Dishevelled-2的过表达促进人食管鳞状细胞癌的增殖和迁移。
Overexpression of Dishevelled-2 contributes to proliferation and migration of human esophageal squamous cell carcinoma.
作者信息
Zhou Guoren, Ye Jinjun, Sun Lei, Zhang Zhi, Feng Jifeng
机构信息
Department of Chemotherapy, Jiangsu Cancer Hospital Affiliated to Nanjing Medical University, 42 Baiziting Raod, Nanjing, 210000, Jiangsu, China.
Department of Radiotherapy, Jiangsu Cancer Hospital Affiliated to Nanjing Medical University, 42 Baiziting Raod, Nanjing, 210000, Jiangsu, China.
出版信息
J Mol Histol. 2016 Jun;47(3):287-95. doi: 10.1007/s10735-016-9674-3. Epub 2016 Apr 15.
Dishevelled-2 (Dvl2) was associated with tumor cell proliferation and migration. We aimed to examine the mechanism of Dvl2 in esophageal squamous cell carcinoma (ESCC). Dvl2 was overexpressed in human ESCC tissues and cell lines ECA109 and TE1 cells. CCK-8 and colony formation assay was performed to evaluate the proliferation in ECA109 cells transfected with Dvl2-shRNA. Wound-healing assay and transwell assay were used to examine the activities of migration and invasion in Dvl2-silenced ESCC cells. Knockdown of Dvl2 significantly reduced ECA109 cell proliferation and migration. Moreover, we demonstrated that the proliferation and migration ability of Dvl2 might through the activation of Wnt pathway by targeting the Cyclin D1 and MMP-9. We came to the conclusion that the proliferation and migration effects of Dvl2 might contribute to malignant development of human ESCC.
Dishevelled-2（Dvl2）与肿瘤细胞的增殖和迁移相关。我们旨在研究Dvl2在食管鳞状细胞癌（ESCC）中的作用机制。Dvl2在人ESCC组织以及细胞系ECA109和TE1细胞中过表达。采用CCK-8和集落形成实验评估转染Dvl2-shRNA的ECA109细胞的增殖情况。利用划痕实验和Transwell实验检测Dvl2沉默的ESCC细胞的迁移和侵袭活性。敲低Dvl2可显著降低ECA109细胞的增殖和迁移能力。此外，我们证明Dvl2的增殖和迁移能力可能是通过靶向细胞周期蛋白D1（Cyclin D1）和基质金属蛋白酶-9（MMP-9）激活Wnt信号通路来实现的。我们得出结论，Dvl2的增殖和迁移作用可能促进了人类ESCC的恶性发展。
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