AUTOCRINE INTERACTION BETWEEN PROLACTIN AND ITS RECEPTOR OCCURS INTRACELLULARLY IN THE 235-1-MAMMOTROPH CELL-LINE

We have previously demonstrated that PRL acts as an autocrine growth f actor in the pituitary tumor GH(3) cell line. In this study we present evidence that the 235-1 cell line also uses PRL as an autocrine growt h factor, and that in this case interaction between PRL and its recept or occurs intracellularly. First, the PRL produced by 235-1 cells was shown to be capable of initiating a proliferative response by placemen t in the Nb-2 bioassay. Second, PRL receptors were demonstrated to be present, but, unusually, primarily in the Golgi complex by light and e lectron microscope immunocytochemistry. Incubation of the cells in ant i-PRL had no effect on 235-1 cell proliferation until interleukin-1 tr eatment caused the PRL receptors to move to the cell surface, whereupo n cell proliferation was inhibited. Specific interference with PRL bio synthesis in noninterleukin-1-treated cells also inhibited cell prolif eration. Thus, the essential elements of an autocrine loop are present and can be demonstrated to be functional by antibody inhibition of gr owth after movement of the receptors to the cell surface and by antise nse inhibition of growth with the receptors in their normal intracellu lar location.