Gene expression and pathway analysis of CTNNB1 in cancer and stem cells
Gene expression and pathway analysis of CTNNB1 in cancer and stem cells作者机构:Division of Risk Assessment National Institute of Health Sciences Laboratory of Protein Informatics Institute for Protein Research Osaka University Department of Translational Oncology National Cancer Center Research Institute Department of Pathology Kobe University of Graduate School of Medicine
出 版 物:《World Journal of Stem Cells》 (世界干细胞杂志(英文版)(电子版))
年 卷 期:2016年第8卷第11期
页 面:384-395页
核心收录:
学科分类:1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学]
基 金:Japan Society for the Promotion of Science, JSPS, (26460418) Japan Society for the Promotion of Science, JSPS
主 题:β-catenin CTNNB1 Epithelial-mesenchymal transition Mesenchymal stem cell Stem cell
摘 要:AIM To investigate β-catenin(CTNNB1) signaling in cancer and stem cells, the gene expression and pathway were analyzed using *** The expression of the catenin β 1(CTNNB1) gene, which codes for β-catenin, was analyzed in mesenchymal stem cells(MSCs) and gastric cancer(GC) cells. Beta-catenin signaling and the mutation of related proteins were also analyzed using the cB ioP ortal for Cancer Genomics and HOMology modeling of Complex Structure(HOMCOS) *** The expression of the CTNNB1 gene was up-regulated in GC cells compared to MSCs. The expression of EPH receptor A8(EPHA8), synovial sarcoma translocation chromosome 18(SS18), interactor of little elongation complex ELL subunit 1(ICE1), patched 1(PTCH1), mutS homolog 3(MSH3) and caspase recruitment domain family member 11(CARD11) were also shown to be altered in GC cells in the cB ioP ortal for Cancer Genomics analysis. 3D complex structures were reported for E-cadherin 1(CDH1), lymphoid enhancer binding factor 1(LEF1), transcription factor 7 like 2(TCF7L2) and adenomatous polyposis coli protein(APC) with β-catenin. CONCLUSION The results indicate that the epithelial-mesenchymal transition(EMT)-related gene CTNNB1 plays an important role in the regulation of stem cell pluripotency and cancer signaling.