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CC 趋化因子配体 2(CCL2)促进前列腺癌的发生和转移。

CC chemokine ligand 2 (CCL2) promotes prostate cancer tumorigenesis and metastasis.

机构信息

Departments of Medicine and Urology, Michigan Center for Translational Pathology and the University of Michigan Comprehensive Cancer Center, University of Michigan, Ann Arbor, MI 48109, United States.

出版信息

Cytokine Growth Factor Rev. 2010 Feb;21(1):41-8. doi: 10.1016/j.cytogfr.2009.11.009. Epub 2009 Dec 14.

Abstract

CCL2 is a chemokine known to recruit monocytes and macrophages to sites of inflammation. A growing body of research suggests CCL2 is progressively overexpressed in tumor beds and may play a role in the clinical progression of solid tumors. Cancer cells derived from several solid tumor types demonstrate functional receptors for CCL2, suggesting this chemokine may achieve tumorigenicity through direct effects on malignant cells; however, a variety of normal host cells that co-exist with cancer in the tumor microenvironment also respond to CCL2. These cells include macrophages, osteoclasts, endothelial cells, T-lymphocytes, and myeloid-derived immune suppressor cells (MDSCs). CCL2 mediated interactions between normal and malignant cells in the tumor microenvironment and plays a multi-faceted role in tumor progression.

摘要

趋化因子 CCL2 已知可募集单核细胞和巨噬细胞至炎症部位。越来越多的研究表明,CCL2 在肿瘤床中逐渐过表达,并可能在实体瘤的临床进展中发挥作用。源自几种实体瘤类型的癌细胞表现出对 CCL2 的功能性受体,这表明这种趋化因子可能通过对恶性细胞的直接作用而实现致瘤性;然而,与肿瘤微环境中的癌症共存的各种正常宿主细胞也对 CCL2 作出反应。这些细胞包括巨噬细胞、破骨细胞、内皮细胞、T 淋巴细胞和髓系来源的免疫抑制细胞 (MDSC)。CCL2 介导肿瘤微环境中正常细胞和恶性细胞之间的相互作用,并在肿瘤进展中发挥多方面的作用。

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