SQSTM1 is a pathogenic target of 5q copy number gains in kidney cancer.

Détails

ID Serval
serval:BIB_63011E6A354B
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
SQSTM1 is a pathogenic target of 5q copy number gains in kidney cancer.
Périodique
Cancer cell
Auteur(s)
Li L., Shen C., Nakamura E., Ando K., Signoretti S., Beroukhim R., Cowley G.S., Lizotte P., Liberzon E., Bair S., Root D.E., Tamayo P., Tsherniak A., Cheng S.C., Tabak B., Jacobsen A., Hakimi A.A., Schultz N., Ciriello G., Sander C., Hsieh J.J., Kaelin W.G.
ISSN
1878-3686 (Electronic)
ISSN-L
1535-6108
Statut éditorial
Publié
Date de publication
09/12/2013
Peer-reviewed
Oui
Volume
24
Numéro
6
Pages
738-750
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
Clear cell renal cell carcinoma (ccRCC) is the most common form of kidney cancer and is often linked to loss of chromosome 3p, which harbors the VHL tumor suppressor gene, loss of chromosome 14q, which includes HIF1A, and gain of chromosome 5q. The relevant target(s) on chromosome 5q is not known. Here, we show that 5q amplification leads to overexpression of the SQSTM1 oncogene in ccRCC lines and tumors. Overexpression of SQSTM1 in ccRCC lines promoted resistance to redox stress and increased soft agar growth, while downregulation of SQSTM1 decreased resistance to redox stress, impaired cellular fitness, and decreased tumor formation. Therefore, the selection pressure to amplify 5q in ccRCC is driven, at least partly, by SQSTM1.
Mots-clé
Adaptor Proteins, Signal Transducing/genetics, Adaptor Proteins, Signal Transducing/physiology, Animals, Base Sequence, Carcinoma, Renal Cell/genetics, Cell Line, Tumor, Chromosomes, Human, Pair 5, Gene Dosage, Humans, Kidney Neoplasms/genetics, Mice, Molecular Sequence Data, NF-E2-Related Factor 2/analysis, NF-E2-Related Factor 2/physiology, Sequestosome-1 Protein
Pubmed
Web of science
Open Access
Oui
Création de la notice
06/07/2018 11:02
Dernière modification de la notice
20/08/2019 14:19
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