BTG3 upregulation induces cell apoptosis and suppresses invasion in esophageal adenocarcinoma

被引：26

作者：

Du, Yuwen ^{[1
]}

Liu, Pingping ^{[1
]}

Zang, Wenqiao ^{[1
]}

Wang, Yuanyuan ^{[1
]}

Chen, Xiaonan ^{[1
]}

Li, Min ^{[1
]}

Zhao, Guoqiang ^{[1
]}

机构：

[1] Zhengzhou Univ, Coll Basic Med Sci, Zhengzhou 450001, Peoples R China

来源：

MOLECULAR AND CELLULAR BIOCHEMISTRY | 2015年 / 404卷 / 1-2期

关键词：

Esophageal adenocarcinoma; BTG3; Proliferation; Migration; DOWN-REGULATION; LUNG-CANCER; EARLY EVENT; TUMOR; CARCINOMA; SURVIVAL; PROTEIN; TOB; PHOSPHORYLATION; CARCINOGENESIS;

D O I：

10.1007/s11010-015-2363-9

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

B cell translocation gene 3 (BTG3) is a tumor suppressor by inhibiting cell proliferation, migration, and regulating cell cycle progression in several tumors. However, its role in esophageal adenocarcinoma (EAC) remains unknown. Here, we detected the expression of BTG3 in EAC tissues and subsequent progression. BTG3 expression was significant decreased in EAC tissues and cell lines detected by real-time RT-PCR and Western blot. Relationships of BTG3 with EAC clinicopathology were analyzed statistically. The decrease expression of BTG3 is associated with lymph node metastases. In vitro assay demonstrated that overexpression of BTG3 significantly suppressed colony formation and proliferation of EAC cells. The suppressed migration and invasion abilities found in BTG3-overexpressing EAC cells. Our findings suggested that BTG3 is suppressor in the progression of EAC.

引用

页码：31 / 38

页数：8

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