Fragment N2, a caspase-3-generated RasGAP fragment, inhibits breast cancer metastatic progression

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State: Public
Version: Author's accepted manuscript
Serval ID
serval:BIB_1FACF08B8A65
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Fragment N2, a caspase-3-generated RasGAP fragment, inhibits breast cancer metastatic progression
Journal
International Journal of Cancer. Journal International Du Cancer
Author(s)
Barras D., Lorusso G., Lhermitte B., Viertl D., Rüegg C., Widmann C.
ISSN
1097-0215 (Electronic)
ISSN-L
0020-7136
Publication state
Published
Issued date
2014
Peer-reviewed
Oui
Volume
135
Number
1
Pages
242-247
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't Publication Status: ppublish
Abstract
The p120 RasGAP protein negatively regulates Ras via its GAP domain. RasGAP carries several other domains that modulate several signaling molecules such as Rho. RasGAP is also a caspase-3 substrate. One of the caspase-3-generated RasGAP fragments, corresponding to amino acids 158-455 and called fragment N2, was previously reported to specifically sensitize cancer cells to death induced by various anticancer agents. Here, we show that fragment N2 inhibits migration in vitro and that it impairs metastatic progression of breast cancer to the lung. Hence, stress-activated caspase-3 might contribute to the suppression of metastasis through the generation of fragment N2. These results indicate that the activity borne by fragment N2 has a potential therapeutic relevance to counteract the metastatic process.
Keywords
Apoptosis/genetics, Breast Neoplasms, Caspase 3/chemistry, Caspase 3/genetics, Cell Line, Tumor, Cell Movement/genetics, Disease Progression, Female, Gene Expression Regulation, Neoplastic, Humans, Neoplasm Metastasis/genetics, Peptide Fragments/chemistry, Peptide Fragments/genetics, Transfection, ras GTPase-Activating Proteins/genetics
Pubmed
Web of science
Create date
24/01/2014 9:16
Last modification date
20/08/2019 12:55
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