期刊
CANCER CELL
卷 29, 期 5, 页码 697-710出版社
CELL PRESS
DOI: 10.1016/j.ccell.2016.03.003
关键词
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资金
- NIH [R01-CA175336, F32-CA189659, T32CA09302, R01-CA157510]
- American Lung Association Biomedical Research Grant
- Stanford Cancer Institute support grant [NIH P30-CA124435]
- Stanford Dean's Fellowship
- American Lung Association Fellowship
- Stanford Biomedical Informatics Training Grant from the National Library of Medicine [LM-07033]
- Bio-X Stanford Interdisciplinary Graduate Fellowship
- Stanford Graduate Fellowship
- National Science Foundation Predoctoral fellowship
- Alfred Sloan Fellowship
- Deutsche Forschungsgemeinschaft [HA 2263/2]
- Koln Fortune Program of the Medical Faculty of the University of Cologne
The ability of cancer cells to establish lethal metastatic lesions requires the survival and expansion of single cancer cells at distant sites. The factors controlling the clonal growth ability of individual cancer cells remain poorly understood. Here, we show that high expression of the transcription factor ARNTL2 predicts poor lung adenocarcinoma patient outcome. Arntl2 is required for metastatic ability in vivo and clonal growth in cell culture. Arntl2 drives metastatic self-sufficiency by orchestrating the expression of a complex pro-metastatic secretome. We identify Clock as an Arntl2 partner and functionally validate the matricellular protein Smoc2 as a pro-metastatic secreted factor. These findings shed light on the molecular mechanisms that enable single cancer cells to form allochthonous tumors in foreign tissue environments.
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