Prolactin and luteinizing hormone‐releasing hormone receptors in human benign prostatic hyperplasia and prostate cancer

Kádár, Tibor; Ben-David, M.; Pontes, J. Edson; Fekete, M.

doi:10.1002/pros.2990120403

Cited by 35 publications

(18 citation statements)

References 42 publications

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“…The detection of membrane receptors for LH-RH in human and hamster pancreatic cancers and their absence in normal pancreas raises the intriguing possibility that LH-RH acting as a growth factor along with EGF might be involved in complex interactions that contribute to the appearance or promotion of pancreatic cancer. The demonstration of binding sites for [ D -T~~~I -L H -R H in pancreatic cancer is in agreement with similar findings on human breast, ovarian, and prostate cancers (17,(39)(40)(41)(42)(43). The exact mechanism by which LH-RH agonists inhibit the growth of these tumors is incompletely understood, but sex hormone deprivation would be among the principal effects in the case of prostate carcinoma, estrogen-dependent breast neoplasms, and possibly pancreatic cancer (3,17,(25)(26)(27)(28).…”

Section: Discussionsupporting

confidence: 88%

“…The occurrence of SS-14 receptors in pancreatic cancers is also of potential interest, since it has been suggested that somatostatin analogs have direct antiproliferative effects on various tumors in addition to the inhibitory properties on the secretion of various hormones (18,24,26,(43)(44)(45)(46). Antitumor activity of somatostatin analogs on pancreatic cancers could be mediated through the inhibition of the secretion or action of gastrointestinal hormones such as gastrin and cholecystokinin (CCK), interference with the effects of growth factors, and directly through receptors for SS-14 located on the tumor cells (3,13,18,23-28,34,40,47).…”

Section: Discussionmentioning

confidence: 99%

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Membrane Receptors for Peptides in Experimental and Human Pancreatic Cancers

et al. 1989

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Membrane receptors for [D-Trp6]-luteinizing hormone-releasing hormone ([D-T~P~I-LH-RH), somatostatin , and epidermal growth factor (EGF) were investigated in experimental N-nitrosobis-(2-oxopropyl)-amine (BOP)-induced pancreatic cancers of hamsters and in specimens of normal human pancreas and human pancreatic cancer obtained from autopsies. Membrane receptors for [ D -T~~~I -L H -R H were absent in the pancreas of normal hamsters, but appeared after the carcinoma was induced with BOP. Binding capacity of SS-14 receptors was lower in membranes of BOP-induced pancreatic cancers than in the normal pancreas. In the BOP-induced pancreatic cancers, the receptors were also characterized following in vivo treatment of hamsters with microcapsules of the agonist [ D -T~~~I -L H -R H , somatostatin analog RC-160, and the combination of both peptides, which resulted in significant tumor inhibition. Therapy with [ D -T~~~I -L H -R H and RC-160, alone or in combination, decreased the binding capacity of receptors for [ D -T~~I -L H -R H , but increased B,,, for SS-14. There were no significant changes in characteristics of the EGF receptor following these therapies. Membranes from human pancreatic cancers showed binding sites for [ D -T~~I -L H -R H , but no binding was detected in normal human pancreas. The presence of receptors for LH-RH in pancreatic tumors of hamster and humans raises the intriguing possibility that LH-RH could be involved in complex interactions that contribute to the appearance of pancreatic cancer. The binding capacity of receptors for SS-14 in human pancreatic cancer membranes was lower, while B,, for EGF was higher, as compared to normal pancreas. Observed changes in receptors and tumor suppression suggest that the agonist [ D -T~~~I -L H -R H and somatostatin analogs might exert some direct inhibitory effects on experimental pancreatic cancer of hamsters. It is possible that LH-RH agonists and somatostatin analogs could also be used for treatment of human pancreatic cancer. The presence of membrane receptors for [ D -T~~~I -L H -R H , SS-14, and EGF in specimens of human pancreatic cancer also implies that this malignancy might be responsive to hormonal manipulations. Key Words: Binding sites for luteinizing hormone-releasing hormone (LH-RH)-Somatostatin-Epidermal growth factor-Hormonal manipulations-Pancreatic carcinoma.Adenocarcinoma of the exocrine pancreas is almost invariably fatal. In the United States, the in-~ cidence of this adenocarcinoma is increasing and more than 26,000 new cases are diagnosed every year (1-3). This malignancy is now the fifth leading cause of cancer-related deaths among adult Americans (1-3). Early diagnosis of pancreatic carcinoma is difficult and current modalities of treatment are unsatisfactory (1-6). Several studies indicate that 521

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Membrane Receptors for Peptides in Experimental and Human Pancreatic Cancers

et al. 1989

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“…The medical therapy for BPH and prostate carcinomas with GnRH analogues was presumed to work by decreasing testicular androgens through decreased LH levels and also by direct action of GnRH analogues on prostate tissue [42,43]. Because testicular androgens are already low, the therapeutic benefit of treatment with GnRH analogues may come from direct action as well as (in part) through decreased LH levels due to desensitization of anterior pituitary gland.…”

Section: Discussionmentioning

confidence: 99%

Expression of Luteinizing Hormone/Human Chorionic Gonadotropin Receptor Gene in Benign Prostatic Hyperplasia and in Prostate Carcinoma in Humans

Tao

Bao

Ackermann

et al. 1997

Biology of Reproduction

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The findings that normal rat prostates express functional LH/hCG receptors led us to test the hypothesis that benign prostatic hyperplasia (BPH) and prostate carcinomas may also express this receptor gene. The data revealed the presence of LH/hCG receptor transcripts and receptor protein in normal and hyperplastic but not in atrophic glands present in BPH tissue. Smooth muscle and blood vessels in stroma of BPH tissue also contained receptors. Prostate carcinomas contain lower and more heterogeneous receptor levels than BPH tissue. Two human prostate cancer cell lines (LNCaP and DU 145) that were investigated showed the presence of a major 4.5-kilobase transcript and several minor transcripts and also the protein of LH/hCG receptors. However, androgen-sensitive LNCaP cells contained more receptors than androgen-insensitive DU 145 cells. In summary, we demonstrate for the first time that BPH and prostate cancer tissues and cell lines express LH/hCG receptor gene. These findings suggest that higher LH levels in aged men may play a role in BPH and/or prostate carcinomas.

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“…It is becoming clear that prolactin (PRL) is implicated in prostate growth (11)(12)(13)(14)(15) and in the development and regulation of BPH and prostate cancer (16)(17)(18)(19)(20). Some authors reported that PRL may promote the growth and proliferation of prostate cells in synergism with androgens (21), whereas others suggested that PRL has an independent action on prostatic growth and metabolism (22)(23)(24).…”

Section: Introductionmentioning

confidence: 99%

Effects of sulpiride on mRNA levels of steroid 5α‐reductase isozymes in prostate of adult rats

et al. 2007

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SummaryProlactin (PRL) is implicated in prostate growth and in the development and regulation of benign prostatic hypertrophy (BPH) and prostate cancer (PCa). PRL may exert its effects on prostate in synergism with androgens. The most active androgen in the prostate is the 5a-dihydrotestosterone (DHT) obtained from testosterone by the 5a-reductase (5a-R) enzyme, which is expressed in the prostate as two isozymes, 5a-R1 and 5a-R2. In this study, sulpiride, a prolactin-secretion inductor, was administered to male rats. mRNA levels of 5a-R1 and 5a-R2 were measured in prostate of controls and sulpiride-treated rats, using one-step quantitative RT-PCR coupled with laserinduced fluorescence capillary electrophoresis (LIF-CE). Results demonstrated that sulpiride-induced hyperprolactinemia is associated with an increase in mRNA levels of both 5a-R1 and 5a-R2 in prostate of adult rats. Although a direct effect of sulpiride on prostate gland cannot be ruled out, hyperprolactinemia may be a factor to be considered in aging males, in whom prostatic diseases such as BPH and PCa are more frequent. IUBMBIUBMB Life, 60(1): [68][69][70][71][72] 2008

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Prolactin and luteinizing hormone‐releasing hormone receptors in human benign prostatic hyperplasia and prostate cancer

Cited by 35 publications

References 42 publications

Membrane Receptors for Peptides in Experimental and Human Pancreatic Cancers

Membrane Receptors for Peptides in Experimental and Human Pancreatic Cancers

Expression of Luteinizing Hormone/Human Chorionic Gonadotropin Receptor Gene in Benign Prostatic Hyperplasia and in Prostate Carcinoma in Humans

Effects of sulpiride on mRNA levels of steroid 5α‐reductase isozymes in prostate of adult rats

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