Document Detail


GRIM-1, a novel growth suppressor, inhibits rRNA maturation by suppressing small nucleolar RNAs.
MedLine Citation:
PMID:  21931644     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We have recently isolated novel IFN-inducible gene, Gene associated with Retinoid-Interferon-induced Mortality-1 (GRIM-1), using a genetic technique. Moderate ectopic expression of GRIM-1 caused growth inhibition and sensitized cells to retinoic acid (RA)/IFN-induced cell death while high expression caused apoptosis. GRIM-1 depletion, using RNAi, conferred a growth advantage. Three protein isoforms (1α, 1β and 1γ) with identical C-termini are produced from GRIM-1 mRNA. We show that GRIM-1 isoforms interact with NAF1 and DKC1, two essential proteins required for box H/ACA sno/sca RNP biogenesis and suppresses box H/ACA RNA levels in mammalian cells by delocalizing NAF1. Suppression of these small RNAs manifests as inefficient rRNA maturation and growth suppression. Interestingly, yeast Shq1p also caused growth suppression in mammalian cells. Consistent with its growth-suppressive property, GRIM-1 expression is lost in a number of human primary prostate tumors. Our observations support a recent study that GRIM-1 might act as a co-tumor suppressor in the prostate.
Authors:
Shreeram C Nallar; Limei Lin; Varsha Srivastava; Padmaja Gade; Edward R Hofmann; Hafiz Ahmed; Sekhar P Reddy; Dhananjaya V Kalvakolanu
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2011-09-08
Journal Detail:
Title:  PloS one     Volume:  6     ISSN:  1932-6203     ISO Abbreviation:  PLoS ONE     Publication Date:  2011  
Date Detail:
Created Date:  2011-09-20     Completed Date:  2012-03-01     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  101285081     Medline TA:  PLoS One     Country:  United States    
Other Details:
Languages:  eng     Pagination:  e24082     Citation Subset:  IM    
Affiliation:
Department of Microbiology and Immunology, University of Maryland School of Medicine, University of Maryland Marlene and Stewart Greenebaum Cancer Center, Baltimore, Maryland, United States of America.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis / drug effects,  genetics
Apoptosis Regulatory Proteins / genetics*,  metabolism
Cell Cycle Proteins / genetics,  metabolism
Cell Growth Processes / drug effects,  genetics
Cell Line, Tumor
Gene Expression Regulation, Neoplastic*
HeLa Cells
Humans
Immunohistochemistry
Interferon-beta / pharmacology
Male
Neoplasms / genetics,  metabolism,  pathology
Nuclear Proteins / genetics,  metabolism
Prostatic Neoplasms / genetics,  metabolism,  pathology
Protein Binding
Protein Isoforms / genetics,  metabolism
RNA, Ribosomal / genetics*,  metabolism
RNA, Small Nucleolar / genetics*,  metabolism
RNA, Small Untranslated / genetics,  metabolism
Reverse Transcriptase Polymerase Chain Reaction
Ribonucleoproteins / genetics,  metabolism
Saccharomyces cerevisiae Proteins / genetics,  metabolism
Tretinoin / pharmacology
Grant Support
ID/Acronym/Agency:
CA105005/CA/NCI NIH HHS; CA133935-01/CA/NCI NIH HHS; CA78282/CA/NCI NIH HHS; ES11863/ES/NIEHS NIH HHS; HL66109/HL/NHLBI NIH HHS; R01 CA105005-09/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Apoptosis Regulatory Proteins; 0/Cell Cycle Proteins; 0/DKC1 protein, human; 0/NAF1 protein, human; 0/Nuclear Proteins; 0/Protein Isoforms; 0/RNA, Ribosomal; 0/RNA, Small Nucleolar; 0/RNA, Small Untranslated; 0/Ribonucleoproteins; 0/Saccharomyces cerevisiae Proteins; 0/Shq1 protein, S cerevisiae; 302-79-4/Tretinoin; 77238-31-4/Interferon-beta
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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