Aberrant expression of Golgi protein 73 is indicative of a poor outcome in hepatocellular carcinoma
Aberrant expression of Golgi protein 73 is indicative of a poor outcome in hepatocellular carcinoma
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DOI：
10.3892/or.2016.4601
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发表时间：
2016-04-01
期刊：
影响因子：
4.2
通讯作者：
Liu, Yinkun
中科院分区：
文献类型：
--
作者：
Jiang, Kai;Li, Wei;Liu, Yinkun
高尔基蛋白73 （GP73）是一种常驻的高尔基ii型膜蛋白，在肝细胞中经常上调。在本研究中，shrna介导的肝细胞癌（HCC）细胞系（MHCC97H, HCCLM3）中GP73表达的抑制导致细胞运动和侵袭的显著抑制，并导致上皮-间质转化表型的回归。相比之下，GP73在SMMC7721细胞系中过表达可恢复EMT标志物的表达，促进细胞运动和侵袭。western blot和免疫组化分析显示，GP73在肝癌转移组织中也有高表达。Kaplan-Meier生存分析显示，GP73高表达患者的生存期明显低于GP73低表达患者（p=0.027）。我们的研究结果证明了GP73在HCC转移中的重要作用，并表明GP73是HCC治疗的候选靶点。
Golgi protein 73 (GP73), a resident Golgi type-II membrane protein, is often upregulated in hepatocytes. In the present study, shRNA-mediated suppression of GP73 expression in hepatocellular carcinoma (HCC) cell lines (MHCC97H, HCCLM3) resulted in a significant inhibition of cell motility and invasion and also led to the regression of epithelial-mesenchymal transition phenotypes. In contrast, overexpression of GP73 in the SMMC7721 cell line retrieved the expression of EMT markers, and promoted cell motility and invasion. High expression of GP73 was also found in HCC tissues with metastasis, as detected by western blot and immunohistochemistry analyses. Kaplan-Meier survival analysis showed that the survival of patients with high GP73 expression was significantly poorer than that of patients with low GP73 expression (p=0.027). Our findings demonstrated an important role of GP73 in HCC metastasis, and indicated that GP73 is a candidate target for HCC therapy.