Journal
ONCOTARGET
Volume 6, Issue 6, Pages 4266-4273Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.2887
Keywords
ovarian cancer; macrophages; monocytes; catecholamines; MCP1
Categories
Funding
- NIH [CA101642, CA109298, P50CA083639, P50CA098258, U54CA151668, CA016672, U54CA96300, U54CA96297]
- Cancer Prevention and Research Institute of Texas (CPRIT) [RP140106]
- Ovarian Cancer Research Foundation [DOD-PC0-80359-P1, NIH/NCI P50 CA093459, 5RC2GM09259, 5U54CA151668, U54 CA 096300-08]
- Ovarian Cancer Research Fund Program Project Development Grant, Department of Defense [OC073399, W81XWH-10-1-0158, OC100237]
- Bettyann Asche Murray Distinguished Professorship
- RGK Foundation
- Gilder Foundation
- Blanton-Davis Ovarian Cancer Research Program
- [CA140933]
- [CA104825]
- CDMRP [546115, OC100237] Funding Source: Federal RePORTER
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Increased adrenergic signaling facilitates tumor progression, but the underlying mechanisms remain poorly understood. We examined factors responsible for stress-mediated effects on monocyte/macrophage recruitment into the tumor microenvironment, and the resultant effects on tumor growth. In vitro, MCP1 was significantly increased after catecholamine exposure, which was mediated by cAMP and PKA. Tumor samples from mice subjected to daily restraint stress had elevated MCP1 gene and protein levels, increased CD14+ cells, and increased infiltration of CD68+ cells. hMCP1 siRNA-DOPC nanoparticles significantly abrogated daily restraint stress-induced tumor growth and inhibited infiltration of CD68+ and F4/80+ cells. In ovarian cancer patients, elevated peripheral blood monocytes and tumoral macrophages were associated with worse overall survival. Collectively, we demonstrate that increased adrenergic signaling is associated with macrophage infiltration and mediated by tumor cell-derived MCP1 production.
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