Vasculogenic mimicry in hepatocellular carcinoma contributes to portal vein invasion.
Vasculogenic mimicry in hepatocellular carcinoma contributes to portal vein invasion.
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肝细胞癌中的血管生成拟态有助于门静脉侵袭
DOI：
10.18632/oncotarget.12867
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发表时间：
2016-11-22
期刊：
影响因子：
--
通讯作者：
Yanqing L
中科院分区：
文献类型：
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作者：
Jue C;Zhifeng W;Zhisheng Z;Lin C;Yayun Q;Feng J;Hao G;Shintaro I;Hisamitsu T;Shiyu G;Yanqing L
门静脉侵犯（PVI）在肝细胞癌（HCC）中很常见，并且是根治性肿瘤切除或肝移植后肿瘤复发的主要原因。血管生成拟态（VM）是一种由肿瘤细胞组成的独立的血管系统，与肝癌预后不良有关。本研究旨在探讨VM与门静脉侵犯的关系。共44例接受解剖性肝切除术的HCC患者被纳入本研究，并被分为PVI组和无PVI组。采用CD 34-PAS双染法检测各组VM的发生率。免疫组化法检测VM形成的调控分子Notch 1、波形蛋白和基质金属蛋白酶（MMPs）。进行分析以探索PVI、VM和VM调节分子的关联。PVI占40.91%（18/44），VM占38.64%（17/44）。PVI组VM的发生率为72.22%（13/18），非PVI组VM的发生率为15.38%（4/26）（P<0.001），VM的形成与PVI呈正相关（r=0.574，P<0.001）。在HCC患者中，VM形成调节分子如Notch 1、Vimentin、MMP-2和MMP-9被发现与PVI相关。总之，我们的研究结果表明，VM的形成，单独与其调节分子，是促进因素PVI在肝细胞癌。
Portal vein invasion (PVI) is common in hepatocellular carcinoma (HCC) and largely contributes to tumor recurrence after radical tumor resection or liver transplantation. Vasculogenic mimicry (VM) was an independent vascular system lined with tumor cells and associated with poor prognosis of HCC. The present study was conducted to evaluate the relationship between VM and portal vein invasion. A total of 44 HCC cases receiving anatomic liver resection were included in the study and were divided into groups with and without PVI. The prevalence of VM in each group was examined by CD34-PAS dual staining. The regulatory molecules of VM formation such as Notch1, Vimentin and matrix metalloproteinases (MMPs) were investigated by immunohistochemical staining. Analysis was performed to explore the association of PVI, VM and the VM regulatory molecules. PVI was found in 40.91% (18/44) cases and VM was found in 38.64% (17/44) cases in total samples. The incidence of VM was 72.22% (13/18) in PVI group while it was 15.38% (4/26) in non-PVI group (P<0.001), VM formation was positively correlated with PVI (r=0.574, P<0.001). The VM forming regulatory molecules such as Notch1, Vimentin, MMP-2 and MMP-9 were found to be correlated with PVI in HCC patients. Taken together, our results suggested that VM formation, alone with its regulatory molecules, is the promoting factor of PVI in hepatocellular carcinoma.