MiR200-upregulated Vasohibin 2 promotes the malignant transformation of tumors by inducing epithelial-mesenchymal transition in hepatocellular carcinoma.
MiR200-upregulated Vasohibin 2 promotes the malignant transformation of tumors by inducing epithelial-mesenchymal transition in hepatocellular carcinoma.
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MiR200上调的Vasohibin 2通过诱导肝细胞癌上皮间质转化促进肿瘤恶性转化
DOI：
10.1186/s12964-014-0062-x
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发表时间：
2014-10-01
期刊：
影响因子：
--
通讯作者：
Gao W
中科院分区：
文献类型：
--
作者：
Xue X;Zhang Y;Zhi Q;Tu M;Xu Y;Sun J;Wei J;Lu Z;Miao Y;Gao W
背景肝细胞癌（HCC）的恶性行为（包括生长和转移）通常依赖于肿瘤转化和血管生成。此前，我们报道Vasohibin2（VASH2）优先在肝细胞癌（HCC）肿瘤组织中表达并促进血管生成。在此，我们进一步研究了VASH2在HCC肿瘤进展中的作用。结果生物信息学分析和荧光素酶报告基因检测证实了miR-200a/b/c对VASH2的转录后调控。然后，我们使用两种代表性肝癌细胞系 HepG2 和 Hep3B 细胞来研究 VASH2 在肿瘤中的作用。 HepG2 细胞中 VASH2 敲除抑制上皮间质转化 (EMT)，但 Hep3B 细胞中 VASH2 过表达促进 EMT。 Western blot分析显示VASH2通过ZEB1/2通路促进EMT。结论VASH2在体内外促进侵袭，减少细胞凋亡，增加干细胞比例。这些结果表明HCC细胞中VASH2的表达通过诱导EMT促进肿瘤的恶性转化。
BackgroundHepatocellular carcinoma (HCC) typically relies on tumor transformation and angiogenesis for its malignant behavior, including growth and metastasis. Previously, we reported that Vasohibin2 (VASH2) is preferentially expressed in hepatocellular carcinoma (HCC) tumor tissues and promotes angiogenesis. Here, we further investigated the role of VASH2 in HCC tumor progression.ResultsBioinformatics analyses and luciferase reporter gene assays confirmed the post-transcriptional regulation ofVASH2bymiR-200a/b/c. We then used HepG2 and Hep3B cells, two representative hepatic cancer cell lines, to examine the role of VASH2 in tumors. VASH2 knockdown in HepG2 cells inhibited epithelial-mesenchymal transition (EMT), but VASH2 overexpression in Hep3B cells promoted EMT. Western blot analyses showed that VASH2 promoted EMT through the ZEB1/2 pathway.ConclusionVASH2 promoted invasion, reduced apoptosis and increased the proportion of stem cells in vitro and in vivo. These results indicated that VASH2 expression in HCC cells promotes the malignant transformation of tumors by inducing EMT.
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影响因子：
11.2
作者：
Wang Z;Li Y;Kong D;Banerjee S;Ahmad A;Azmi AS;Ali S;Abbruzzese JL;Gallick GE;Sarkar FH
通讯作者：
Sarkar FH
影响因子：
11.2
作者：
Spaderna, Simone;Schmalhofer, Otto;Brabletz, Thomas
通讯作者：
Brabletz, Thomas
影响因子：
158.5
作者：
Llovet, Josep M.;Ricci, Sergio;Bruix, Jordi
通讯作者：
Bruix, Jordi
影响因子：
13.5
作者：
Ding, Wei;You, Hanning;Dang, Hien;LeBlanc, Francis;Galicia, Vivian;Lu, Shelly C.;Stiles, Bangyan;Rountree, C. Bart
通讯作者：
Rountree, C. Bart
影响因子：
5
作者：
Song, Kyoung Doo;Choi, Dongil;Lee, Won Jae
通讯作者：
Lee, Won Jae