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[1]袁华尊,孙保存,赵秀兰,等.Amotl2促进肝细胞肝癌血管生成拟态及EMT形成[J].天津医科大学学报,2016,22(04):277-282.
　YUAN Hua-zun,SUN Bao-cun,ZHAO Xiu-lan,et al.Amotl2 promotes vasculogenic mimicry and epithelial-mesenchymal transition in hepatocellular carcinoma[J].Journal of Tianjin Medical University,2016,22(04):277-282.
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《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:
22卷
期数:
2016年04期
页码:
277-282
栏目:
基础医学
出版日期:
2016-07-19

文章信息/Info

Title:
Amotl2 promotes vasculogenic mimicry and epithelial-mesenchymal transition in hepatocellular carcinoma
文章编号:
1006-8147（2016）04-0277-06
作者:
?袁华尊1; 孙保存1; 2; 赵秀兰1; 2; 张丹芳1; 刘铁菊1; 赵 楠1; 董学易1; 刘 芳1
（1.天津医科大学病理学教研室，天津 300070；2.天津医科大学总医院病理科，天津 300052）
Author(s):
YUAN Hua-zun1;  SUN Bao-cun1; 2; ZHAO Xiu-lan1; 2;  ZHANG Dan-fang1;  LIU Tie-jun1;  ZHAO Nan1; DONG Xue-yi1;  LIU Fang1
(1. Department of Pathology, Tianjin Medical University, Tianjin 300070, China; 2. Department of Pathology, General Hospital，Tianjin Medical University, Tianjin 300052, China )
关键词:
肝细胞肝癌;  Amotl2;  上皮间充质转化 ;  血管生成拟态 ;  迁移;  侵袭
Keywords:
hepatocellular carcinoma;  Amotl2;  epithelial-mesenchymal transition;  vasculogenic mimicry; migration;  invasion

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分类号:
Q7
DOI:
-
文献标志码:
A
摘要:
目的：研究Amotl2对肝癌细胞迁移侵袭能力的影响及其在诱导肝癌上皮间充质转化（EMT）及血管生成中的作用。方法：将Amotl2过表达质粒和干扰质粒分别转染至肝癌细胞系HepG2和Bel7402中，Western blot检测转染前、后HepG2和Bel7402中Amotl2、EMT相关蛋白（E-cadherin、Vimentin）表达变化情况；划痕、侵袭实验检测Amotl2对肝癌细胞迁移和侵袭能力的影响；三维培养检测Amotl2对HCC细胞形成血管样结构的影响。结果：促进Amotl2表达后HepG2表现出EMT样改变，E-cadherin表达下降、Vimentin表达上升、细胞迁移侵袭和三维成管的能力增强。抑制Amotl2表达后Bel7402由间质样表型转变为上皮样表型，E-cadherin表达上升、Vimentin表达下降、细胞迁移侵袭和三维成管的能力减弱。结论：Amotl2可能通过诱导EMT促进原发性肝癌的迁移侵袭能力和血管生成拟态的形成。
Abstract:
Objective: To examine the expression of Amotl2 in hepatocellular carcinoma (HCC) cells and its effect on the migration and invasion. To evaluate the functions of Amotl2 in inducing epithelial-mesenchymal transition (EMT). Methods: A cDNA sequence containing Amotl2 over-expression plasmid was inserted into HepG2 cells to induce exogenous expression of Amotl2 protein while the Amotl2 shRNA sequence plasmid was inserted into Bel7402 to interfere the quantity of Amotl2 protein. The expression of Amotl2, EMT-related protein (E-cadherin, Vimentin) in HepG2 cells and Bel7402 cells were analyzed by Western blot before and after transfection; In wound healing assays, cell motility was assessed by measuring the movement of cells into a scarped and the invasion assay was used to determine the function of invasive potential；Matrigel 3D culture was utilized as a well-established in vitro model for investigating vasculogenic mimicry（VM） formation. Results: After transfection, the HepG2 cells showed significant changes from epithelial phenotype to interstitial phenotype. Accordingly, up-regulation group presented an E-cadherin expression down-regulated and Vimentin expression up-regulated in HepG2-Amotl2 cells and its motility and invasiveness were enhanced; the transfected Bel7402 cells were converted from interstitial phenotype toepithelial phenotype, which increased E-cadherin expression and decreased Vimentin expression and its motility and invasiveness were inhibited. Conclusion: Amotl2 may affect hepatocellular carcinoma migration, invasion and VM formation by regulating the epithelial-mesenchymal transition process.

参考文献/References:

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备注/Memo

备注/Memo:
基金项目 国家自然科学基金重点项目基金资助（81230050）, 国家自然科学基金面上项目基金资助（81572872）

作者简介 袁华尊（1988-），男，硕士在读，研究方向：肿瘤病理学；

通信作者：孙保存，E-mail：sunbaocun@aliyun.com。

更新日期/Last Update: 2016-07-12