Specific low affinity binding sites for gonadotropin-releasing hormone in human endometrial carcinomata

Pahwa, G. S.; Kullander, Stig; Vollmer, G.; Oberheuser, F; Knüppen, R.; Emons, G.

doi:10.1016/0028-2243(91)90091-x

Cited by 42 publications

(16 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The low affinity/high capacity site had similar characteristics as the low affin ity LHRH binding sites previously described in biopsy material from human epithelial ovarian cancers (9, 11), human placenta (10), breast (3), or endometrial cancer (18,19). The second class of binding sites for LHRH found in EFO-21 and EFO-27 seems to be identical with the high affinity LHRH-binding site described by Fekete et However, the relative reduction of cell growth in these experiments after 2 to 6 days was less marked than in the first series with daily addition of the analogue.…”

Section: Discussionsupporting

confidence: 59%

High affinity binding and direct antiproliferative effects of luteinizing hormone-releasing hormone analogs in human endometrial cancer cell lines

Emons¹

1993

Journal of Clinical Endocrinology & Metabolism

105

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 59%

High affinity binding and direct antiproliferative effects of luteinizing hormone-releasing hormone analogs in human endometrial cancer cell lines

Emons¹

1993

Journal of Clinical Endocrinology & Metabolism

105

View full text Add to dashboard Cite

“…c[Gly ]-GnRH) did not display the perfect sigmoidal IP stimulation exhibited by others; this was suggestive of a second low affinity binding site. The precise interaction of the ligand with the GnRHR is unknown and low-affinity interactions have been proposed in some tissues (Pahwa et al 1991). It is also possible that this may reflect a non-specific interaction of a hydrophobic analogue at the very high dose (10 5 M) when this was observed.…”

Section: Discussionmentioning

confidence: 99%

Identification of new gonadotrophin-releasing hormone partial agonists

Leaños‐Miranda

Ulloa‐Aguirre²,

Cervini³

et al. 2006

Journal of Endocrinology

View full text Add to dashboard Cite

GnRH agonists or antagonists are currently utilized as therapeutic agents in a number of diseases. A side-effect of prolonged treatment with GnRH analogues is hypoestrogenism. In this study, we tested the in vitro potency of different GnRH analogues originally found to be partial agonists (i.e. analogues with decreased efficacy for activating or stimulating their cognate receptor) as well as novel analogues, to identify compounds that might potentially be useful for partial blockade of gonadotrophin release.

show abstract

“…The high‐affinity GnRH‐binding sites are commonly regarded as being the same as the GnRHR of the pituitary gland. Whereas in most of the reported cases, both the low‐affinity and high‐affinity GnRHR have been found in extrapituitary tissues [30–33], in some cases, only low‐affinity GnRHR could be detected [10,18,34], and in others, e.g. in endometrial cancers and nonmalignant endometrial specimens, only the high‐affinity GnRHR has been demonstrated [14].…”

Section: Localization Of Gnrh Receptor (Gnrhr) In Peripheral Reproducmentioning

confidence: 99%

Gonadotropin‐releasing hormone: GnRH receptor signaling in extrapituitary tissues

2008

View full text Add to dashboard Cite

Gonadotropin‐releasing hormone (GnRH) has historically been known as a pituitary hormone; however, in the past few years, interest has been raised in locally produced, extrapituitary GnRH. GnRH receptor (GnRHR) was found to be expressed in normal human reproductive tissues (e.g. breast, endometrium, ovary, and prostate) and tumors derived from these tissues. Numerous studies have provided evidence for a role of GnRH in cell proliferation. More recently, we and others have reported a novel role for GnRH in other aspects of tumor progression, such as metastasis and angiogenesis. The multiple actions of GnRH could be linked to the divergence of signaling pathways that are activated by GnRHR. Recent observations also demonstrate cross‐talk between GnRHR and growth factor receptors. Intriguingly, the classical Gαq–11‐phospholipase C signal transduction pathway, known to function in pituitary gonadotropes, is not involved in GnRH actions at nonpituitary targets. Herein, we review the key findings on the role of GnRH in the control of tumor growth, progression, and dissemination. The emerging role of GnRHR in actin cytoskeleton remodeling (small Rho GTPases), expression and/or activity of adhesion molecules (integrins), proteolytic enzymes (matrix metalloproteinases) and angiogenic factors is explored. The signal transduction mechanisms of GnRHR in mediating these activities is described. Finally, we discuss how a common GnRHR may mediate different, even opposite, responses to GnRH in the same tissue/cell type and whether an additional receptor(s) for GnRH exists.

show abstract

Specific low affinity binding sites for gonadotropin-releasing hormone in human endometrial carcinomata

Cited by 42 publications

References 30 publications

High affinity binding and direct antiproliferative effects of luteinizing hormone-releasing hormone analogs in human endometrial cancer cell lines

High affinity binding and direct antiproliferative effects of luteinizing hormone-releasing hormone analogs in human endometrial cancer cell lines

Identification of new gonadotrophin-releasing hormone partial agonists

Gonadotropin‐releasing hormone: GnRH receptor signaling in extrapituitary tissues

Contact Info

Product

Resources

About