This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Balakrishnan, A. Articles by Nandi, S. Search for Related Content PubMed PubMed Citation Articles by Balakrishnan, A. Articles by Nandi, S.

Differential Proliferative Response to Linoleate in Cultures of Epithelial Cells from Normal Human Breast and Fibroadenomas¹

Cancer Research Laboratory, University of California, Berkeley, California 94720 [A. B., S. C., G. B., W. I., J. Y., S. N.], Department of Anatomy, University of California, San Francisco, California 94143 [J. E.], and Department of Surgery, Division of Surgical Oncology, University of Illinois at Chicago, College of Medicine, Chicago, Illinois [C. B., T. D.]

Human breast epithelial cells isolated from normal breast tissues of premenopausal women demonstrated direct evidence of a proliferative effect by linoleate (18:26) or prostaglandin E₂ (PGE₂) in the presence of insulin and epidermal growth factor in serum-free cultures within a collagen gel matrix. Neither epidermal growth factor nor 18:26 by itself was capable of stimulating growth but together they stimulated proliferation synergistically. Epithelial cells isolated from fibroadenomas on the other hand failed to exhibit any growth stimulation due to 18:26 or PGE₂. The linoleate-stimulated growth in normal breast epithelial cells was inhibited by indomethacin, a cyclooxygenase inhibitor, which however could be reversed by PGE₂.

The proliferative response of normal breast epithelial cells to 18:26 was accompanied by a greater conversion of [¹⁴C]18:26 to arachidonic acid and [¹⁴C]20:46 to prostaglandins than that seen in epithelial cells from fibroadenomas. The turnover of [¹⁴C]18:26 in the phospholipids of normal cells was higher than in fibroadenomas indicating a possible role of phospholipids in mediating the 18:26 effect in normal cells.

Both normal and fibroadenoma cells can proliferate in response to cholera toxin and glucocorticoids when supplemented to the insulin- and epidermal growth factor-containing medium. From the results it appears that, unlike normal cells, fibroadenoma cells may have a specific defect in the PGE₂-responsive cyclic AMP-generating mechanism whereas cholera toxin-induced mechanism is operative in both types of cells.

¹ This work was supported in part by American Cancer Society Grant PDT 252, NIH Grant CA05388, NIH Grant CA40160, and NIH Grant CA09041.

² To whom requests for reprints should be addressed, at Cancer Research Laboratory, 3510 Life Sciences Building, University of California, Berkeley, CA 94720.

Received 3/28/88. Revised 8/23/88. Revised 11/ 7/88. Accepted 11/10/88.

This article has been cited by other articles:

				L. D. Yee, D. C. Young, T. J. Rosol, A. M. VanBuskirk, and S. K. Clinton Dietary (n-3) Polyunsaturated Fatty Acids Inhibit HER-2/neu-Induced Breast Cancer in Mice Independently of the PPAR{gamma} Ligand Rosiglitazone J. Nutr., May 1, 2005; 135(5): 983 - 988. [Abstract] [Full Text] [PDF]

				R. Natarajan, R. Esworthy, W. Bai, J.-L. Gu, S. Wilczynski, and J. Nadler Increased 12-Lipoxygenase Expression in Breast Cancer Tissues and Cells. Regulation by Epidermal Growth Factor J. Clin. Endocrinol. Metab., June 1, 1997; 82(6): 1790 - 1798. [Abstract] [Full Text] [PDF]