Ribosomal protein S6 kinase and PKC in human mammary tumor cells.

Abstract

It is well established that 17-β estradiol (E2) influences the growth of human breast cancer (Patterson et al. 1982; Edwards et al. 1979; Maass and Jonat 1983; Howat et al. 1985), but it is unclear wheter E2 acts directly or indirectly on the proliferation of target cells (Soto and Sonnenschein 1987; Dickson and Lippman 1987; King 1985). At present, there is increasing evidence that polypeptide growth factors (GF) also regulate the growth of human breast cancer (Dickson and Lippman 1987; King 1985; Dickson et al. 1986; Dickson et al. 1986). Therefore, E2 may in part promote the growth through the regulation of autostimulatory and autoinhibitory GFs (Soto and Sonnenschein 1987; Dickson and Lippman 1987; Knabbe et al. 1987). Consequently, the hormone dependency of breast tumor cells may be limited not only to functional estrogen receptors (ER) but also to functional growth factor receptors (GF-R). Such GF-Rs are likely to represent important growth-regulatory elements in the estrogen-induced autocrine or paracrine growth mechanisms of human breast cancer (Fitzpatrick et al. 1984; Macias et al. 1986; Sainsbury et al. 1985; Wyss et al. 1987; Sainsbury et al. 1987; Furlanetto and DiCarlo 1984).