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葡萄糖调节蛋白94通过AKT和eNOS介导肝细胞癌的进展。

Glucose-regulated protein 94 mediates cancer progression via AKT and eNOS in hepatocellular carcinoma.

作者信息

Huang Chien-Yu, Batzorig Uyanga, Cheng Wan-Li, Huang Ming-Te, Chen Wei- Yu, Wei Po-Li, Chang Yu-Jia

机构信息

Division of General Surgery, Department of Surgery, Shuang Ho Hospital, Taipei Medical University, Taipei, Taiwan.

Mongolian National University of Medical Sciences, Ulaanbaatar, Mongolia.

出版信息

Tumour Biol. 2016 Apr;37(4):4295-304. doi: 10.1007/s13277-015-4254-9. Epub 2015 Oct 22.

Abstract

Hepatocellular carcinoma (HCC) is a crucial health issue worldwide. High glucose-regulated protein 94 (GRP94) expression has been observed in different types of cancer, suggesting a link between tumor progression and GRP94 expression. However, the mechanisms underlying the role of GRP94 in HCC progression remain unclear. We used specific small hairpin RNA (shRNA) to manipulate GRP94 expression in HCC cells. Tissue arrays, MTT assays, xCELLigence assays, and in vivo xenograft model were performed to identify clinicopathological correlations and to analyze cell growth. We found that high GRP94 expression reflected a poor response and a lower survival rate. In vitro and in vivo studies showed that silencing GRP94 suppressed cancer progression. Mechanistically, GRP94 knockdown reduced AKT, phospho-AKT, and eNOS levels but did not influence the AMPK pathway. Our results demonstrated that GRP94 is a key molecule in HCC progression that modulates the AKT pathway and eNOS levels. Our findings suggest that GRP94 may be a new prognostic and therapeutic target for HCC.

摘要

肝细胞癌(HCC)是一个全球性的重要健康问题。在不同类型的癌症中均观察到高葡萄糖调节蛋白94(GRP94)的表达,这表明肿瘤进展与GRP94表达之间存在联系。然而,GRP94在HCC进展中作用的潜在机制仍不清楚。我们使用特异性短发夹RNA(shRNA)来调控HCC细胞中GRP94的表达。通过组织芯片、MTT实验、xCELLigence实验以及体内异种移植模型来确定临床病理相关性并分析细胞生长情况。我们发现高GRP94表达反映出较差的反应和较低的生存率。体外和体内研究表明,沉默GRP94可抑制癌症进展。从机制上来说,GRP94基因敲低可降低AKT、磷酸化AKT和eNOS的水平,但不影响AMPK信号通路。我们的结果表明,GRP94是HCC进展中的关键分子,可调节AKT信号通路和eNOS水平。我们的研究结果表明,GRP94可能是HCC的一个新的预后和治疗靶点。

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