Missing-in-metastasis B (MIM-B) combined with caveolin-1 promotes metastasis of hepatocellular carcinoma.
Missing-in-metastasis B (MIM-B) combined with caveolin-1 promotes metastasis of hepatocellular carcinoma.
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DOI：
10.18632/oncotarget.20735
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发表时间：
2017-11-10
期刊：
影响因子：
--
通讯作者：
Tang ZY
中科院分区：
文献类型：
--
作者：
Huang XY;Huang ZL;Niu T;Wu ZQ;Xu B;Xu YH;Huang XY;Zheng Q;Zhou J;Chen Z;Tang ZY
越来越多的证据表明转移缺失B（MIM-B）促进肿瘤转移。在这里，我们试图更好地了解MIM-B促进肝细胞癌（HCC）肿瘤转移的机制。我们进行了共聚焦显微镜分析来确定MIM-B和小窝蛋白-1的分布，并进行了免疫共沉淀试验来检测MIM-B和小窝蛋白-1之间的体外相互作用。我们用transwell法分析肝癌细胞的侵袭能力。采用免疫组化和Western blotting方法检测肝癌组织中关键基因和部分分子标志物表达水平的变化。我们发现MIM-B与小窝蛋白-1共定位，并证明MIM-B和小窝蛋白-1在体外相互作用。抑制MIM-B和小窝蛋白-1的表达可抑制表皮生长因子受体信号通路。我们在Hep 3B细胞中过表达MIM-B和caveolin-1，这增强了Hep 3B细胞的侵袭力。此外，在MIM-B和小窝蛋白-1表达被抑制的细胞中，MHCC 97 H细胞侵袭力显著降低。此外，我们发现MIM-B和小窝蛋白-1在肝癌组织中的表达水平高于配对的正常组织。此外，MIM-B和caveolin-1表达上调的HCC患者的预后显著差于对照组（P < 0.001），并且MIM-B和caveolin-1高表达水平的HCC患者通常发生肺转移（P < 0.001）。MIM-B和caveolin-1联合应用促进了肝癌的转移，并且MIM-B和caveolin-1的表达水平升高与肝癌患者的不良预后相关，因此MIM-B和caveolin-1可能成为肝癌诊断和治疗的新靶点。
Increasing amounts of evidence indicate that Missing in metastasis B (MIM-B) promotes cancer metastasis. Here, we sought to better understand the mechanism through which MIM-B promotes tumor metastasis in hepatocellular carcinoma (HCC). We performed confocal microscopy analysis to determine the distributions of MIM-B and caveolin-1 and conducted co-immunoprecipitation assays to detect the interactions between MIM-B and caveolin-1 in vitro. We performed transwell assays to analyze the invasive ability of HCC cells. Changes in the expression levels of key genes and some molecular makers were detected by immunohistochemistry and western blotting in HCC tissue samples. We found that MIM-B co-localizes with caveolin-1 and demonstrated that MIM-B and caveolin-1 interact in vitro. Repressing MIM-B and caveolin-1 expression inhibited the epidermal growth factor receptor signaling pathway. We overexpressed MIM-B and caveolin-1 in Hep3B cells, which enhanced Hep3B cell invasiveness. Furthermore, MHCC97H cell invasiveness was significantly decreased in cells in which MIM-B and caveolin-1 expression was inhibited. Additionally, we found that MIM-B and caveolin-1 were expressed at higher levels in HCC tissues than in paired normal tissues. Moreover, HCC patients with MIM-B and caveolin-1 up-regulation experienced significantly worse outcomes than controls (P < 0.001), and HCC patients with high MIM-B and caveolin-1 expression levels often developed pulmonary metastasis (P < 0.001). MIM-B combined with caveolin-1 promotes metastasis of HCC, and elevated MIM-B and caveolin-1 expression levels are associated with a poor prognosis in HCC patients; therefore, MIM-B and caveolin-1 may represent novel targets for the diagnosis and treatment of HCC.
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