Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
Volume 1773, Issue 7, Pages 1028-1038Publisher
ELSEVIER
DOI: 10.1016/j.bbamcr.2007.04.009
Keywords
cyclin D1; C-myc; E-cadherin; LEF-1; cancer; transcription; nucleus; cytoplasm; membrane; reepithelialization
Categories
Funding
- NHLBI NIH HHS [R01 HL047125, HL047125] Funding Source: Medline
- NIAID NIH HHS [R21 AI072291, AI072291, R21 AI072291-01] Funding Source: Medline
- NIEHS NIH HHS [ES013483, R21 ES013483, R21 ES013483-02, R21 ES013483-01] Funding Source: Medline
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beta-Catenin binds to the cytoplasmic region of the type I membrane glycoprotein MUC1. In the current study, we utilized HEK293T cells expressing the full-length MUC1 protein, or a CD8/MUC1 fusion protein containing only the MUC1 cytoplasmic tail, to investigate the effects of beta-catenin binding to MUC1 on downstream beta-catenin-dependent events. Compared with HEK293T cells transfected with empty vector or CD8 alone, expression of the MUC1 cytoplasmic tail inhibited beta-catenin binding to E-cadherin, decreased translocation of beta-catenin into the nucleus, reduced activation of the LEF-1 transcription factor, and blocked expression of the cyclin D1 and c-Myc proteins. Furthermore, expression of MUC1 was associated with decreased cell proliferation, either in the context of the transfected HEK293T cells, or when comparing wild type (Mucl(+/+)) vs. knockout (Mucl(-/-)) mouse primary tracheal epithelial cells. We conclude that MUC1 inhibits cell proliferation through a beta-catenin/ LEF-1/cyclin D1/c-Myc pathway. (C) 2007 Elsevier B.V. All rights reserved.
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