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前列腺癌肿瘤微环境中的免疫介质

Immune mediators in the tumor microenvironment of prostate cancer.

作者信息

Dai Jinlu, Lu Yi, Roca Hernan, Keller Jill M, Zhang Jian, McCauley Laurie K, Keller Evan T

机构信息

Department of Urology and Biointerfaces Institute, University of Michigan, Ann Arbor, MI, 48109, USA.

Center for Translational Medicine, Guangxi Medical University, Nanning, Guangxi, 520021, P. R. China.

出版信息

Chin J Cancer. 2017 Mar 14;36(1):29. doi: 10.1186/s40880-017-0198-3.

Abstract

Prostate cancer tissue is composed of both cancer cells and host cells. The milieu of host components that compose the tumor is termed the tumor microenvironment (TME). Host cells can be those derived from the tissue in which the tumor originates (e.g., fibroblasts and endothelial cells) or those recruited, through chemotactic or other factors, to the tumor (e.g., circulating immune cells). Some immune cells are key players in the TME and represent a large proportion of non-tumor cells found within the tumor. Immune cells can have both anti-tumor and pro-tumor activity. In addition, crosstalk between prostate cancer cells and immune cells affects immune cell functions. In this review, we focus on immune cells and cytokines that contribute to tumor progression. We discuss T-regulatory and T helper 17 cells and macrophages as key modulators in prostate cancer progression. In addition, we discuss the roles of interleukin-6 and receptor activator of nuclear factor kappa-B ligand in modulating prostate cancer progression. This review highlights the concept that immune cells and cytokines offer a potentially promising target for prostate cancer therapy.

摘要

前列腺癌组织由癌细胞和宿主细胞组成。构成肿瘤的宿主成分环境被称为肿瘤微环境(TME)。宿主细胞可以是源自肿瘤起源组织的细胞(如成纤维细胞和内皮细胞),也可以是通过趋化因子或其他因素被募集到肿瘤的细胞(如循环免疫细胞)。一些免疫细胞是TME中的关键参与者,并且占肿瘤内发现的非肿瘤细胞的很大比例。免疫细胞可以具有抗肿瘤和促肿瘤活性。此外,前列腺癌细胞与免疫细胞之间的相互作用会影响免疫细胞功能。在本综述中,我们关注有助于肿瘤进展的免疫细胞和细胞因子。我们将调节性T细胞、辅助性T细胞17和巨噬细胞作为前列腺癌进展中的关键调节因子进行讨论。此外,我们还讨论了白细胞介素-6和核因子κB受体激活剂配体在调节前列腺癌进展中的作用。本综述强调了免疫细胞和细胞因子为前列腺癌治疗提供潜在有前景靶点的概念。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1908/5351274/40474adb1c1c/40880_2017_198_Fig1_HTML.jpg

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