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PMID: 1633879 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Loss of transcriptional repression contributes to the ectopic expression of the calcitonin/alpha-CGRP gene in a human lung carcinoma cell line.

FEBS letters ·Vol. 306 ·No. 2-3 ·1992-07-20 ·Pages 229-33

Symes AJ, Craig RK, Brickell PM

Abstract

The calcitonin/alpha-CGRP (CT/CGRP) gene is ectopically expressed in a wide variety of neoplasia. We have investigated the molecular mechanisms responsible for this ectopic expression in the human cell line BEN, which is derived from a poorly differentiated squamous cell lung carcinoma. We show that a trans-acting factor which represses expression of the CT/CGRP gene in HeLa cells is absent or inactive in BEN cells, and have localised the repressor binding site to a 53 bp fragment 1500 bp upstream of the transcription start site.

MeSH Terms
Base Sequence Binding Sites Calcitonin Gene-Related Peptide/genetics Carcinoma, Squamous Cell/genetics,metabolism DNA, Neoplasm/metabolism Gene Expression Regulation, Neoplastic HeLa Cells Humans Lung Neoplasms/genetics,metabolism Molecular Sequence Data Repressor Proteins/metabolism Restriction Mapping Transcription, Genetic Transfection Tumor Cells, Cultured
Chemicals
DNA, Neoplasm Repressor Proteins Calcitonin Gene-Related Peptide
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Symes A J
Medical Molecular Biology Unit, University College and Middlesex School of Medicine, London, UK.
Craig R K
Brickell P M
Article Info
Journal
FEBS letters
Abbr.
FEBS Lett
ISSN
0014-5793
Published
1992-07-20
Pages
229-33
Language
English
Region
England
NLM ID
0155157
Subset
IM
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