ArticleProceedings of the National Academy of Sciences of the United States of America2002
Expression of a splice variant of the receptor for GHRH in 3T3 fibroblasts activates cell proliferation responses to GHRH analogs.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 73 citations in OpenAlex.
- Growth hormone-releasing hormone receptor (GHRH-R) and its signaling.Reviews in endocrine & metabolic disorders · 2025Review
- Growth hormone-releasing hormone and its analogues in health and disease.Nature reviews. Endocrinology · 2025Review
- Characterization of Somatotrope Cell Expansion in Response to GHRH in the Neonatal Mouse Pituitary.Endocrinology · 2023Article
- GH-dependent growth of experimentally induced carcinomas in vivo.Endocrine-related cancer · 2023Review
- Expression of Growth Hormone-Releasing Hormone and Its Receptor Splice Variants in Primary Human Endometrial Carcinomas: Novel Therapeutic Approaches.Molecules (Basel, Switzerland) · 2022Article
- Constitutive signal bias mediated by the human GHRHR splice variant 1.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Suppression of reactive oxygen species in endothelial cells by an antagonist of growth hormone-releasing hormone.Journal of biochemical and molecular toxicology · 2021Article
- Splice variant of growth hormone-releasing hormone receptor drives esophageal squamous cell carcinoma conferring a therapeutic target.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- GHRH antagonists support lung endothelial barrier function.Tissue barriers · 2019Article
- Growth hormone-releasing hormone is produced by adipocytes and regulates lipolysis through growth hormone receptor.International journal of obesity (2005) · 2017Article
- Article
- Growth Hormone-Releasing Hormone and Its Analogues: Significance for MSCs-Mediated Angiogenesis.Stem cells international · 2016Review
- Growth hormone-releasing hormone receptor splice variant 1 is frequently expressed in oral squamous cell carcinomas.Hormones & cancer · 2012Article
- Acceleration of wound healing by growth hormone-releasing hormone and its agonists.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Antiproliferative effect of growth hormone-releasing hormone (GHRH) antagonist on ovarian cancer cells through the EGFR-Akt pathway.Reproductive biology and endocrinology : RB&E · 2010Article
- Stimulation of proliferation of MCF-7 breast cancer cells by a transfected splice variant of growth hormone-releasing hormone receptor.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Potentiation of mammary cancer inhibition by combination of antagonists of growth hormone-releasing hormone with docetaxel.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- The expression of the pituitary growth hormone-releasing hormone receptor and its splice variants in normal and neoplastic human tissues.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Effective treatment of experimental human non-Hodgkin's lymphomas with antagonists of growth hormone-releasing hormone.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Antagonist of growth hormone-releasing hormone induces apoptosis in LNCaP human prostate cancer cells through a Ca2+-dependent pathway.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The stimulatory effects of growth hormone-releasing hormone (GHRH) and the antiproliferative action of GHRH antagonists have been demonstrated in various cancers, but the receptors that mediate these responses are not clearly identified. Recently, we reported that human cancer cell lines express splice variants (SVs) of the receptors for GHRH. SV1 exhibits the greatest similarity to the pituitary GHRH receptor and is most likely to be functional. To ascertain whether SV1 mediates mitogenic effects on nonpituitary tissues, we expressed SV1 in 3T3 mouse fibroblasts and studied the properties of the transfected cells. Radioligand binding assays with (125)I-labeled GHRH antagonist JV-1-42 detected high affinity (K(d) = 0.58 +/- 0.17 nM) binding sites for GHRH with a maximal binding capacity (B(max)) of 103 +/- 17.4 fmol/mg of membrane protein in 3T3 cells transfected with pcDNA3-SV1, whereas the control cells transfected with the empty vector did not show any GHRH binding. Cell proliferation studies showed that cells expressing SV1 are much more sensitive to GHRH analogs than the pcDNA3 controls. Thus, the expression of SV1 augments the stimulatory responses to GHRH(1-29)NH(2) or GHRH agonist JI-38 and inhibitory responses to GHRH antagonist JV-1-38 as compared with pcDNA3 controls. The stimulation of SV1-expressing cells by GHRH or JI-38 is followed by an increase in cAMP production, but no GH release occurs. Vasoactive intestinal peptide had no effect, and its antagonist JV-1-53 did not inhibit the proliferation of SV1-expressing cells stimulated by GHRH. Our results suggest that SV1 could mediate responses of nonpituitary cells and various tumors to GHRH and GHRH antagonists. 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.
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