β-Catenin/TCF pathway plays a vital role in selenium induced-growth inhibition and apoptosis in esophageal squamous cell carcinoma (ESCC) cells

被引:30
作者
Zhang, Wei [1 ,2 ,3 ,4 ]
Yan, Shuang [1 ,2 ,3 ,4 ]
Liu, Mei [1 ,2 ,3 ,4 ]
Zhang, Guo [1 ,2 ,3 ,4 ]
Yang, Shangbin [1 ,2 ,3 ,4 ]
He, Shun [1 ,2 ,3 ,4 ]
Bai, Jinfeng [1 ,2 ,3 ,4 ]
Quan, Lanping [1 ,2 ,3 ,4 ]
Zhu, Hongxia [1 ,2 ,3 ,4 ]
Dong, Yan [5 ]
Xu, Ningzhi [1 ,2 ,3 ,4 ]
机构
[1] Chinese Acad Med Sci, Lab Cell & Mol Biol, Beijing 100021, Peoples R China
[2] Chinese Acad Med Sci, State Key Lab Mol Oncol, Inst Canc, Beijing 100021, Peoples R China
[3] Chinese Acad Med Sci, Canc Hosp, Beijing 100021, Peoples R China
[4] Peking Union Med Coll, Beijing 100021, Peoples R China
[5] Tulane Univ, Sch Med, Dept Struct & Cellular Biol, New Orleans, LA 70112 USA
关键词
beta-catenin; Selenium; Apoptosis; PROSTATE-CANCER CELLS; BREAST-CANCER; ANDROGEN RECEPTOR; METHYLSELENINIC ACID; COLORECTAL ADENOMAS; TOENAIL SELENIUM; GENE-EXPRESSION; DOWN-REGULATION; PREVENTION; RISK;
D O I
10.1016/j.canlet.2010.04.001
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Epidemiological and experimental studies have indicated selenium could reduce the risk of some cancers. In our present study, growth inhibition and apoptosis were detected upon methylseleninic acid (MSA) treatment in human esophageal squamous cell carcinoma cell lines EC9706 and KYSE150. MSA reduced p-catenin protein levels, while there was no significant change observed on transcriptional levels. Moreover, we found MSA accelerated the degradation of beta-catenin and activated glycogen synthase kinase 3 beta (GSK-3 beta). Some targets of beta-catenin/TCF pathway and apoptosis-related genes altered after MSA treatment. Notably, utilizing the inducible 293-TR/beta-catenin cell line, we found the apoptotic phenotypes induced by MSA were partially reversed by the overexpression of beta-catenin. Overall, our data indicate the effects induced by MSA in ESCC cells may act on the inhibition of beta-catenin/TCF pathway. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:113 / 122
页数:10
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