Erythropoietin Stimulates Tumor Growth via EphB4
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...
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| Published in | Cancer cell Vol. 28; no. 5; pp. 610 - 622 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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United States
Elsevier Inc
09.11.2015
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| 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.
[Display omitted]
•EphB4 functions as a canonical Epo receptor•rhEpo-mediated EphB4 activation triggers downstream signaling via STAT3•rhEpo induces EphB4-mediated functional and biological effects•EphB4 expression negatively correlates with clinical outcome
Pradeep et al. identify EphB4 as an erythropoietin (Epo) receptor promoting rhEpo-induced tumor growth and progression via Stat3 signaling. In human ovarian and breast cancer samples, expression of EphB4 rather than of the canonical EpoR correlates with decreased disease-specific survival in rhEpo-treated patients. |
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| AbstractList | 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. 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. [Display omitted] •EphB4 functions as a canonical Epo receptor•rhEpo-mediated EphB4 activation triggers downstream signaling via STAT3•rhEpo induces EphB4-mediated functional and biological effects•EphB4 expression negatively correlates with clinical outcome Pradeep et al. identify EphB4 as an erythropoietin (Epo) receptor promoting rhEpo-induced tumor growth and progression via Stat3 signaling. In human ovarian and breast cancer samples, expression of EphB4 rather than of the canonical EpoR correlates with decreased disease-specific survival in rhEpo-treated patients. 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. |
| Author | Hansen, Jean M. Hung, Mien-Chie Goodman, Blake Gharpure, Kshipra Rodriguez-Aguayo, Cristian Ladbury, John E. Coleman, Robert L. Han, Hee Dong Xiong, Chiyi Schneider, Armin Danes, Christopher Matsuo, Koji Li, Chun Pradeep, Sunila Wen, Yunfei Alpay, S. Neslihan Stein, Martin A. Zand, Behrouz Mora, Edna M. Haghpeykar, Shyon Nagaraja, Archana S. Hu, Wei Liu, Jinsong Brock, Stephan Nick, Alpa M. Vivas-Mejia, Pablo Pecot, Chad V. Dalton, Heather J. Jaladurgam, Padmavathi Wu, Sherry Y. Cho, Min Soon Sood, Anil K. Lopez-Berestein, Gabriel Huang, Jie Mangala, Lingegowda S. Ozpolat, Bulent Stagg, Loren J. Urbauer, Diana Previs, Rebecca A. Nishimura, Masato Noh, Kyunghee Stone, Rebecca L. Rupaimoole, Rajesha Kruger, Carola Jackson, David B. Armaiz-Peña, Guillermo N. |
| AuthorAffiliation | 1 Department of Gynecologic Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77584 12 Sygnis AG, Germany 4 Department of Surgical Oncology, Chapel Hill, NC 10 Department of Biochemistry and Molecular Biology and Center for Biomolecular Structure and Function, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030 6 Division of Hematology/Oncology, Chapel Hill, NC 13 Molecular & Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA 15 Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA 9 Center for RNA Interference and Non-coding RNA, The University of Texas MD Anderson Cancer Center 77030, USA 14 Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA 2 Department of Surgery, School of Medicine, University of Puerto Rico, San Juan, Puerto Rico 5 Department of Benign Hematology, Chapel Hill, NC 11 Department of Experimental Therape |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26481148$$D View this record in MEDLINE/PubMed |
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| Publisher_xml | – name: Elsevier Inc |
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| Title | Erythropoietin Stimulates Tumor Growth via EphB4 |
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