JDP2 inhibits the epithelial-to-mesenchymal transition in pancreatic cancer BxPC3 cells

被引:12
|
作者
Liu, Zhe [1 ]
Du, Ruixia [2 ]
Long, Jin [1 ]
Dong, Anbing [1 ]
Fan, Jianpeng [1 ]
Guo, Kejian [1 ]
Xu, Yuanhong [1 ]
机构
[1] China Med Univ, Hosp 1, Dept Pancreat Gastroenterol Surg, Shenyang 110001, Peoples R China
[2] Shenyang Med Univ, Fengtian Hosp, Dept Otorhinolaryngol, Shenyang, Peoples R China
关键词
Epithelial-to-mesenchymal; JDP2; Pancreatic cancer; TGF-beta; 1; EGF; JUN DIMERIZATION PROTEIN-2; ACTIVATING TRANSCRIPTION FACTOR-2; AP-1 REPRESSOR PROTEIN; DOWN-REGULATION; METASTASIS; EXPRESSION; ANGIOGENESIS; PROGRESSION; INDUCTION; CARCINOMA;
D O I
10.1007/s13277-012-0404-5
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Pancreatic carcinoma is one of the most malignant and aggressive cancers. Increased motility and invasiveness of pancreatic cancer cells are believed to be associated with epithelial-to-mesenchymal transition (EMT). However, the molecular basis of EMT in pancreatic cancer cells is poorly understood. In this study, we examined the relationship between Jun dimerization protein 2 (JDP2), which is an AP-1 inhibitor, and EMT in human pancreatic carcinoma cells. We demonstrated that transforming growth factor-beta 1 (TGF-beta 1) promoted epidermal growth factor (EGF)-induced EMT in co-treated human pancreatic BxPC3 cells and that JDP2 overexpression reversed the EMT that was induced by co-treatment with TGF-beta 1 and EGF. These results suggest that EGF plays a principal role in EMT through its association with TGF-beta 1 in human pancreatic BxPC3 cells and that JDP2 may be a molecular target for pancreatic carcinoma intervention.
引用
收藏
页码:1527 / 1534
页数:8
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