Erythropoietin Stimulates Tumor Growth via EphB4
Copyright policy )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 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.
- University of Queensland Australia
- University of North Carolina at Chapel Hill United States
- University of Queensland Australia
- The University of Texas System United States
- University of Puerto Rico System United States
Adult, Cancer Research, Blotting, Western, Receptor, EphB4, Mice, Nude, Breast Neoplasms, Kaplan-Meier Estimate, Recombinant-Human-Erythropoietin, Retinal Neovascularization, Ovarian-Cancer, Cell Line, Tumor, 616, Animals, Humans, Erythropoietin, Aged, Aged, 80 and over, Ovarian Neoplasms, Proliferative Retinopathy, Mouse Model, Progression, Agents, Cell Biology, Middle Aged, Promotes, Gene Expression Regulation, Neoplastic, Mice, Inbred C57BL, Oncology, Disease Progression, MCF-7 Cells, Female, Angiogenesis, Receptor Specificity, Protein Binding
Adult, Cancer Research, Blotting, Western, Receptor, EphB4, Mice, Nude, Breast Neoplasms, Kaplan-Meier Estimate, Recombinant-Human-Erythropoietin, Retinal Neovascularization, Ovarian-Cancer, Cell Line, Tumor, 616, Animals, Humans, Erythropoietin, Aged, Aged, 80 and over, Ovarian Neoplasms, Proliferative Retinopathy, Mouse Model, Progression, Agents, Cell Biology, Middle Aged, Promotes, Gene Expression Regulation, Neoplastic, Mice, Inbred C57BL, Oncology, Disease Progression, MCF-7 Cells, Female, Angiogenesis, Receptor Specificity, Protein Binding
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