JOE Society for Endocrinology Archive
HOME HELP CONTACT US SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Journal of Endocrinology (1999) 163, 269-280       DOI: 10.1677/joe.0.1630269
© 1999 Society for Endocrinology
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (9)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Csernus, V
Right arrow Articles by Groot, K
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Csernus, V
Right arrow Articles by Groot, K
Journal of Endocrinology, Vol 163, Issue 2, 269-280
Copyright © 1999 by Society for Endocrinology

Articles

Effect of GHRH and peptides from the vasoactive intestinal peptide family on cAMP production of human cancer cell lines in vitro

V Csernus, AV Schally, and K Groot


Antagonistic analogs of GHRH inhibit growth of various human cancers both in vivo and in vitro. To elucidate the mechanism of direct action of the antagonistic analogs of GHRH on tumor cells, cultured human cancer cells were exposed to GHRH, vasoactive intestinal peptide (VIP), secretin, glucagon, neuropeptide-Y (NPY), pituitary adenylate cyclase-activating peptide (PACAP), and VIP analogs in a superfusion system, and changes in cAMP and IGF-II release from the cells were measured. Various human cancer cell lines, such as mammary (MDAMB-468 and ZR-75-1), prostatic (PC-3), pancreatic (SW-1990 and Capan-2), ovarian (OV-1063), and colorectal (LoVo) responded to pulsatile stimuli with GHRH (0.5-20 nM), VIP (0.02-10 nM), and PACAP-38 (0.05-5 nM) with a rapid, transient increase in cAMP release from the cells. The VIP antagonist, PG-97-269, and the adenylate cyclase inhibitor, MDL-12330A, but not SQ-22536 or pertussis toxin, blocked the cAMP responses to these peptides. Stimulation of the cells with 100 nM secretin, glucagon or NPY did not alter the cAMP release. Our results suggest that GHRH receptors different from the type expressed in the pituitary are involved in mediating these effects. As cAMP is a potent second messenger controlling a wide variety of intracellular functions, including those required for cell growth, our results indicate that GHRH might have a direct stimulatory effect on growth of human cancers. Blockade of the autocrine/paracrine action of GHRH with its antagonistic analogs may provide a new approach to tumor control.


This article has been cited by other articles:


Home page
 Proc. Natl. Acad. Sci. USAHome page
R. Busto, A. V. Schally, J. L. Varga, M. O. Garcia-Fernandez, K. Groot, P. Armatis, and K. Szepeshazi
The expression of growth hormone-releasing hormone (GHRH) and splice variants of its receptor in human gastroenteropancreatic carcinomas
PNAS, September 3, 2002; 99(18): 11866 - 11871.
[Abstract] [Full Text] [PDF]

Home page
 J. Clin. Endocrinol. Metab.Home page
I. Chatzistamou, A. V. Schally, J. L. Varga, K. Groot, P. Armatis, R. Busto, and G. Halmos
Antagonists of Growth Hormone-Releasing Hormone and Somatostatin Analog RC-160 Inhibit the Growth of the OV-1063 Human Epithelial Ovarian Cancer Cell Line Xenografted into Nude Mice
J. Clin. Endocrinol. Metab., May 1, 2001; 86(5): 2144 - 2152.
[Abstract] [Full Text]

Home page
 Proc. Natl. Acad. Sci. USAHome page
R. D. Kineman
Antitumorigenic actions of growth hormone-releasing hormone antagonists
PNAS, January 18, 2000; 97(2): 532 - 534.
[Full Text] [PDF]


HOME HELP CONTACT US SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1999 by the Society for Endocrinology.