Long non-coding RNA DICER1-AS1-low expression in arsenic-treated A549 cells inhibits cell proliferation by regulating the cell cycle pathway.
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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DOI：
10.1016/j.etap.2021.103617
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发表时间：
2021-02
影响因子：
4.3
通讯作者：
C. Jiang;Mingjun Sun;Shuting Li;J. Tan;Mengjie Wang;Yuefeng He
中科院分区：
文献类型：
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作者：
C. Jiang;Mingjun Sun;Shuting Li;J. Tan;Mengjie Wang;Yuefeng He
砷是一种具有多种毒性的环境污染物，严重威胁着人类的健康。三氧化二砷在体外实验中可以抑制细胞增殖，但其潜在机制尚不完全清楚。LncRNA也参与砷诱导的毒理反应。在我们的研究中，我们发现lncRNA DICER 1-AS 1的表达被亚砷酸钠以剂量依赖的方式显著抑制。DICER 1-AS 1基因沉默可抑制A549细胞的增殖和细胞周期进程。重要的是，DICER 1-AS 1沉默诱导p21上调和Cyclin A2、Cyclin E2、CDK 1和PCNA下调。总之，我们的研究提供了一个新的lncRNA主导的调控机制参与砷诱导的细胞增殖抑制。
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.