Kidney cancer cells secrete IL-8 to activate Akt and promote migration of mesenchymal stem cells
Kidney cancer cells secrete IL-8 to activate Akt and promote migration of mesenchymal stem cells
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肾癌细胞分泌IL-8激活Akt促进间充质干细胞迁移
DOI：
10.1016/j.urolonc.2013.10.018
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发表时间：
2014-07-01
影响因子：
2.7
通讯作者：
Xu Ke-Wei
中科院分区：
文献类型：
--
作者：
Bi Liang-kuan;Zhou Nan;Xu Ke-Wei
背景：间充质干细胞(MSCs)是一种多潜能的成体干细胞，具有向癌细胞归巢的能力。因此，MSCs在肿瘤的发生、转移和耐药中发挥着重要作用。目前，MSCs在肾癌中归巢的机制尚不清楚。方法：采用酶联免疫吸附试验检测肾癌患者和肾癌细胞培养上清液中IL-8的水平。免疫荧光染色和逆转录聚合酶链式反应检测MSCs中IL-8的主要受体。结果：肾癌患者血清IL-8水平明显升高，2株肾癌细胞株均可分泌IL-8。MSCs高表达IL-8受体(CXCR2)。阻断IL-8或CXCR2可降低MSCs的迁移能力。结论：肾癌细胞分泌IL-8，通过CXCR2激活Akt信号通路，诱导MSCs迁移，这可能是MSCs归巢的重要机制之一。(C)2014 Elsevier Inc.保留所有权利。
Background: Mesenchymal stem cells (MSCs) are multipotent adult stem cells that have the capability of homing to cancer cells. Thus, MSCs play an important role in the development, metastasis, and drug resistance of cancers. The mechanisms underlying the homing of MSCs in kidney cancer are still poorly understood.Methods: In the present study, enzyme-linked immunosorbent assay was used to measure the level of IL-8 in patients with kidney cancer and in the culture medium of kidney cancer cells. Immunofluorescence staining and reverse transcription polymerase chain reaction were utilized to explore the main receptor for IL-8 in MSCs. Transwell migration assay was performed to measure the migration ability of MSCs and Western blot test was performed to test the activation of signaling pathways.Results: The serum level of IL-8 was markedly increased in patients with kidney cancer, and 2 kidney cancer cell lines were found to secrete IL-8. MSCs had high expression of the IL-8 receptor (CXCR2). Blocking IL-8 or CXCR2 could decrease the migration ability of MSCs. IL-8 could significantly increase Akt phosphorylation in MSCs.Conclusions: Kidney cancer cells secrete IL-8 to activate the Akt signaling pathway via CXCR2 on MSCs, inducing the migration of MSCs, which may be one of the important mechanisms underlying the homing of MSCs in kidney cancer. (C) 2014 Elsevier Inc. All rights reserved.