The transcriptional repressor Snail promotes mammary tumor recurrence

Breast cancer recurrence is a fundamental clinical manifestation of tumor progression and represents the principal cause of death from this disease. Using a conditional transgenic mouse model for the recurrence of HER2/neu-induced mammary tumors, we demonstrate that the transcriptional repressor Sna...

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Bibliographic Details
Published in:	Cancer cell Vol. 8; no. 3; pp. 197 - 209
Main Authors:	Moody, Susan E., Perez, Denise, Pan, Tien-chi, Sarkisian, Christopher J., Portocarrero, Carla P., Sterner, Christopher J., Notorfrancesco, Kathleen L., Cardiff, Robert D., Chodosh, Lewis A.
Format:	Journal Article
Language:	English
Published:	United States Elsevier Inc 01-09-2005
Subjects:	Animals Breast Neoplasms - genetics Epithelial Cells - pathology Female Gene Expression Regulation, Neoplastic Humans Mammary Neoplasms, Experimental - genetics Mammary Neoplasms, Experimental - pathology Mesoderm - pathology Mice Mice, Transgenic Neoplasm Recurrence, Local - genetics Neoplasm Recurrence, Local - pathology Receptor, ErbB-2 - genetics Snail Family Transcription Factors Transcription Factors - genetics Transcription Factors - metabolism
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Summary:	Breast cancer recurrence is a fundamental clinical manifestation of tumor progression and represents the principal cause of death from this disease. Using a conditional transgenic mouse model for the recurrence of HER2/neu-induced mammary tumors, we demonstrate that the transcriptional repressor Snail is spontaneously upregulated in recurrent tumors in vivo and that recurrence is accompanied by epithelial-to-mesenchymal transition (EMT). Consistent with a causal role for Snail in these processes, we show that Snail is sufficient to induce EMT in primary tumor cells, that Snail is sufficient to promote mammary tumor recurrence in vivo, and that high levels of Snail predict decreased relapse-free survival in women with breast cancer. In aggregate, our observations strongly implicate Snail in the process of breast cancer recurrence.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	1535-6108 1878-3686
DOI:	10.1016/j.ccr.2005.07.009