TY - JOUR
T1 - Epithelial-Mesenchymal Transition (EMT) Is Not Sufficient for Spontaneous Murine Breast Cancer Metastasis
AU - Lou, Yuanmei
AU - Preobrazhenska, Olena
AU - auf dem Keller, Ulrich
AU - Sutcliffe, Margaret
AU - Barclay, Lorena
AU - McDonald, Paul C.
AU - Roskelley, Calvin
AU - Overall, Christopher M.
AU - Dedhar, Shoukat
PY - 2008
Y1 - 2008
N2 - 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.
AB - 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.
U2 - 10.1002/dvdy.21658
DO - 10.1002/dvdy.21658
M3 - Journal article
SN - 1058-8388
VL - 237
SP - 2755
EP - 2768
JO - Developmental Dynamics
JF - Developmental Dynamics
IS - 10
ER -