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 Google Scholar Google Scholar Articles by Shain, S. A. Articles by Koger, J. D. Search for Related Content PubMed PubMed Citation Articles by Shain, S. A. Articles by Koger, J. D.

Differences in Responsiveness of Clonally Derived AXC/SSh Rat Prostate Cancer Cells to Secreted or Prototypic Mitogens¹

Department of Cellular and Molecular Biology, Southwest Foundation for Biomedical Research, San Antonio, Texas 78284

AXC/SSh rat prostate cancer cells elaborate heat-sensitive, heparinbinding mitogens which include members of the fibroblast growth factor (FGF)-like family of growth factors. The quantity of FGF-like growth factors, relative to total growth factor production, was cell line specific as was prostate cancer cell response to secreted or the prototypic mitogens basic FGF (bFGF), acidic FGF (aFGF), or epidermal growth factor (EGF). C3 cell proliferation, assayed either by cell counting or thymidine incorporation, was not affected by mitogens secreted by C3, D1, T1, or T5 prostate cancer cells or by bFGF, aFGF, or EGF. In contrast, C3, D1, T1, or T5 cell-secreted mitogens enhanced proliferation of T1 and T5 Cells, and proliferation of D1, T1, and T5 cells was enhanced by bFGF, aFGF, and EGF. D1 cell response to prototypic mitogens was 3- to 12-fold less than that of T1 or T5 cells. By comparison, the NRKF cell response to prototypic mitogens was qualitatively comparable but quantitatively greater than that of rat prostate cancer cells. The relative and absolute bFGF or aFGF concentrations necessary for half-maximum stimulation of prostate cancer or normal rat kidney fibroblast cell thymidine incorporation were comparable to that known to effect half-maximum increase in proliferation of mesoderm-derived cells. Similarly, the EGF concentration required for half-maximum prostate cancer or normal rat kidney fibroblast cell thymidine incorporation was comparable to that known to effect half-maximum fibroblast thymidine incorporation or granulosa cell proliferation. Our data establish that prostate cancer cell response to prototypic mitogens is representative of that of nonneoplastic cells and imply that C3 cell insensitivity to prostate cancer cell or prototypic mitogens represents defects in cellular response mechanisms. The basis for C3 cell unresponsiveness or D1 cell-diminished responsiveness remains to be elaborated.

¹ These studies were supported in part by Grant DK 39766 from the Department of Health and Human Services.

² Effective September 1, 1989, address correspondence to Dr. Shain at Department of Obstetrics and Gynecology, University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78284.

Received 1/11/89. Revised 4/ 5/89. Accepted 4/13/89.