Journal
CANCER CELL
Volume 15, Issue 5, Pages 416-428Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2009.03.016
Keywords
-
Categories
Funding
- ACS [IRG-110376]
- Susan G. Komen Foundation [KGO81310]
- NCI [RO1-CA125454]
- NIH [R01 CA104748, R01 DK48498, T32CA117834]
Ask authors/readers for more resources
The increased motility and invasiveness of tumor cells are reminiscent of epithelial-mesenchymal transition (EMT), which occurs during embryonic development, wound healing, and metastasis. In this study, we found that Snail is stabilized by the inflammatory cytokine TNF alpha through the activation of the NF-kappa B pathway. We demonstrated that NF-kappa B is required for the induction of COP9 signalosome 2 (CSN2), which, in turn, blocks the ubiquitination and degradation of Snail. Furthermore, we showed that the expression of Snail correlated with the activation of NF-kappa B in cancer cell lines and metastatic tumor samples. Knockdown of Snail expression inhibited cell migration and invasion induced by inflammatory cytokines and suppressed inflammation-mediated breast cancer metastasis. Our study provides a plausible mechanism for inflammation-induced metastasis.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available