| Literature DB >> 26481148 |
Sunila Pradeep1, Jie Huang1, Edna M Mora2, Alpa M Nick1, Min Soon Cho3, Sherry Y Wu1, Kyunghee Noh1, Chad V Pecot4, Rajesha Rupaimoole1, Martin A Stein5, Stephan Brock5, Yunfei Wen1, Chiyi Xiong6, Kshipra Gharpure1, Jean M Hansen1, Archana S Nagaraja1, Rebecca A Previs1, Pablo Vivas-Mejia7, Hee Dong Han8, Wei Hu1, Lingegowda S Mangala8, Behrouz Zand1, Loren J Stagg9, John E Ladbury9, Bulent Ozpolat10, S Neslihan Alpay10, Masato Nishimura1, Rebecca L Stone1, Koji Matsuo1, Guillermo N Armaiz-Peña1, Heather J Dalton1, Christopher Danes1, Blake Goodman1, Cristian Rodriguez-Aguayo10, Carola Kruger11, Armin Schneider11, Shyon Haghpeykar1, Padmavathi Jaladurgam1, Mien-Chie Hung12, Robert L Coleman1, Jinsong Liu13, Chun Li9, Diana Urbauer14, Gabriel Lopez-Berestein15, David B Jackson5, Anil K Sood16.
Abstract
While recombinant human erythropoietin (rhEpo) has been widely used to treat anemia in cancer patients, concerns about its adverse effects on patient survival have emerged. A lack of correlation between expression of the canonical EpoR and rhEpo's effects on cancer cells prompted us to consider the existence of an alternative Epo receptor. Here, we identified EphB4 as an Epo receptor that triggers downstream signaling via STAT3 and promotes rhEpo-induced tumor growth and progression. In human ovarian and breast cancer samples, expression of EphB4 rather than the canonical EpoR correlated with decreased disease-specific survival in rhEpo-treated patients. These results identify EphB4 as a critical mediator of erythropoietin-induced tumor progression and further provide clinically significant dimension to the biology of erythropoietin.Entities:
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Year: 2015 PMID： 26481148 PMCID： PMC4643364 DOI： 10.1016/j.ccell.2015.09.008
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743