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The role of semaphorin 7A and its receptor plexin C1 in the migration of NSCLC cells

机译:信号素7a及其受体丛C1在NSCLC细胞迁移中的作用

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摘要

We aim to explore the role of semaphorin 7A (SEMA7A) and its receptor plexin C1 in the migration of NSCLC cells. In the present study, expression of SEMA7A and plexin C1 in A549 cells and H1299 cellswere detected by western blot. The effect of interaction between SEMA7A and plexin C1 in cell migration and migration related signaling pathway was detected using recombinant SEMA7A and plexin C1 small interfering RNA (siRNA). Both cells showed an increase in SEMA7A and plexinC1 expression comparedwith normal alveolar epithelial cells. In addition, SEMA7A activated tumor migration by increasing phosphorylation of its related protein FAK, LIMKII and actin-binding protein cofilin, which are also downstream targets of plexin C1. However, SEMA7A failed to activate cell migration and its related protein FAK, LIMKII and cofilin when plexin C1 was silenced. These results suggest that the interaction between SEMA7A and plexin C1 promoted migration of A549 cells and H1299 cells and this effect worked through actin-binding protein cofilin signaling activation.
机译:我们的目标是探讨信号素7a(sema7a)及其受体丛c1在Nsclc细胞迁移中的作用。在本研究中,Sema7a和Plexin C1在A549细胞和Western印迹中检测到的H1299细胞中的表达。使用重组Sema7a和Plexin C1小干扰RNA(siRNA)检测Sema7a和plexin c1之间的相互作用在细胞迁移和迁移相关信号通路中的影响。两种细胞显示出与正常肺泡上皮细胞相比的Sema7a和plexinc1表达的增加。此外,通过增加其相关蛋白质Fak,Limkii和肌动蛋白结合蛋白钴蛋白的磷酸化,Sema7a活化的肿瘤迁移,这也是Plexin C1的下游靶标。然而,当丛林C1沉默时,Sema7a未能激活细胞迁移及其相关的蛋白质Fak,Limkii和Cofilin。这些结果表明Sema7a和Plexin C1之间的相互作用促进了A549细胞和H1299细胞的迁移,并且通过肌动蛋白结合蛋白钴蛋白信号激活来改变这种效果。

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  • 来源
    《RSC Advances》 |2017年第89期|共9页
  • 作者单位

    Fourth Mil Med Univ Tangdu Hosp Dept Respirat Xian 710038 Shaanxi Peoples R China;

    Fourth Mil Med Univ Tangdu Hosp Dept Respirat Xian 710038 Shaanxi Peoples R China;

    Fourth Mil Med Univ Tangdu Hosp Dept Respirat Xian 710038 Shaanxi Peoples R China;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 化学;
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