NOV promoted the growth and migration of pancreatic cancer cells

被引：17

作者：

Cui, Lei ^{[1
]}

Xie, Rong ^{[1
]}

Dang, Shenchun ^{[1
]}

Zhang, Qing ^{[1
]}

Mao, Shengfa ^{[1
]}

Chen, Jixiang ^{[1
]}

Qu, Jianguo ^{[1
]}

Zhang, Jianxin ^{[1
,2
]}

机构：

[1] Jiangsu Univ, Affiliated Hosp, Dept Gen Surg, Zhenjiang 212003, Jiangsu, Peoples R China

[2] Jiangsu Univ, Affiliated Hosp, Zhenjiang 212003, Jiangsu, Peoples R China

来源：

TUMOR BIOLOGY | 2014年 / 35卷 / 04期

关键词：

NOV; Pancreatic cancer; Cancer metastasis; EMT; CCN FAMILY; METASTASIS; EXPRESSION; REGULATOR;

D O I：

10.1007/s13277-013-1418-3

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

NOV, a member of the CCN (Cyr61, CTGF and NOV) family, is involved in diverse biological processes, such as cell adhesion, proliferation and angiogenesis. However, its function in pancreatic cancer remains poorly understood. Here, we found that the expression of NOV was up-regulated in pancreatic cancer tissues. Moreover, over-expression of NOV in pancreatic cancer cells promoted cell proliferation and migration, while knock down the expression of NOV impaired the tumorigenecity of pancreatic cancer cells in vitro and in vivo. Mechanistically, NOV induced epithelial-mesenchymal transition (EMT) and regulated the expression of multiple EMT marker. Taken together, our study suggested the important role of NOV in pancreatic cancer and NOV might be an important therapeutic target.

引用

页码：3195 / 3201

页数：7

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