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

Details

Serval ID
serval:BIB_63011E6A354B
Type
Article: article from journal or magazin.
Collection
Publications
Title
SQSTM1 is a pathogenic target of 5q copy number gains in kidney cancer.
Journal
Cancer cell
Author(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
Publication state
Published
Issued date
09/12/2013
Peer-reviewed
Oui
Volume
24
Number
6
Pages
738-750
Language
english
Notes
Publication types: Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Abstract
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.
Keywords
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
Yes
Create date
06/07/2018 11:02
Last modification date
20/08/2019 14:19
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