Document Detail


Molecular cloning of TA16, a transcriptional repressor that may mediate glucocorticoid-induced growth arrest of leiomyosarcoma cells.
MedLine Citation:
PMID:  9259324     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The DDT1 MF2 smooth muscle tumor cell line was derived from an estrogen/androgen-induced leiomyosarcoma that arose in the ductus deferens of a Syrian hamster. The growth of this cell line is arrested at the G0/G1 phase of the cell cycle after treatment with glucocorticoids. To identify the putative gene(s) that are potentially involved in this hormone-induced cell growth arrest, we have used a differential screening technique to clone those genes whose expression is induced or up-regulated by glucocorticoids. A number of glucocorticoid response genes were thereby isolated from the leiomyosarcoma cells. One of these clones, termed TA16, was found to be markedly up-regulated by glucocorticoids in DDT1 MF2 cells, but only marginally changed in GR1 cells, a glucocorticoid-resistant variant that was selected from the wild type DDT1 MF2 cell. Isolation and sequencing of its intact cDNA indicated that the TA16 encodes a protein 485 amino acids long, and its sequence is closely homologous to a novel transcriptional repressor that presumably represses the transcription activity of some zinc finger transcriptional factors through a direct interaction. Transfection assays demonstrated that introduction of an antisense TA16 cDNA expression vector, controlled by an MMTV promoter, into the DDT1 MF2 cell significantly relieved the glucocorticoid-induced cell growth arrest. This finding suggests that TA16 might participate in the mediation of glucocorticoid-induced cell cycle arrest in leiomyosarcoma cells.
Authors:
W Fan; J X Ma; L Cheng; J S Norris
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Molecular endocrinology (Baltimore, Md.)     Volume:  11     ISSN:  0888-8809     ISO Abbreviation:  Mol. Endocrinol.     Publication Date:  1997 Aug 
Date Detail:
Created Date:  1997-10-06     Completed Date:  1997-10-06     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8801431     Medline TA:  Mol Endocrinol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1342-52     Citation Subset:  IM    
Affiliation:
Department of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston 29425, USA.
Data Bank Information
Bank Name/Acc. No.:
GENBANK/U17253;  U47007;  U47008;  U88975
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MeSH Terms
Descriptor/Qualifier:
Amino Acid Sequence
Animals
Base Sequence
Cell Division / drug effects,  genetics
Cloning, Molecular
Cricetinae
Drug Resistance, Neoplasm / genetics
Gene Expression Regulation, Neoplastic / drug effects
Glucocorticoids / pharmacology*
Humans
Leiomyosarcoma / drug therapy,  genetics*
Mice
Molecular Sequence Data
Oligonucleotides, Antisense
Polymerase Chain Reaction / methods
RNA, Messenger / genetics
Rats
Repressor Proteins / genetics*,  metabolism
Sequence Analysis, DNA
Sequence Homology, Amino Acid
Signal Transduction
Transcription Factors*
Transfection
Tumor Cells, Cultured
Grant Support
ID/Acronym/Agency:
CA-58846/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Glucocorticoids; 0/NAB1 protein, human; 0/Nab1 protein, mouse; 0/Nab1 protein, rat; 0/Oligonucleotides, Antisense; 0/RNA, Messenger; 0/Repressor Proteins; 0/TA16 protein, Mesocricetus auratus; 0/Transcription Factors

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


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