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

机译：信号蛋白7A及其受体plexin C1在NSCLC细胞迁移中的作用

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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 cells were 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 plexin C1 expression compared with 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：我们旨在探讨信号量7A（SEMA7A）及其受体plexin C1在NSCLC细胞迁移中的作用。在本研究中，通过western blot检测SEMA7A和plexin C1在A549细胞和H1299细胞中的表达。使用重组SEMA7A和plexin C1小干扰RNA（siRNA）检测了SEMA7A和plexin C1之间相互作用对细胞迁移和迁移相关信号通路的影响。与正常肺泡上皮细胞相比，两种细胞均显示出SEMA7A和plexin C1表达的增加。此外，SEMA7A通过增加其相关蛋白FAK，LIMKII和肌动蛋白结合蛋白cofilin的磷酸化来激活肿瘤迁移，它们也是plexin C1的下游靶标。但是，当plexin C1沉默时，SEMA7A无法激活细胞迁移及其相关蛋白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，并且这种作用通过肌动蛋白结合蛋白cofilin信号激活而起作用。

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