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粒细胞集落刺激因子对神经生长的非靶向作用促进前列腺癌的发展。

Granulocyte colony-stimulating factor off-target effect on nerve outgrowth promotes prostate cancer development.

机构信息

Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY.

出版信息

Int J Cancer. 2015 Feb 15;136(4):982-8. doi: 10.1002/ijc.29046. Epub 2014 Jul 9.

DOI:10.1002/ijc.29046
PMID:24975135
Abstract

The hematopoietic growth factor granulocyte colony-stimulating factor (G-CSF) has a role in proliferation, differentiation and migration of the myeloid lineage and in mobilizing hematopoietic stem and progenitor cells into the bloodstream. However, G-CSF has been newly characterized as a neurotrophic factor in the brain. We recently uncovered that autonomic nerve development in the tumor microenvironment participates actively in prostate tumorigenesis and metastasis. Here, we found that G-CSF constrains cancer to grow and progress by, respectively, supporting the survival of sympathetic nerve fibers in 6-hydroxydopamine-sympathectomized mice and also, promoting the aberrant outgrowth of parasympathetic nerves in transgenic or xenogeneic prostate tumor models. This provides insight into how neurotrophic growth factors may control tumor neurogenesis and may lead to new antineurogenic therapies for prostate cancer.

摘要

造血生长因子粒细胞集落刺激因子 (G-CSF) 在髓系细胞的增殖、分化和迁移中起作用,并将造血干细胞和祖细胞动员到血液中。然而,G-CSF 最近被新确定为大脑中的神经营养因子。我们最近发现,肿瘤微环境中的自主神经发育积极参与前列腺肿瘤发生和转移。在这里,我们发现 G-CSF 通过分别支持 6-羟多巴胺去交感神经小鼠中交感神经纤维的存活以及促进转基因或异种前列腺肿瘤模型中副交感神经的异常生长来限制癌症的生长和进展。这为神经生长因子如何控制肿瘤神经发生提供了新的见解,并可能为前列腺癌带来新的抗神经发生治疗方法。

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