH) contributes to hepatocellular carcinoma (HCC) invasiveness, but the role of ASPH hydroxylase activity in this process remains to be defined. As such, the current study investigated the role of ASPH hydroxylase activity in downstream signalling of HCC tumorgenesis and, specifically, metastasis development. Over-expression of wild-type ASPH, but not a hydroxylase mutant, promoted HCC cell migration in vitro, as well as intrahepatic and distant metastases in vivo. The enhanced migration and epithelial to mesenchymal transition (EMT) activation was notably absent in response to hydroxylase activity blockade. Vimentin, a regulator of EMT, interacted with ASPH and likely mediated the effect of ASPH hydroxylase activity with cell migration. The enhanced hydroxylase activity in tumor tissues predicted worse prognoses of HCC patients. Collectively, the hydroxylase activity of ASPH affected HCC metastasis through interacting with vimentin and regulating EMT. As such, ASPH might be a promising therapeutic target of HCC.
机译：天冬氨酰（天冬酰胺）-β-羟化酶（ASPH）的过表达有助于肝细胞癌（HCC）的侵袭，但在此过程中ASPH羟化酶活性的作用尚待确定。因此，本研究调查了ASPH羟化酶活性在HCC肿瘤发生，特别是转移发生的下游信号传导中的作用。野生型ASPH的过表达，而不是羟化酶突变体的过表达，在体外促进HCC细胞迁移，并在体内促进肝内和远处转移。响应羟化酶活性阻滞，明显缺乏增强的迁移和上皮向间质转化（EMT）活化。波形蛋白（EMT的调节剂）与ASPH相互作用，并可能通过细胞迁移介导ASPH羟化酶活性的影响。肿瘤组织中羟化酶活性的增强预示了HCC患者的预后较差。总的来说，ASPH的羟化酶活性通过与波形蛋白相互作用和调节EMT来影响HCC转移。因此，ASPH可能是HCC的有希望的治疗靶标。

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