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Biochem Biophys Res Commun. 2007 Oct 26;362(3):740-6. Epub 2007 Aug 24.

Down-regulation of MUC1 in cancer cells inhibits cell migration by promoting E-cadherin/catenin complex formation.

Author information

1
Department of Surgery, Rhode Island Hospital, Brown University, 2 Dudley Street, Suite 470, Providence, RI 02905, USA.

Abstract

MUC1, a tumor associated glycoprotein, is over-expressed in most cancers and can promote proliferation and metastasis. The objective of this research was to study the role of MUC1 in cancer metastasis and its potential mechanism. Pancreatic (PANC1) and breast (MCF-7) cancer cells with stable 'knockdown' of MUC1 expression were created using RNA interference. beta-Catenin and E-cadherin protein expression were upregulated in PANC1 and MCF-7 cells with decreased MUC1 expression. Downregulation of MUC1 expression also induced beta-catenin relocation from the nucleus to the cytoplasm, increased E-cadherin/beta-catenin complex formation and E-cadherin membrane localization in PANC1 cells. PANC1 cells with 'knockdown' MUC1 expression had decreased in vitro cell invasion. This study suggested that MUC1 may affect cancer cell migration by increasing E-cadherin/beta-catenin complex formation and restoring E-cadherin membrane localization.

PMID:
17764657
DOI:
10.1016/j.bbrc.2007.08.074
[Indexed for MEDLINE]

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