期刊
ONCOGENE
卷 35, 期 33, 页码 4302-4311出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2015.497
关键词
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资金
- National Institutes of Health (NIH) grant [R01 5R01-CA127727]
- American Cancer Society Post-doctoral Fellowship [PF-11-036-01-DDC]
- NIH T32 Training Grant [5T32CA009111]
- NIH NRSA postdoctoral fellowship [F32-CA165482]
- NIH NRSA Fellowship [1F32CA142095]
- Duke Cancer Institute
- Department of Orthopedics
- Genitourinary Oncology Laboratory
The cascade that culminates in macrometastases is thought to be mediated by phenotypic plasticity, including epithelial-mesenchymal and mesenchymal-epithelial transitions (EMT and MET). Although there is substantial support for the role of EMT in driving cancer cell invasion and dissemination, much less is known about the importance of MET in the later steps of metastatic colonization. We created novel reporters, which integrate transcriptional and post-transcriptional regulation, to test whether MET is required for metastasis in multiple in vivo cancer models. In a model of carcinosarcoma, metastasis occurred via an MET-dependent pathway; however, in two prostate carcinoma models, metastatic colonization was MET independent. Our results provide evidence for both MET-dependent and MET-independent metastatic pathways.
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