期刊
CANCER CELL
卷 27, 期 6, 页码 780-796出版社
CELL PRESS
DOI: 10.1016/j.ccell.2015.04.017
关键词
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资金
- Sander Stiftung
- Association of International Cancer Research
- ERC Advanced Investigator Grant from the European research Council [294293]
- Deutsche Forschungsgemeinschaft [SFB-TR23]
- Hartmut Hoffmann-Berling International Graduate School for Molecular and Cellular Biology
Cancer pain is a debilitating disorder and a primary determinant of the poor quality of life. Here, we report a non-vascular role for ligands of the Vascular Endothelial Growth Factor (VEGF) family in cancer pain. Tumor-derived VEGF-A, PLGF-2, and VEGF-B augment pain sensitivity through selective activation of VEGF receptor 1 (VEGFR1) expressed in sensory neurons in human cancer and mouse models. Sensory-neuron-specific genetic deletion/silencing or local or systemic blockade of VEGFR1 prevented tumor-induced nerve remodeling and attenuated cancer pain in diverse mouse models in vivo. These findings identify a therapeutic potential for VEGFR1-modifying drugs in cancer pain and suggest a palliative effect for VEGF/VEGFR1-targeting anti-angiogenic tumor therapies.
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