IL-7/IL-7 receptor axis stimulates prostate cancer cell invasion and migration via AKT/NF-κB pathway
IL-7/IL-7 receptor axis stimulates prostate cancer cell invasion and migration via AKT/NF-κB pathway
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DOI：
10.1016/j.intimp.2016.08.017
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发表时间：
2016-11-01
影响因子：
5.6
通讯作者：
Wang, Zhongyang
中科院分区：
文献类型：
--
作者：
Qu, Hu;Zou, Zihao;Wang, Zhongyang
IL-7通过IL-7受体（IL-7R）在肿瘤进展中起重要作用。据报道，IL-7在前列腺癌组织中表达升高，并与预后不良密切相关。然而，IL-7及其受体在前列腺癌细胞侵袭中的生物学功能尚不清楚。在我们的研究中，我们发现前列腺癌细胞中IL-7和IL-7R的表达均上调。IL-7能剂量依赖性地促进前列腺癌细胞的侵袭和迁移，而IL-7R的下调则能减弱IL-7的作用。此外，IL-7/IL-7R轴诱导了ART和NF-kappa B的激活，而阻断ART则抑制了IL-7介导的NF-kappa B活性。此外，IL-7/IL-7R轴增加了前列腺癌细胞MMP-3和MMP-7的表达，而抑制nf - κ B和MMPs活性可抑制IL-7介导的细胞侵袭和迁移。综上所述，这些数据表明IL-7/IL-7R轴可能通过激活AKT/NF-kappa B通路和上调MMP-3和MMP-7表达参与前列腺癌细胞的侵袭和迁移。因此，阻断IL-7/IL-7R轴可能为治疗前列腺癌提供一种潜在的治疗策略。(C) 2016 Elsevier B.V.版权所有
IL-7, acting via IL-7 receptor (IL-7R), plays an important role in tumor progression. Elevated IL-7 expression has been reported to be observed in prostate cancer tissues and closely associated with poor prognosis. However, the biological functions of IL-7 and its receptor in prostate cancer cell invasiveness remain unclear. In our study, we found that the expressions of IL-7 and IL-7R were both upregulated in prostate cancer cells. IL-7 dose-dependently promoted the invasion and migration of prostate cancer cells, whereas knockdown of IL-7R attenuated the effect of IL-7. Further, IL-7/IL-7R axis induced the activation of ART and NF-kappa B, whereas blocking of ART suppressed IL-7-mediated NF-kappa B activity. Moreover, IL-7/IL-7R axis increased MMP-3 and MMP-7 expression of prostate cancer cells, whereas inhibition of NF-kappa B as well as MMPs activity suppressed IL-7-mediated cell invasion and migration. Together, these data identify IL-7/IL-7R axis to be involved in prostate cancer cell invasion and migration, probably via activating AKT/NF-kappa B pathway and upregulating MMP-3 and MMP-7 expression. Therefore, blocking IL-7/IL-7R axis may provide a potential therapeutic strategy to treat prostate cancer. (C) 2016 Elsevier B.V. All rights reserved.