Document Detail


An alternative pathway for expression of p56lck from type I promoter transcripts in colon carcinoma.
MedLine Citation:
PMID:  9416836     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The lymphoid-specific protein tyrosine kinase, p56lck which is essential for both T cell development and function, is aberrantly expressed in colon and small lung carcinoma lines. In this paper, we demonstrate p56lck is also expressed in colon tumour biopsies due predominantly or exclusively to the use of the lck type I promoter. In T leukaemia lines, the lck type I promoter requires binding sites for both Ets- and Myb-related transcription factors. In contrast, in colon tumour lines the activation of the lck type I promoter requires the Ets but not the Myb binding site. In these lines, a consensus binding site for HMG-related transcription factors, AACAAAG, is required for efficient lck type I promoter activity. Sox-4 is a candidate transcription factor for binding and activating the lck type l promoter in colon carcinoma cells. Co-expression of Ets-1 and Sox-4, but neither protein alone, was sufficient to activate the lck type l promoter in HeLa cells which do not normally express lck transcripts. These results suggest that aberrant expression of p56lck from the lck type l promoter in colon carcinoma arises from transcriptional activation mediated by Ets- and HMG-related transcription factors.
Authors:
S McCracken; C S Kim; Y Xu; M Minden; N G Miyamoto
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Oncogene     Volume:  15     ISSN:  0950-9232     ISO Abbreviation:  Oncogene     Publication Date:  1997 Dec 
Date Detail:
Created Date:  1998-01-15     Completed Date:  1998-01-15     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8711562     Medline TA:  Oncogene     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  2929-37     Citation Subset:  IM    
Affiliation:
The AMGEN Research Institute/Princess Margaret Hospital, Toronto, Ontario, Canada.
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MeSH Terms
Descriptor/Qualifier:
Alternative Splicing*
Animals
Binding Sites / genetics
Carcinoma / enzymology,  genetics
Colonic Neoplasms / enzymology*,  genetics*
Drug Synergism
Hela Cells
High Mobility Group Proteins / genetics,  physiology
Humans
Jurkat Cells
Lymphocyte Specific Protein Tyrosine Kinase p56(lck) / biosynthesis,  genetics*
Mice
Mice, SCID
Neoplasms, Multiple Primary / enzymology,  genetics
Promoter Regions, Genetic*
Proto-Oncogene Protein c-ets-1
Proto-Oncogene Proteins / physiology
Proto-Oncogene Proteins c-ets
Regulatory Sequences, Nucleic Acid
SOXC Transcription Factors
Trans-Activators / physiology
Transcription Factors / physiology
Transcription, Genetic*
Tumor Cells, Cultured
Chemical
Reg. No./Substance:
0/ETS1 protein, human; 0/Ets1 protein, mouse; 0/High Mobility Group Proteins; 0/Proto-Oncogene Protein c-ets-1; 0/Proto-Oncogene Proteins; 0/Proto-Oncogene Proteins c-ets; 0/SOX4 protein, human; 0/SOXC Transcription Factors; 0/Sox4 protein, mouse; 0/Trans-Activators; 0/Transcription Factors; EC 2.7.10.2/Lymphocyte Specific Protein Tyrosine Kinase p56(lck)

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


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