BACKGROUND. Although essential, androgens alone are not sufficient to induc
e normal growth and functionality of the prostate. Nonandrogenic hormones m
ust also be involved in the proliferation of the prostate cancer cells whic
h do not respond to antiandrogenic therapy and which thus become androgen-i
ndependent. Prolactin, but also growth hormone and luteinizing hormone, are
potentially able to act on both normal and abnormal prostatic cells.
METHODS. In this review we summarize data from the literature concerning th
e physiological and pathological implications of prolactin, growth hormone,
and luteinizing hormone on the prostate.
RESULTS. In rodent prostates, prolactin and growth hormone can induce a var
iety of effects independently of androgens (e.g., transactivation of certai
n genes, or synthesis of the major secretion products). Moreover, hyperprol
actinemia is responsible for inflammation and dysplasia of the gland, while
growth hormone promotes the development of prostate tumors in vivo in the
mouse and rat. Growth hormone acts on the gland directly, through prostatic
growth hormone receptors, and/or indirectly via the stimulation of insulin
-like growth factor-I (IGF-I) synthesis in the liver. Luteinizing hormone r
eceptor is expressed in rat and human prostates. Luteinizing hormone increa
ses the amount of various transcripts in the rat prostate through an androg
en-independent pathway.
CONCLUSIONS. Prolactin, growth hormone, and luteinizing hormone, alone or s
ynergistically with androgens, play physiologically significant roles in th
e normal prostate. The involvement of these hormones in the development of
benign prostatic hyperplasia and prostatic carcinoma is an issue that needs
to be addressed. (C) 1999 Wiley-Liss, Inc.