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.

砷是一种具有多种毒性的环境污染，会引起公共卫生问题。三氧化二砷可在体外实验中抑制细胞增殖，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，我们发现亚砷酸钠以剂量依赖的方式显着抑制了lncRNA DICER1-AS1的表达。DICER1-AS1沉默降低A549细胞增殖并抑制细胞周期进程。重要的是，DICER1-AS1沉默诱导p21的上调和Cyclin A2，Cyclin E2，CDK1和PCNA的下调。总之，我们的研究提供了一种新的lncRNA调控机制，参与了砷诱导的细胞增殖抑制。