Journal
DEVELOPMENTAL CELL
Volume 45, Issue 6, Pages 681-+Publisher
CELL PRESS
DOI: 10.1016/j.devcel.2018.05.027
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Funding
- NIH [R01-CA169123, F31-CA177163-01A1, R35-CA210263, K12-CA076931, K08-DK109292]
- American Cancer Society
- Penn Center for Molecular Studies in Digestive and Liver Diseases from the National Institute of Diabetes and Digestive and Kidney Diseases [P30-DK050306]
- Genome Technology Center and Cancer Center at the Laura and Isaac Perlmutter Cancer Center at NYU [P30-CA016087]
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Epithelial-mesenchymal transition (EMT) is strongly implicated in tumor cell invasion and metastasis. EMT is thought to be regulated primarily at the transcriptional level through the repressive activity of EMT transcription factors. However, these classical mechanisms have been parsed out almost exclusively in vitro, leaving questions about the programs driving EMT in physiological contexts. Here, using a lineage-labeled mouse model of pancreatic ductal adenocarcinoma to study EMT in vivo, we found that most tumors lose their epithelial phenotype through an alternative program involving protein internalization rather than transcriptional repression, resulting in a partial EMT'' phenotype. Carcinoma cells utilizing this program migrate as clusters, contrasting with the single-cell migration pattern associated with traditionally defined EMT mechanisms. Moreover, many breast and colorectal cancer cell lines utilize this alternative program to undergo EMT. Collectively, these results suggest that carcinoma cells have different ways of losing their epithelial program, resulting in distinct modes of invasion and dissemination.
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