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

Détails

Ressource 1Télécharger: 5_24347041_Postprint.pdf (15739.38 [Ko])
Etat: Public
Version: Author's accepted manuscript
ID Serval
serval:BIB_1FACF08B8A65
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Fragment N2, a caspase-3-generated RasGAP fragment, inhibits breast cancer metastatic progression
Périodique
International Journal of Cancer. Journal International Du Cancer
Auteur⸱e⸱s
Barras D., Lorusso G., Lhermitte B., Viertl D., Rüegg C., Widmann C.
ISSN
1097-0215 (Electronic)
ISSN-L
0020-7136
Statut éditorial
Publié
Date de publication
2014
Peer-reviewed
Oui
Volume
135
Numéro
1
Pages
242-247
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't Publication Status: ppublish
Résumé
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.
Mots-clé
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
Création de la notice
24/01/2014 9:16
Dernière modification de la notice
20/08/2019 12:55
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