Studies on 17-1A antigen gene regulation in nonexpressing A549 and A431 cells, as compared to expressing pancreatic carcinoma (Capan 2) cells, reveal a complex mechanism of repression of this gene.

Abstract	Elements controlling high expression of the 17-1A antigen gene in pancreatic carcinoma cells (Capan 2) reside within the two regions: proximal (-193 to +3) and distal (-877 to -518). We demonstrate here that some factors present in nuclear extracts from nonexpressing cells bind specifically to the control elements, important for gene expression. Our results suggest that nonexpressing cells may either lack at least one of the factors necessary for activation or may contain their modified forms. A major difference between expressing and nonexpressing cells was found in the region containing core enhancer sequence. Moreover, nonexpressing cells display a complex pattern of DNA-protein interactions in this region, suggesting that these cells contain factors acting negatively mainly on the enhancer sequence. Our results however, indicate that the mechanism of repression is much more complicated than expected.
Authors	B Siemieniako, E Wiland, W H Trzeciak
Journal	Cell biology international (Cell Biol Int) Vol. 18 Issue 11 Pg. 1009-17 (Nov 1994) ISSN: 1065-6995 [Print] England
PMID	7894386 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
Chemical References	Antigens, Neoplasm DNA, Neoplasm DNA-Binding Proteins Neoplasm Proteins RNA, Messenger RNA, Neoplasm carcinoma-associated antigen 17-1A
Topics	Antigens, Neoplasm (biosynthesis, genetics) Base Sequence Carcinoma (genetics, pathology) Carcinoma, Squamous Cell (genetics, pathology) DNA, Neoplasm (genetics) DNA-Binding Proteins (metabolism) Enhancer Elements, Genetic Gene Expression Regulation, Neoplastic HeLa Cells (metabolism) Humans Lung Neoplasms (genetics, pathology) Molecular Sequence Data Neoplasm Proteins (biosynthesis, genetics, metabolism) Pancreatic Neoplasms (genetics, pathology) Promoter Regions, Genetic RNA, Messenger (biosynthesis) RNA, Neoplasm (biosynthesis) Transcription, Genetic Tumor Cells, Cultured (metabolism)

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