魏威①, 朱东望②, 孙保存①③, 赵秀兰①, 张艳辉③, 董学易①, 刘芳①, 张丹芳①, 赵楠①. Prdx1 通过P38MAPK通路影响肺癌VM的形成*[J]. 中国肿瘤临床, 2016, 43(22): 981-985. DOI: 10.3969/j.issn.1000-8179.2016.22.947
引用本文: 魏威①, 朱东望②, 孙保存①③, 赵秀兰①, 张艳辉③, 董学易①, 刘芳①, 张丹芳①, 赵楠①. Prdx1 通过P38MAPK通路影响肺癌VM的形成*[J]. 中国肿瘤临床, 2016, 43(22): 981-985. DOI: 10.3969/j.issn.1000-8179.2016.22.947
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Wei WEI1, Dongwang ZHU2, Baocun SUN1, 3, Xiulan ZHAO1, Yanhui ZHANG3, Xueyi DONG1, Fang LIU1, Danfang ZHANG1. Prdx1 promotes vasculogenic mimicry formation of lung cancer via P38MAPK signaling[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2016, 43(22): 981-985. DOI: 10.3969/j.issn.1000-8179.2016.22.947
Citation: Wei WEI1, Dongwang ZHU2, Baocun SUN1, 3, Xiulan ZHAO1, Yanhui ZHANG3, Xueyi DONG1, Fang LIU1, Danfang ZHANG1. Prdx1 promotes vasculogenic mimicry formation of lung cancer via P38MAPK signaling[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2016, 43(22): 981-985. DOI: 10.3969/j.issn.1000-8179.2016.22.947
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Prdx1 通过P38MAPK通路影响肺癌VM的形成*

Prdx1 promotes vasculogenic mimicry formation of lung cancer via P38MAPK signaling

    摘要
  • 摘要: 目的：检测Prdx 1 在肺癌中的表达，探讨Prdx 1 对肺癌血管生成拟态（vasculoenic mimicry，VM）形成的影响，并深入研究其影响机制。方法：利用CD31/PAS 双重染色及免疫组织化学法检测并分析VM及Prdx 1 的表达关系。将Prdx 1 表达质粒转染至肺癌细胞系A 549、H 1299中，诱导Prdx 1 外源性升降表达。Westernblot检测转染前、后Prdx 1、EMT 相关蛋白（E-cadherin 、Vimentin）、VM相关蛋白（VE-cadherin、VEGF）、P 38MAPK 通路相关蛋白（P 38、P-P 38）表达变化情况；A 549-Prdx1 细胞系加入P 38MAPK 通路的抑制剂SB203580后，检测（P 38，P-P 38、VEGF）的表达变化情况；三维，划痕和侵袭实验检测Prdx 1 对细胞成管、迁移、侵袭能力的影响。结果：Prdx 1 与患者VM的形成、淋巴结转移、不良预后密切相关。Prdx 1 升表达高E-cadherin 表达下调，Vimentin 表达上调，VE-cadherin、VEGF表达上调，P 38MAPK 中P 38表达不变，P-P 38表达上调。细胞的迁移侵袭成管能力显著增强。Prdx 1 低表达后与上述结果相反。A 549-Prdx1 细胞系中加入P 38MAPK 通路抑制剂SB203580后，VEGF高P-P 38随剂量的增加而降低，而P 38总蛋白不变。结论：Prdx 1 在肺癌中高表达，可能通过P 38MAPK 通路影响患者VM的形成。

     

    Abstract: Objective:To analyze the effect of Prdx 1 on lung cancer by investigating its expression and role in vasculogenic mimicry (VM) formation. Methods:The relationship between VM existence and Prdx1 expression was detected and analyzed by CD31/PAS du-al staining and immunohistochemical staining. A 549 and H1299cells were transfected with Prdx 1-expressing plasmids to induce exoge-nous Prdx1 protein expression. Changes in the expression levels of Prdx1, EMT-related proteins (E-cadherin and Vimentin), VM-related proteins (VE-cadherin and VEGF), and P38MAPK signaling-related proteins (P38and P-P38) were detected by Western blot after trans -fection. Furthermore, changes in the expression levels of P 38MAPK signaling-related proteins (P38and P-P38) and VM-related protein (VEGF) in A 549 -Prdx1 cells were detected by Western blot after using SB 203580. The effects of Prdx 1 gene transfection on migration capacity were determined by an in vitro wound-healing assay, whereas the role of Prdx1 transfection in invasive potential was deter -mined by an invasion assay. The role of Prdx 1 transfection on tube structure formation potential was determined by three-dimensional culture. Results: Immunohistochemistry staining showed that Prdx 1 expression was positively associated with VM, metastasis, and poor prognosis. Western blot showed that after Prdx 1 was increased, E- cadherin expression was downregulated, whereas Vimentin, VE- cadherin, VEGF, and P- P38expression levels were upregulated in A 549 cells. Moreover, P38expression was unchanged. Wound healing, invasion, and three-dimensional culture assays showed that the migration, invasion, and tube structure formation potentials of A 549 cells significantly increased, whereas suppressing Prdx1 in H 1299cells yielded the opposite results. After adding the P38MAPK pathway inhibitor, VEGF and P- P38expression levels decreased as inhibitor dosage increased, whereas P 38expression remained the same. Conclusion: Prdx 1, which is highly expressed in lung cancer specimens, was closely associated with VM. This association may promote VM formation via P 38MAPK signaling.

     

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