Over‐expression of the epidermal growth factor receptor in human breast cancer cells fails to induce an Estrogen‐independent phenotype

Publisher Website
Google Scholar
Abstract
An association exists in primary human breast tumors between high epidermal growth factor receptor (EGFR) expression and a reduced number or even absence of estrogen receptors (ER). To determine whether an increase in EGFR expression might alter the estrogen responsiveness of an ERpositive human breast cancer cell line, ZR 75‐1 cells were cotransfected with a plasmid containing the full‐length cDNA for the human EGFR under the transcriptional control of the Harvey murine sarcoma virus (HaMSV) long terminal repeat (LTR) and with a pSV2neo plasmid. Two of the isolated G4 18‐resistant clones were found to constitutively express EGFR levels 15‐ to 60‐fold higher than those found on nontransfected ZR 75‐ I cells. The EGFR in these clones were functionally normal since EGF could increase their autophosphorylation and since EGF could enhance the transphosphorylation of p185erbe‐2. No change was seen in either the number or affinity of ER in these clones. In addition, the ability of estrogen to stimulate the anchorage‐dependent and anchorageindependent growth of these clones was not significantly modified. These results suggest that an increase in EGFR expression alone is not sufficient to induce a hormoneindependent phenotype in vitro in human breast cancer cells.