MRC2 expression correlates with TGFβ1 and survival in hepatocellular carcinoma.

MRC2 expression correlates with TGFβ1 and survival in hepatocellular carcinoma.
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DOI:
10.3390/ijms150915011
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发表时间:
2014-08-26
影响因子:
5.6
通讯作者:
Zheng X
Zheng X
中科院分区:
生物学2区
文献类型:
--
作者:
Gai X;Tu K;Lu Z;Zheng X

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MRC2(甘露糖受体C型2)是甘露糖受体家族中的一种结构性循环内吞受体,已被发现与肿瘤转移密切相关。本研究旨在探讨MRC2在肝细胞癌中的表达及其对肝细胞癌术后预后的意义。应用免疫组织化学方法检测96例肝癌组织中MRC2和转化生长因子β-1的表达,发现肝癌组织中MRC2的表达明显高于癌旁肝组织。MRC2高表达的人肝细胞癌术后预后较差。单因素分析显示,分期高、Edmonson-Steiner分级高、肝内转移、门静脉侵犯、高MRC2和高转化生长因子β-1是预后不良的因素。多因素分析显示,肝内转移、高MRC2和高转化生长因子β1是影响预后的独立因素。转化生长因子β-1可显著上调HUH7细胞MRC2的表达、细胞迁移和侵袭能力。此外,下调mrc2基因可抑制转化生长因子β1对细胞迁移和侵袭的影响。这些数据表明,MRC2的过度表达预示着肝细胞癌切除后的不良预后,并且MRC2可能与转化生长因子β1上调肝癌细胞的迁移和侵袭有关。
MRC2 (Mannose Receptor C Type 2) is a constitutively recycling endocytic receptor belonging to the mannose receptor family, which has been found to be closely involved with cancer metastasis. This study attempted to determine MRC2 expression on hepatocellular carcinoma (HCC) and its significance on postsurgical prognosis of HCCs. The expression of both MRC2 and transforming growth factor (TGFβ1) was detected in tumor tissues and adjacent liver tissues from 96 HCCs by immunohistochemistry staining, and it was found that MRC2 expression in HCC tissues was significantly higher than in adjacent liver tissues. HCCs with higher MRC2 expression had worse prognosis after liver resection. Univariate analysis showed that advanced TNM staging of HCC, higher Edmonson-Steiner classification, intrahepatic metastases, portal vein invasion, higher MRC2 and higher TGFβ1 were the poor prognostic factors. Furthermore, multivariate analysis revealed that intrahepatic metastases, higher MRC2 and higher TGFβ1 were the independent prognostic factors. TGFβ1 treatment up-regulated MRC2 expression, cell migration and invasion of Huh7 cells notably. In addition, knockdown of MRC2 repressed the effect of TGFβ1 on cell migration and invasion. These data suggest that MRC2 overexpression predicts poor prognosis of HCCs after liver resection and MRC2 potentially contributed to TGFβ1-driven up-regulation of cell migration and invasion in HCC.
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