Expression of growth hormone-releasing hormone (GHRH) and splice variants of GHRH receptors in human experimental prostate cancers

@article{Ponowski2002ExpressionOG,
  title={Expression of growth hormone-releasing hormone (GHRH) and splice variants of GHRH receptors in human experimental prostate cancers},
  author={Artur Płonowski and Andrew V. Schally and Rebeca Busto and Magdalena Krupa and J{\'o}zsef L. Varga and G{\'a}bor Halmos},
  journal={Peptides},
  year={2002},
  volume={23},
  pages={1127-1133}
}
Expression of growth hormone-releasing hormone and its receptor splice variants in human prostate cancer.
TLDR
The presence of GHRH and its tumoral receptor SVs in prostate cancers suggests the possible existence of an autocrine mitogenic loop and the antitumor effects of G HRH antagonists in prostate cancer could be exerted in part by interference with this local GHRh system.
The expression of growth hormone-releasing hormone (GHRH) and splice variants of its receptor in human gastroenteropancreatic carcinomas
TLDR
The finding of SV1 receptor in human cancers provides an approach to an antitumor therapy based on the blockade of this receptor by specific GHRH antagonists.
Expression of Growth Hormone-Releasing Hormone and Its Receptor Splice Variants in Primary Human Endometrial Carcinomas: Novel Therapeutic Approaches
TLDR
The findings suggest the possible existence of an autocrine loop in EC based on GHRH and its tumoral SV receptors, and the antiproliferative effects of GHRh antagonists on EC are likely to be exerted in part by the local SVs and G HRH system.
The Immunohistochemical Expression of Growth Hormone-Releasing Hormone Receptor Splice Variant 1 Is a Favorable Prognostic Marker in Colorectal Cancer
TLDR
The immunohistochemical expression of SV-1 seems to be a favorable prognostic factor in CRC, and Kaplan-Meier and Cox univariate survival analyses indicated an improved survival time in patients with high SV- 1 compared with those with low GHRH-R expression, but this difference was not statistically significant.
The Expression of Growth Hormone-Releasing Hormone (GHRH) and its Receptor Splice Variants in Human Breast Cancer Lines; The Evaluation of Signaling Mechanisms in the Stimulation of Cell Proliferation
TLDR
The presence of SV1 of G HRH receptors in human cancers provides a rationale for antitumor therapy based on the blockade of this receptor by specific GHRH antagonists, and suggests that SVs of G hrH receptors could mediate the responses to GHRh and GHRD antagonists in breast cancer through Ca2+-, cAMP- and PKC-dependent mechanisms.
Antiproliferative effect of growth hormone-releasing hormone (GHRH) antagonist on ovarian cancer cells through the EGFR-Akt pathway
TLDR
The present study demonstrates that the inhibitory effect of the GHRH antagonist JMR-132 on proliferation is due, in part, to an interference with the EGFR-Akt pathway in ovarian cancer cells.
Growth hormone-releasing hormone (GHRH) antagonists inhibit the proliferation of androgen-dependent and -independent prostate cancers
TLDR
It is demonstrated that GHRH antagonists inhibit androgens-independent prostate cancers and, after combination with androgen deprivation, also androgen-sensitive tumors and the therapy with G HRH antagonist could be considered for the management of both androgen -dependent or - independent prostate cancers.
Cellular mechanisms of growth inhibition of human endometrial cancer cell line by an antagonist of growth hormone-releasing hormone.
TLDR
Results demonstrate that MZ-5-156 can directly inhibit the proliferation of human endometrial cancer cells, which express mRNA for GHRH and SV1 of G HRH receptor, presumably through the induction of p53-dependent apoptosis coupled with the up-regulation of Fas, phospho-p53 (Ser46), p53AIP1, and caspase-8, -9, and -3, and the down- regulation of Bcl-2.
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TLDR
The findings support the view that distinct receptors are expressed on human cancer cells, which may mediate the antiproliferative effect of GHRH antagonists.
Human renal cell carcinoma expresses distinct binding sites for growth hormone-releasing hormone.
TLDR
The presence of specific receptor proteins that bind GHRH antagonists in CAKI-1 RCC supports the view that distinct binding sites that mediate the inhibitory effect of G HRH antagonists are present on various human cancers.
Expression of a splice variant of the receptor for GHRH in 3T3 fibroblasts activates cell proliferation responses to GHRH analogs
TLDR
The presence of SV1 in several human cancer cell lines provides a rationale for antitumor therapy based on the blockade of this receptor by specific GHRH antagonists, and suggests that SV1 could mediate responses of nonpituitary cells and various tumors to G HRH and GHRh antagonists.
Expression of growth hormone-releasing hormone (GHRH) messenger ribonucleic acid and the presence of biologically active GHRH in human breast, endometrial, and ovarian cancers.
TLDR
The presence of biologically and immunologically active G HRH and messenger ribonucleic acid for GHRH in human breast, endometrial, and ovarian cancers supports the hypothesis that locally produced GHRh may play a role in the proliferation of these tumors.
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TLDR
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TLDR
The cloning of a cDNA encoding a human GHRH-R from an acromegalic pituitary cDNA library is reported, which is a member of the secretin family of G-protein-coupled receptors and has 47%, 42%, 35%, and 28% identity with receptors for vasoactive intestinal peptide, secretin, calcitonin, and PTH, respectively.
Growth hormone-releasing hormone antagonist MZ-5-156 inhibits growth of DU-145 human androgen-independent prostate carcinoma in nude mice and suppresses the levels and mRNA expression of insulin-like growth factor II in tumors.
TLDR
It is suggested that GH-RH antagonist MZ-5-156 may inhibit the growth of DU-145 human androgen-independent prostate cancers through a reduction in the production and mRNA expression of IGF-II by the tumor tissue.
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TLDR
The results indicate that GH-RH antagonist MZ-4-71 suppresses growth of PC-3, DU-145 and Dunning AT-1 androgen-independent prostate cancers, through diminution of GH release and the resulting decrease in the secretion of hepatic IGF-I, or through mechanisms involving a lowering of tumour IGF-i levels and possibly an inhibition of tumours IGF- I and IGF-II production.
Antagonists of growth hormone-releasing hormone and vasoactive intestinal peptide inhibit tumor proliferation by different mechanisms: evidence from in vitro studies on human prostatic and pancreatic cancers.
TLDR
Because GHRH antagonists inhibit the proliferation of LNCaP cells more powerfully than VPAC-R antagonists and also suppress the growth ofVPAC- R-negative MiaPaCa-2 cells, it can be concluded that their antiproliferative effect is exerted through a mechanism independent of VPac-R.
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