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

A J Symes; R K Craig; P M Brickell

doi:10.1016/0014-5793(92)81006-8

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

FEBS Lett. 1992 Jul 20;306(2-3):229-33. doi: 10.1016/0014-5793(92)81006-8.

Authors

A J Symes¹, R K Craig, P M Brickell

Affiliation

¹ Medical Molecular Biology Unit, University College and Middlesex School of Medicine, London, UK.

PMID: 1633879
DOI: 10.1016/0014-5793(92)81006-8

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.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Base Sequence
Binding Sites
Calcitonin Gene-Related Peptide / genetics*
Carcinoma, Squamous Cell / genetics*
Carcinoma, Squamous Cell / metabolism
DNA, Neoplasm / metabolism
Gene Expression Regulation, Neoplastic*
HeLa Cells
Humans
Lung Neoplasms / genetics*
Lung Neoplasms / metabolism
Molecular Sequence Data
Repressor Proteins / metabolism*
Restriction Mapping
Transcription, Genetic
Transfection
Tumor Cells, Cultured

Substances

DNA, Neoplasm
Repressor Proteins
Calcitonin Gene-Related Peptide