Epithelial-Mesenchymal Transition (EMT) Is Not Sufficient for Spontaneous Murine Breast Cancer Metastasis

Yuanmei Lou, Olena Preobrazhenska, Ulrich auf dem Keller, Margaret Sutcliffe, Lorena Barclay, Paul C. McDonald, Calvin Roskelley, Christopher M. Overall, Shoukat Dedhar

Research output: Contribution to journalJournal articleResearchpeer-review

Abstract

Epithelial-mesenchymal transition (EMT) has been linked to metastatic propensity. The 4T1 tumor is a clinically relevant model of spontaneous breast cancer metastasis. Here we characterize 4T1-derived cell lines for EMT, in vitro invasiveness and in vivo metastatic ability. Contrary to expectations, 67NR cells, which form primary tumors but fail to metastasize, express vimentin and N-cadherin, but not E-cadherin. 4T1 cells express E-cadherin and ZO-1, but are migratory, invasive, and metastasize to multiple sites. 66c14 cells form lung metastases and display a mixed phenotype, but are not as migratory or invasive as 67NR cells. These findings demonstrate that the metastatic ability of breast cancer cells does not strictly correlate with genotypic and phenotypic properties of EMT per se, and suggest that other processes may govern metastatic capability. Gene expression analysis of primary tumors did not identify differences in EMT markers, but did reveal candidate genes that may influence metastatic ability. Developmental Dynamics 237:2755-2768, 2008. (C) 2008 Wiley-Liss, Inc.
Original languageEnglish
JournalDevelopmental Dynamics
Volume237
Issue number10
Pages (from-to)2755-2768
ISSN1058-8388
DOIs
Publication statusPublished - 2008
Externally publishedYes

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