AI Article Synopsis
- Erythropoietin (EPO), commonly used to treat anemia in cancer patients, may inadvertently promote tumor growth and increase mortality rates due to its effects on the tumor microenvironment.
- In laboratory studies simulating tumor environments, EPO exacerbated the suppression of T cell proliferation through a mechanism involving inducible nitric oxide synthase (iNOS) and IFNγ signaling in macrophages.
- The presence of EPO receptors on specific macrophage populations highlights the potential of EPO to directly enhance T cell suppression in tumors, suggesting a complex role of EPO in cancer progression.
Article Abstract
Erythropoietin (EPO), used to treat anemia in cancer patients, has been reported to accelerate tumor progression and increase mortality. Research of the mechanism for this effect has focused upon EPOR expression by tumor cells. We model the high macrophage to lymphocyte ratio found in tumor microenvironments (TMEs) by culturing peritoneal cavity (PerC) cells that naturally have a high macrophage to T cell ratio. Following TCR ligation, C57BL/6J PerC T cell proliferation is suppressed due to IFNγ-triggered inducible nitric oxide synthase (iNOS) expression. EPO was tested in the PerC culture model and found to increase T cell suppression. This effect could be abrogated by inhibiting iNOS by enzyme inhibition, genetic ablation, or blocking IFNγ signaling. Flow cytometry revealed the EPOR on CD11b(+)F4/80(+) macrophages. These results suggest that EPO could increase T cell suppression in the TME by acting directly on macrophages.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4983461 | PMC |
| http://dx.doi.org/10.1016/j.cellimm.2016.05.004 | DOI Listing |
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