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首页> 外文期刊>Environmental toxicology and pharmacology >Long non-coding RNA DICER1-AS1-low expression in arsenic-treated A549 cells inhibits cell proliferation by regulating the cell cycle pathway
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Long non-coding RNA DICER1-AS1-low expression in arsenic-treated A549 cells inhibits cell proliferation by regulating the cell cycle pathway

机译:在砷处理的A549细胞中长的非编码RNA Dicer1-AS1-LOW表达通过调节细胞周期途径来抑制细胞增殖

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摘要

Arsenic, an environmental pollution with diverse toxicities, incurs public health problems. Arsenic trioxide could inhibit cell proliferation in vitro experiments, but the underlying mechanisms are not fully known. LncRNAs are also involved in the arsenic-induced toxicological responses. In our study, we found that the expression of lncRNA DICER1-AS1 was significantly inhibited by sodium arsenite in a dose-dependent manner. DICER1-AS1 silencing decreased the A549 cell proliferation and inhibited cell cycle progression. Importantly, DICER1-AS1 silencing induced upregulation of p21 and downregulation of Cyclin A2, Cyclin E2, CDK1 and PCNA. In conclusion, our study provided a new lncRNA-dictated regulatory mechanism participating in arsenic-induced inhibition of cell proliferation.
机译:砷,具有不同毒性的环境污染,引发公共卫生问题。 砷三氧化砷可以抑制细胞增殖在体外实验,但下面的机制尚不完全已知。 LNCRNA也参与了砷诱导的毒理学反应。 在我们的研究中,我们发现LNCRNA Dicer1-AS1的表达被剂量依赖性方式显着抑制了砷酸钠。 Dicer1-AS1沉默降低了A549细胞增殖和抑制细胞周期进展。 重要的是,Dicer1-AS1诱导P21,细胞周期蛋白A2,Cyclin E2,CDK1和PCNA的下调的诱导上调。 总之,我们的研究提供了参与砷诱导的细胞增殖抑制的新的LNCRNA标志性机制。

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