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

来源：

TUMOR BIOLOGY | 2012年 / 33卷 / 05期

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

页码：1527 / 1534

页数：8

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