An estrogen-responsive element from the 5'-flanking region of the rat prolactin gene functions in MCF-7 but not in HeLa cells.
We have used MCF-7, the human breast cancer cell line, which is estrogen receptor-positive, and the HeLa cell line, which is estrogen receptor-negative, to study the mechanisms by which estrogen induces prolactin gene transcription. A series of plasmids were constructed which direct the expression of the easily assayed bacterial enzyme chloramphenicol acetyltransferase. We have used these recombinants to show that the estrogen-responsive DNA element (ERE) required for the estrogenic regulation of the rat prolactin gene is functional in MCF-7 cells but not in HeLa cells. Specifically, in MCF-7 cells this element enhances the level of gene activity after estrogen treatment both from its own promoter and from a heterologous (simian virus 40) promoter. Results of these studies also show that in HeLa cells the ERE can mediate estrogenic regulation if cotransfected with a plasmid that can synthesize estrogen receptor.
Somasekhar
M B
MB
Department of Biochemistry, College of Agriculture and Life Sciences, University of Wisconsin-Madison 53706.
Gorski
J
J
D001943:Breast Neoplasms; D002460:Cell Line; D015500:Chloramphenicol O-Acetyltransferase / Q000235:genetics; D004967:Estrogens / Q000494:pharmacology*; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects*; D005796:Genes / Q000187:drug effects*; D006367:HeLa Cells / Q000378:metabolism; D006801:Humans; D011388:Prolactin / Q000235:genetics*; D011401:Promoter Regions, Genetic / Q000187:drug effects*; D014162:Transfection
D004967:Estrogens; D011388:Prolactin; D015500:Chloramphenicol O-Acetyltransferase