Endocrine-paracrine cells of the prostate (also known as APUD or neuroendocrine cells) constitute, in addition to the basal and exocrine secretory cells, a third population of highly specialized epithelial cells in the prostate gland. These endocrine-paracrine cells contain, and most likely secrete, serotonin and calcitonin, as well as variety of other peptides. Little is known of the functional role of these cells, but they probably subserve a paracrine or local regulatory role. They may also regulate via endocrine, lumencrine, or neurocrine mechanisms. These endocrine-paracrine cells probably play a significant role during prostatic growth and differentiation as well as regulating the secretory process of the mature gland. Neuroendocrine differentiation in prostatic carcinoma occurs in the form of the relatively rare small cell carcinoma and carcinoid or carcinoid-like tumor, but most commonly as focal neuroendocrine differentiation in a conventional prostatic adenocarcinoma that is a very frequent, if not ubiquitous phenomenon, and reflects tumor cell heterogeneity mimicking the normal differentiation process. The world's literature on neuroendocrine differentiation in prostatic carcinoma is reviewed. Neuroendocrine differentiation in all types of prostatic carcinoma appears to correlate with a poor prognosis. This correlation is probably multifactorial and may relate to a positive correlation with grade, a direct resistance to hormonal manipulation, and/or autocrine/paracrine growth factor activity due to the secretion of neuroendocrine products. Neuron-specific enolase and chromogranin, as well as other neuroendocrine products, may be useful as serum markers in patients with prostatic carcinoma with neuroendocrine differentiation. New therapeutic strategies need to be developed to treat these tumors. This includes the use of specialized protocols that have been effective against neuroendocrine carcinomas arising in other organ systems.

Neuroendocrine differentiation in carcinoma of the prostate. Diagnostic, prognostic, and therapeutic implications.

Neuroendocrine differentiation in human prostatic carcinoma

Differential effects of peptide hormones bombesin, vasoactive intestinal polypeptide and somatostatin analog RC-160 on the invasive capacity of human prostatic carcinoma cells.

Involvement of corticotropin-releasing factor in restraint stress-induced anorexia and reversion of the anorexia by somatostatin in the rat.

Octapeptide analogues of somatostatin inhibit the clonal growth and vasoactive intestinal peptide-stimulated cyclic AMP formation in human small cell lung cancer cells

https://febs.onlinelibrary.wiley.com/doi/pdf/10.1016/0014-5793%2887%2981021-9

Somatostatin inhibits VIP‐ and isoproterenol‐stimulated cyclic AMP accumulation in rat prostatic epithelial cells

1. The administration of 125 I-labelled growth hormone-releasing factor (GRF) analogue 1-29NH 2 by intravenous, subcutaneous or intraperitoneal injection to rats leads to rapid (i.v.) or slow (s.c. and i.p.) increases in plasma radioactivity followed by extensive breakdown of the peptide. 2. Tissues possessing GRF-like immunoreactivity such as gastric antrum (but not fundus), duodenum and ileum showed in vivo specific uptake of 125 I-GRF probably mediated by vasoactive intestinal peptide (VIP) receptors. 3. Pituitary (the primary target organ for GRF) but neither thyroid nor parathyroid exhibited specific uptake of 125 I-GRF.

Tissue and plasma distribution of exogenous growth hormone-releasing factor analogue (GRF1-29NH2) after intravenous, subcutaneous and intraperitoneal injection in the rat.

M.A. Fernandez-Gonzalez

Papers

Somatostatin inhibits VIP‐ and isoproterenol‐stimulated cyclic AMP accumulation in rat prostatic epithelial cells

Tissue and plasma distribution of exogenous growth hormone-releasing factor analogue (GRF1-29NH2) after intravenous, subcutaneous and intraperitoneal injection in the rat.