EPO induced the activation of PI3K/AKT and MAPK pathways in human breast cancer cell lines.
Here, we have examined the functional role of the EPO-EPOR axis in pre-clinical models of breast cancer. Numerous tumor cells express the EPO receptor (EPOR), posing a risk that EPO treatment would enhance tumor growth, but the mechanisms involved in breast tumor progression are poorly understood. Clinical studies have indicated decreased survival in some groups of cancer patients treated with EPO. Anemia is common in breast cancer patients and can be treated with blood transfusions or with recombinant erythropoietin (EPO) to stimulate red blood cell production. Received: FebruAccepted: FebruPublished: MaAbstractīreast cancer is a leading cause of cancer-related deaths. Keywords: EPO, EPOR, breast cancer, MYC, apoptosis ** These authors have contributed equally to this work Lappin 1,**ġ Centre for Cancer Research and Cell Biology, Queen’s University Belfast, Belfast BT9 7AE, UKĢ School of Pharmacy, Queen’s University Belfast, Belfast BT9 7AE, UKģ Institute of Laboratory Animal Science, University of Veterinary Medicine Vienna, Vienna A-1210, AustriaĤ Division of Medical Biochemistry, Biocenter, Innsbruck Medical University, Innsbruck A-6020, Austriaĥ Institute of Integrative Biology, University of Liverpool, Liverpool L69 3BX, UKĦ Northern Ireland Molecular Pathology Laboratory, Belfast Health & Social Care Trust, Queen’s University Belfast, Belfast BT9 7AE, UKħ Department of Pathology, The University of Hong Kong, Hong Kong Special Administrative Region Hong Kong 999077, ChinaĨ Northern Ireland Centre for Stratified Medicine, Biomedical Sciences Research Institute, Ulster University, Londonderry BT47 6SB, UKĩ Institute of Cancer Therapeutics, University of Bradford, Bradford, West Yorkshire BD7 1DP, UK Mills 1, Perry Maxwell 6, Mohamed El-Tanani 1,9,** and Terence R. Davidson 1, Thomas Rülicke 3, Sophie Schober 3, Ludger Hengst 4, Heidelinde Jaekel 4, Angela Platt-Higgins 5, Philip S. McCrudden 2, Shu-Dong Zhang 1,8, Gareth W.