Cardiff University | Prifysgol Caerdydd ORCA
Online Research @ Cardiff 
WelshClear Cookie - decide language by browser settings

Induction of signalling in non-erythroid cells by pharmacological levels of erythropoietin

Dunlop, Elaine A., Percy, M. J., Boland, M. P., Maxwell, A. P. and Lappin, T. R. 2006. Induction of signalling in non-erythroid cells by pharmacological levels of erythropoietin. Neurodegenerative Diseases 3 (1-2) , pp. 94-100. 10.1159/000092099

Full text not available from this repository.

Abstract

Erythropoiesis is maintained by the hormone erythropoietin (Epo) binding to its cognate receptor (EpoR) on erythroid progenitor cells. The Epo-EpoR interaction initiates a signal transduction process that regulates the survival, growth and differentiation of these cells. Originally perceived as highly lineage-restricted, Epo is now recognised to have pleiotropic effects extending beyond the maintenance of red cell mass. Functional interactions between Epo and EpoR have been demonstrated in numerous cells and tissues. EpoR expression on neoplastic cells leads to concern that recombinant human erythropoietin, used to treat anaemia in cancer patients, may augment tumour growth. Here we demonstrate that EPO, at pharmacological concentrations, can activate three major signalling cascades, viz. the Jak2/STAT5, Ras/ERK and PI3K/Akt pathways in non-small cell lung carcinoma (NSCLC) cell lines. EpoR synthesis is normally under the control of GATA-1, but NSCLC cells exhibit decreased GATA-1 levels compared to GATA-2, -3 and -6, suggesting that GATA-1 is not essential for EpoR production. The increased Epo-induced signalling was not associated with a growth advantage for the NSCLC cells.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
Subjects: R Medicine > R Medicine (General)
Publisher: Karger
ISSN: 1660-2862
Last Modified: 04 Jun 2017 06:42
URI: http://orca-mwe.cf.ac.uk/id/eprint/63786

Citation Data

Cited 58 times in Google Scholar. View in Google Scholar

Cited 44 times in Scopus. View in Scopus. Powered By Scopus® Data

Actions (repository staff only)

Edit Item Edit Item