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C-X-C基序趋化因子配体5通过诱导血红素氧合酶-1表达发挥抗氧化作用，在人前列腺基质细胞和癌细胞中依赖于C-X-C基序趋化因子受体2。

The C-X-C Motif Chemokine Ligand 5, Which Exerts an Antioxidant Role by Inducing HO-1 Expression, Is C-X-C Motif Chemokine Receptor 2-Dependent in Human Prostate Stroma and Cancer Cells.

作者信息

Chang Kang-Shuo, Chen Syue-Ting, Hsu Shu-Yuan, Sung Hsin-Ching, Lin Wei-Yin, Tsui Ke-Hung, Lin Yu-Hsiang, Hou Chen-Pang, Juang Horng-Heng

机构信息

Department of Anatomy, College of Medicine, Chang Gung University, Kwei-Shan, Tao-Yuan 33302, Taiwan.

Department of Urology, Chang Gung Memorial Hospital-Linkou, Kwei-Shan, Tao-Yuan 33302, Taiwan.

出版信息

Antioxidants (Basel). 2024 Dec 5;13(12):1489. doi: 10.3390/antiox13121489.

DOI:10.3390/antiox13121489
PMID:39765818
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11673138/
Abstract

While the C-X-C motif chemokine ligand 5 (CXCL5) is recognized as an inflammatory mediator and a potent attractant for immune cells, its functions within the human prostate remain unclear. This study explored the expression, functions, and regulatory mechanisms of CXCL5 in prostate stroma and cancer cells. CXCL5 secreted from prostate cancer cells enhanced neutrophil migration. CXCL5 induced cell proliferation and invasion of prostate cancer cells in vitro and tumorigenesis in a xenograft animal model. C-X-C motif chemokine receptor 2 (CXCR2) has been identified on the surface of prostate fibroblasts and cancer cells. The supernatant of LNCaP cells or CXCL5 overexpression enhanced the migration and contraction of prostate myofibroblast WPMY-1 cells; however, pretreatment with SB225002, a CXCR2 inhibitor, can reverse these effects. CXCL5 evinces antioxidant properties by upregulating heme oxygenase-1 (HO-1) to counteract HO-induced reactive oxygen species (ROS) in a CXCR2-dependent manner in WPMY-1 and prostate cancer cells. Our findings illustrate that CXCL5, through HO-1, plays a role in antioxidation, and determine that the CXCL5/CXCR2/HO-1 pathway facilitates antioxidative communication between fibroblasts and cancer cells in the prostate. Therefore, targeting the CXCL5/CXCR2 signaling pathway could provide a new strategy for managing oxidative stress within the prostate.

摘要

虽然C-X-C基序趋化因子配体5（CXCL5）被认为是一种炎症介质和免疫细胞的强效吸引剂，但其在人前列腺中的功能仍不清楚。本研究探讨了CXCL5在前列腺基质和癌细胞中的表达、功能及调控机制。前列腺癌细胞分泌的CXCL5增强了中性粒细胞的迁移。CXCL5在体外诱导前列腺癌细胞的增殖和侵袭，并在异种移植动物模型中诱导肿瘤发生。已在前列腺成纤维细胞和癌细胞表面鉴定出C-X-C基序趋化因子受体2（CXCR2）。LNCaP细胞的上清液或CXCL5过表达增强了前列腺肌成纤维细胞WPMY-1细胞的迁移和收缩；然而，用CXCR2抑制剂SB225002预处理可逆转这些作用。CXCL5通过上调血红素加氧酶-1（HO-1）以CXCR2依赖的方式在WPMY-1细胞和前列腺癌细胞中抵消HO诱导的活性氧（ROS），从而表现出抗氧化特性。我们的研究结果表明，CXCL5通过HO-1发挥抗氧化作用，并确定CXCL5/CXCR2/HO-1途径促进前列腺中纤维母细胞与癌细胞之间的抗氧化通讯。因此，靶向CXCL5/CXCR2信号通路可为管理前列腺内的氧化应激提供新策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2726/11673138/c80f26592254/antioxidants-13-01489-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2726/11673138/3beb67f5efbd/antioxidants-13-01489-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2726/11673138/8481d0b5e72a/antioxidants-13-01489-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2726/11673138/abfdf2e3bcb7/antioxidants-13-01489-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2726/11673138/93a4f9363c44/antioxidants-13-01489-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2726/11673138/c80f26592254/antioxidants-13-01489-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2726/11673138/3beb67f5efbd/antioxidants-13-01489-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2726/11673138/837c72ef0cde/antioxidants-13-01489-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2726/11673138/ad0d47ff8418/antioxidants-13-01489-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2726/11673138/8481d0b5e72a/antioxidants-13-01489-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2726/11673138/abfdf2e3bcb7/antioxidants-13-01489-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2726/11673138/93a4f9363c44/antioxidants-13-01489-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2726/11673138/c80f26592254/antioxidants-13-01489-g007.jpg

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