Abstract |
The TRIM family of genes is largely studied because of their roles in development, differentiation and host cell antiviral defenses; however, roles in cancer biology are emerging. Loss of heterozygosity of the TRIM3 locus in ∼20% of human glioblastomas raised the possibility that this NHL-domain containing member of the TRIM gene family might be a mammalian tumor suppressor. Consistent with this, reducing TRIM3 expression increased the incidence of and accelerated the development of platelet-derived growth factor -induced glioma in mice. Furthermore, TRIM3 can bind to the cdk inhibitor p21(WAF1/CIP1). Thus, we conclude that TRIM3 is a tumor suppressor mapping to chromosome 11p15.5 and that it might block tumor growth by sequestering p21 and preventing it from facilitating the accumulation of cyclin D1-cdk4.
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Authors | Y Liu, R Raheja, N Yeh, D Ciznadija, A M Pedraza, T Ozawa, E Hukkelhoven, H Erdjument-Bromage, P Tempst, N P Gauthier, C Brennan, E C Holland, A Koff |
Journal | Oncogene
(Oncogene)
Vol. 33
Issue 3
Pg. 308-15
(Jan 16 2014)
ISSN: 1476-5594 [Electronic] England |
PMID | 23318451
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
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Chemical References |
- Carrier Proteins
- Cyclin-Dependent Kinase Inhibitor p21
- RNA, Messenger
- TRIM3 protein, human
- TRIM3 protein, mouse
- Tumor Suppressor Proteins
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Topics |
- Animals
- Carrier Proteins
(genetics, metabolism)
- Cell Line
- Cell Line, Transformed
- Cell Line, Tumor
- Cyclin-Dependent Kinase Inhibitor p21
(genetics, metabolism)
- Gene Expression Regulation, Neoplastic
- Glioblastoma
(genetics, metabolism, pathology)
- Humans
- Immunoblotting
- Loss of Heterozygosity
- Mice
- Mice, Knockout
- Mutation
- Protein Binding
- RNA Interference
- RNA, Messenger
(genetics, metabolism)
- Tumor Suppressor Proteins
(genetics, metabolism)
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