Use of two MCF-7 cell variants to evaluate the growth regulatory potential of estrogen-induced products

• Published in: Cancer research (Chicago, Ill.) Vol. 46; no. 4; pp. 1904 - 1908
• Main Authors: DAVIDSON, N. E, BRONZERT, D. A, CHAMBON, P, GELMANN, E. P, LIPPMAN, M. E
• Format: Journal Article
• Language: English
• Published: Philadelphia, PA American Association for Cancer Research 01.04.1986
• Subjects: Animal tumors. Experimental tumors; Biological and medical sciences; Breast Neoplasms - genetics; Breast Neoplasms - metabolism; Breast Neoplasms - pathology; Cells, Cultured; Estrogens - pharmacology; Experimental genital and mammary tumors; Female; Growth Substances - biosynthesis; Humans; Medical sciences; Molecular Weight; Neoplasm Proteins - biosynthesis; Neoplasms, Hormone-Dependent - genetics; Neoplasms, Hormone-Dependent - metabolism; Neoplasms, Hormone-Dependent - pathology; Oncogenes; RNA, Neoplasm - analysis; Tumors; Cell culture; Regulation(control); Induction; Estrogen; Development; Tumor; Mammary gland; Sex steroid hormone
• ISSN: 0008-5472; 1538-7445

Two variants of the human estrogen-responsive breast cancer cell line MCF-7, were utilized to study the expression of an estrogen-induced gene, pS2, and an estrogen-induced Mr 52,000 protein. One variant cell line, I13, is growth inhibited after chronic exposure to estrogen. Both the pS2 gene product and the Mr 52,000 protein were produced at maximal levels at a time when I13 growth was inhibited by estrogen. The variant cell line, LY2, selected for its resistance to the growth-inhibitory effects of the antiestrogen, LY117018, grew normally in the presence of this drug, although both pS2 expression and Mr 52,000 protein production were inhibited. These results confirm that the pS2 gene and Mr 52,000 protein are estrogen-regulated elements, but the lack of correlation between their activities and variant cell growth suggests that they are not major autocrine growth-stimulatory agents.