The detection of EBP50 expression using quantum dot immunohistochemistry in pancreatic cancer tissue and down-regulated EBP50 effect on PC-2 cells

被引:14
作者
Ji, Meng-Yao [1 ]
Fan, Di-kun [2 ]
Lv, Xiao-Guang [1 ]
Peng, Xiu-Lan [1 ]
Lei, Xiao-Fei [1 ]
Dong, Wei-Guo [1 ]
机构
[1] Wuhan Univ, Dept Gastroenterol, Renmin Hosp, Wuhan 430060, Hubei, Peoples R China
[2] Ctr Hosp Nanyang, Dept Cardiac Surg, Nanyang, Henan, Peoples R China
关键词
EBP50; Pancreatic cancer; Carcinogenesis; Proliferation; BETA-CATENIN; COLORECTAL-CANCER; GROWTH-FACTOR; NHERF1/EBP50; STABILIZATION; PROGRESSION; INHIBITION; MANAGEMENT; PROTEINS; COFACTOR;
D O I
10.1007/s10735-012-9424-0
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Ezrin-radixin-moesin-binding phosphoprotein 50 (EBP50) is a putative tumor suppressor that is correlated with many human cancers. However, the function of EBP50 in pancreatic cancer (PC) has not been described. In this paper, the EBP50 expression level in PC tissues was characterized. In vitro, the effects of EBP50 down-regulation by siRNA in PC-2 and MiaPaCa-2 cells were evaluated. In addition, possible mechanisms that mediate the influence of EBP50 were examined. Our results show that the EBP50 expression pattern changes during transformation as there is a loss of the normal apical membrane distribution and an ectopic cytoplasmic over-expression of EBP50; furthermore, the EBP50 expression level is subsequently decreased during malignant progression. Down-regulation of EBP50 promoted cancer cell proliferation, increased the colony-forming ability of cells and accelerated the G1-to-S progression. Additionally, the loss of EBP50 accentuated beta-catenin activity, increased cyclin E and phosphorylated Rb expression, and attenuated p27 expression compared to control cells. Our results suggest that EBP50 may function as a potential tumor suppressor.
引用
收藏
页码:517 / 526
页数:10
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