Journal
CANCER LETTERS
Volume 296, Issue 1, Pages 113-122Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2010.04.001
Keywords
beta-catenin; Selenium; Apoptosis
Categories
Funding
- National Natural Science Foundation [39925020, 30672361, 30721001]
- National Basic Research Program [2004CB518701]
- State Key Laboratory of Molecular Oncology program, PR China [SKL-2007-03]
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available