title: beta-Catenin/TCF pathway plays a vital role in selenium induced-growth inhibition and apoptosis in esophageal squamous cell carcinoma (ESCC) cells.
abstract: 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 beta-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 3beta (GSK-3beta). 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.
authors.affiliation: Laboratory of Cell and Molecular Biology & State Key Laboratory of Molecular Oncology, Cancer Institute & Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, PR China.
authors.forename: Wei
authors.initials: W
authors.lastname: Zhang
authors.forename: Shuang
authors.initials: S
authors.lastname: Yan
authors.forename: Mei
authors.initials: M
authors.lastname: Liu
authors.forename: Guo
authors.initials: G
authors.lastname: Zhang
authors.forename: Shangbin
authors.initials: S
authors.lastname: Yang
authors.forename: Shun
authors.initials: S
authors.lastname: He
authors.forename: Jinfeng
authors.initials: J
authors.lastname: Bai
authors.forename: Lanping
authors.initials: L
authors.lastname: Quan
authors.forename: Hongxia
authors.initials: H
authors.lastname: Zhu
authors.forename: Yan
authors.initials: Y
authors.lastname: Dong
authors.forename: Ningzhi
authors.initials: N
authors.lastname: Xu
mesh_terms: D017304:Annexin A5 / Q000235:genetics; D017209:Apoptosis / Q000187:drug effects*; D002455:Cell Division / Q000187:drug effects*; D045744:Cell Line, Tumor; D003114:Colony-Forming Units Assay; D017931:DNA Primers; D004938:Esophageal Neoplasms / Q000473:pathology*; D006801:Humans; D051034:Inhibitor of Apoptosis Proteins; D008869:Microtubule-Associated Proteins / Q000235:genetics; D018307:Neoplasms, Squamous Cell / Q000473:pathology*; D016566:Organoselenium Compounds / Q000494:pharmacology; D016133:Polymerase Chain Reaction; D016755:Proto-Oncogene Proteins c-jun / Q000235:genetics; D016271:Proto-Oncogene Proteins c-myc / Q000235:genetics; D012643:Selenium / Q000494:pharmacology*; D000077022:Survivin; D051822:T Cell Transcription Factor 1 / Q000187:drug effects / Q000235:genetics / Q000502:physiology*; D051176:beta Catenin / Q000187:drug effects / Q000235:genetics / Q000502:physiology*
chemical_list: D017304:Annexin A5; C107489:BIRC5 protein, human; D017931:DNA Primers; D051034:Inhibitor of Apoptosis Proteins; D008869:Microtubule-Associated Proteins; D016566:Organoselenium Compounds; D016755:Proto-Oncogene Proteins c-jun; D016271:Proto-Oncogene Proteins c-myc; D000077022:Survivin; D051822:T Cell Transcription Factor 1; D051176:beta Catenin; C008493:methylselenic acid; D012643:Selenium