c-Fos/ERK promotes the progression from pancreatic intraepithelial neoplasia to pancreatic ductal adenocarcinoma

被引：17
|
作者：
You, Lei
Ren, Xiaoxia
Du, Yongxing
Zhao, Wenjing
Cui, Ming
Chen, Ge [1 ,2 ]
Zhao, Yupei [1 ,2 ]
机构：
[1] Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Gen Surg, 1 Shuai Fu Yuan, Beijing 100730, Peoples R China
[2] Peking Union Med Coll, 1 Shuai Fu Yuan, Beijing 100730, Peoples R China
来源：
ONCOLOGY REPORTS | 2016年 / 36卷 / 06期
关键词：
C-Fos; pancreatic intraepithelial neoplasia; pancreatic ductal adenocarcinoma; Pdx-cre; Kras(G12D) mice; ENGINEERED MOUSE MODELS; CANCER; AP-1; APOPTOSIS; PATHWAYS; ERK1/2; CELLS; MAPK; KRAS;
D O I：
10.3892/or.2016.5169
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Pathogenesis of pancreatic ductal adenocarcinoma (PDAC) is thought to develop through the progression of precursor lesions, known as pancreatic intraepithelial neoplasias (PanIN). In the present study, we showed that c-Fos promoted proliferation, cell cycle and migration in pancreatic cancer cells. Caerulein was used to accelerate the pathogenesis of Pdx-cre; Kras(G12D) mice. During PanIN formation and development of PDAC, the expression of ERK and c-Fos increased concomitantly. When ERK activity was inhibited by U0126, the expression of c-Fos also decreased. Inactivation of ERK/c-Fos suppressed pancreatic lesions concurrently through proliferation, inflammation and apoptosis. Our findings suggest that the ERK/c-Fos pathway is required for PDAC initiation and progression.
引用
收藏
页码：3413 / 3420
页数：8
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