help button home button Endocrine Society Molecular Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bengtson, N. W.
Right arrow Articles by Linzer, D. I. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bengtson, N. W.
Right arrow Articles by Linzer, D. I. H.
Molecular Endocrinology 14 (12): 1934-1943
Copyright © 2000 by The Endocrine Society

Inhibition of Tumor Growth by the Antiangiogenic Placental Hormone, Proliferin-Related Protein

Nancy W. Bengtson and Daniel I. H. Linzer

Department of Biochemistry, Molecular Biology, and Cell Biology Northwestern University Evanston, Illinois 60208

Proliferin-related protein (PRP) is a potent placental antiangiogenic hormone. To test the antiangiogenic potential of PRP to block tumor growth, we engineered tumor cells to express this hormone. Both SV40-transformed BALB/c mouse 3T3 fibroblasts and rat C6 glioma cells have markedly reduced growth rates as tumors in mice if they express high levels of PRP. In both models, the small tumors that form are largely avascular, whereas control tumors are rich in blood vessels, consistent with PRP limiting tumor growth by preventing neovascularization of the tumors. The antiangiogenic effects of PRP are also detected on human endothelial cells, suggesting that the receptor and signaling pathway of this mouse hormone are conserved between mouse and human and may represent useful targets for the development of antiangiogenic therapeutics. That signaling pathway appears to involve an inhibition of arachidonic acid release, based on the ability of arachidonic acid to overcome the antiangiogenic effects of PRP.




This article has been cited by other articles:


Home page
 Proc. Natl. Acad. Sci. USAHome page
R. Ain, G. Dai, J. H. Dunmore, A. R. Godwin, and M. J. Soares
From the Cover: A prolactin family paralog regulates reproductive adaptations to a physiological stressor
PNAS, November 23, 2004; 101(47): 16543 - 16548.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
G. Pandini, E. Medico, E. Conte, L. Sciacca, R. Vigneri, and A. Belfiore
Differential Gene Expression Induced by Insulin and Insulin-like Growth Factor-II through the Insulin Receptor Isoform A
J. Biol. Chem., October 24, 2003; 278(43): 42178 - 42189.
[Abstract] [Full Text] [PDF]

Home page
 Endocr. Rev.Home page
C. V. Clevenger, P. A. Furth, S. E. Hankinson, and L. A. Schuler
The Role of Prolactin in Mammary Carcinoma
Endocr. Rev., February 1, 2003; 24(1): 1 - 27.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
D. O. Wiemers, L.-j. Shao, R. Ain, G. Dai, and M. J. Soares
The Mouse Prolactin Gene Family Locus
Endocrinology, January 1, 2003; 144(1): 313 - 325.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 2000 by The Endocrine Society