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

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 β-catenin protein levels, while there was no significant change observed on transcriptional levels. Moreover, we found MSA accelerated the degradation of β-catenin and activated glycogen synthase kinase 3β (GSK-3β). Some targets of β-catenin/TCF pathway and apoptosis-related genes altered after MSA treatment. Notably, utilizing the inducible 293-TR/β-catenin cell line, we found the apoptotic phenotypes induced by MSA were partially reversed by the overexpression of β-catenin. Overall, our data indicate the effects induced by MSA in ESCC cells may act on the inhibition of β-catenin/TCF pathway.