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Zinc induces epithelial to mesenchymal transition in human lung cancer H460 cells via superoxide anion-dependent mechanism

机译:锌通过超氧阴离子依赖性机制诱导人肺癌H460细胞上皮向间质转化

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Background Epithelial to mesenchymal transition (EMT) has been shown to be a crucial enhancing mechanism in the process of cancer metastasis, as it increases cancer cell capabilities to migrate, invade and survive in circulating systems. This study aimed to investigate the effect of essential element zinc on EMT characteristics in lung cancer cells. Methods The effect of zinc on EMT was evaluated by determining the EMT behaviors using migration, invasion and colony formation assay. EMT markers were examined by western blot analysis. Reactive oxygen species (ROS) were detected by specific fluorescence dyes and flow cytometry. All results were analyzed by ANOVA, followed by individual comparisons with post hoc test. Results The present study has revealed for the first time that the zinc could induce EMT and related metastatic behaviors in lung cancer cells. Results showed that treatment of the cells with zinc resulted in the significant increase of EMT markers N-cadherin, vimentin, snail and slug and decrease of E-cadherin proteins. Zinc-treated cells exhibited the mesenchymal-like morphology and increased cancer cell motility with significant increase of activated FAK, Rac1, and RhoA. Also, tumorigenic abilities of lung cancer cells could be enhanced by zinc. Importantly, the underlying mechanism was found to be caused by the ability of zinc to generate intracellular superoxide anion. Zinc was shown to induce cellular superoxide anion generation and the up-regulation of EMT markers and the induced cell migration and invasion in zinc-treated cells could be attenuated by the treatment of MnTBAP, a specific superoxide anion inhibitor. Conclusion Knowledge gains from this study may highlight the roles of this important element in the regulation of EMT and cancer metastasis and fulfill the understanding in the area of cancer cell biology.
机译:背景技术上皮向间质转化(EMT)已被证明是癌症转移过程中至关重要的增强机制,因为它提高了癌细胞在循环系统中迁移,侵袭和生存的能力。这项研究旨在调查必需元素锌对肺癌细胞EMT特性的影响。方法采用迁移,侵袭和菌落形成试验,通过测定EMT的行为来评估锌对EMT的影响。通过蛋白质印迹分析检查EMT标记。通过特定的荧光染料和流式细胞仪检测活性氧(ROS)。所有结果均通过ANOVA分析,然后通过事后检验进行个别比较。结果本研究首次揭示锌可诱导肺癌细胞EMT和相关的转移行为。结果表明,用锌处理细胞会导致EMT标记N-钙黏着蛋白,波形蛋白,蜗牛和显着增加,而E-钙黏着蛋白减少。锌处理的细胞表现出间充质样形态,并增加了癌细胞的运动性,其中活化的FAK,Rac1和RhoA显着增加。同样,锌可以增强肺癌细胞的致瘤能力。重要的是,发现潜在的机制是由锌产生细胞内超氧阴离子的能力引起的。锌被证明可以诱导细胞超氧阴离子的产生,EMT标记的上调以及锌处理过的细胞中诱导的细胞迁移和侵袭可以通过治疗特定的超氧阴离子抑制剂MnTBAP来减弱。结论从这项研究中获得的知识可能突出了这一重要元素在EMT和癌症转移的调节中的作用,并充实了对癌细胞生物学领域的理解。

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