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首页> 外文期刊>Cellular Physiology and Biochemistry >Mechanisms of RhoGDI2 Mediated Lung Cancer Epithelial-Mesenchymal Transition Suppression
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Mechanisms of RhoGDI2 Mediated Lung Cancer Epithelial-Mesenchymal Transition Suppression

机译：RhoGDI2介导的肺癌上皮-间质转化抑制机制

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biBackground /i/bThe aim of this study was to evaluate the function of RhoGDI2 in lung cancer epithelial-mesenchymal transition (EMT) process and to illustrate the underlying mechanisms that will lead to improvement of lung cancer treatment. biMethods /i/bThe RhoGDI2 knock-down and overexpressing A549 cell lines were first constructed. The influence of RhoGDI2 on cytoskeleton in A549 cells was studied using two approaches G-LISA-based Rac1 activity measurement and immunostaining-based F-actin distribution. The expression levels of key EMT genes were analyzed using real time quantitative polymerase chain reaction (RT-qPCR), western blot and immunostaining in untreated and RhoGDI2 knock-down or overexpressing A549 cells in both iin vivo/i and iin vitro/i experimental settings. biResults /i/bOur study showed that the activity of Rac1, a key gene that is crucial for the initiation and metastasis of human lung adenocarcinoma, causing the redistribution of F-actin with partial loss of cell-cell adhesions and stress fibers, was significantly suppressed by RhoGDI2. RhoGDI2 promoted the expression of EMT marker gene E-cadherin and repressed EMT promoting genes Slug, Snail, α-SMA in both A549 cells and lung and liver organs derived from the mouse models. Knocking-down RhoGDI2 induced abnormal morphology for lung organs. biConclusion /i/bThese findings indicate that RhoGDI2 repressed the activity of Rac1 and may be involved in the rearrangement of cytoskeleton in lung cancer cells. RhoGDI2 suppresses the metastasis of lung cancer mediated through EMT by regulating the expression of key genes such as E-cadherin, Slug, Snail and α-SMA in both iin vivo/i and iin vitro/i models.
机译：背景 本研究的目的是评估RhoGDI2在肺癌上皮-间质转化（EMT）过程中的功能，并阐明将导致RhoGDI2改善的潜在机制。肺癌的治疗。 方法 首先构建了RhoGDI2敲除和过表达的A549细胞系。使用两种方法基于G-LISA的Rac1活性测量和基于免疫染色的F-肌动蛋白分布研究了RhoGDI2对A549细胞中细胞骨架的影响。使用实时定量聚合酶链反应（RT-qPCR），western印迹和免疫染色法对体内和中未经处理的RhoGDI2敲低或过表达的A549细胞的关键EMT基因表达水平进行了分析。 i>体外实验设置。 结果 我们的研究表明，Rac1的活性是关键基因，对人类肺腺癌的发生和转移至关重要，从而导致F-肌动蛋白的重新分布而部分丢失RhoGDI2显着抑制了细胞间粘附和应力纤维的表达。 RhoGDI2在源自小鼠模型的A549细胞以及肺和肝器官中均促进了EMT标记基因E-钙粘着蛋白的表达，并抑制了EMT促进基因Slug，Snail，α-SMA。敲低RhoGDI2诱导肺脏器官形态异常。 结论 这些发现表明RhoGDI2抑制了Rac1的活性，并可能参与了肺癌细胞骨架的重排。 RhoGDI2通过调节E-cadherin，Slug，Snail和α-SMA等关键基因在体内和体外的表达来抑制通过EMT介导的肺癌转移。 >型号。

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