ADP-核糖基化因子样肿瘤抑制基因 1 是小鸟苷三磷酸酶 Ras 超家族的成员，已知该家族参与人类癌症多阶段发展的多种调控途径。此外，据报道，与对照相比，癌细胞系和肿瘤组织中 ADP-核糖基化因子样抑癌基因 1 的表达水平显着降低。因此，ADP-核糖基化因子样肿瘤抑制基因1基因的调节缺陷似乎在包括肺癌在内的人类癌症的形成和发展中具有关键的肿瘤抑制作用。此外，调节ADP-核糖基化因子样抑癌基因1表达的microRNA此前尚未被描述过。因此，本研究旨在揭示miR-16-5p对ADP-核糖基化因子样抑癌基因1基因调控的影响。采用A549肺腺癌细胞。对于 miR-16-5p 合成的 microRNA 模拟物和抑制剂的过表达和沉默实验，分别使用。借助实时定量聚合酶链式反应实现基因表达分析。MiR-16-5p 被确定为 ADP-核糖基化因子样抑癌基因 1 的预测靶标，并直接靶向 ADP-核糖基化因子-的表达。就像过表达和沉默实验所揭示的抑癌基因 1 一样。具体而言，发现miR-16-5p过表达的A549细胞显示ADP-核糖基化因子样肿瘤抑制基因1基因表达减少，而miR16-5p抑制的细胞显示表达增加。这些发现可能表明miR-16-5p是转录后调节ADP核糖基化因子样肿瘤抑制基因1表达的直接调节性microRNA。总的来说，miR-16-5p似乎是转录后参与的关键调节分子。 ADP-核糖基化因子样抑癌基因 1 的调节，可能是肺癌中该基因下调的原因。

ADP-ribosylation factor-like tumor suppressor gene 1 is a member of the Ras superfamily of small guanosine triphosphatases that are known to be involved in multiple regulatory pathways in the multistage development of human cancers. Also, ADP-ribosylation factor-like tumor suppressor gene 1 expression levels have been reported to be dramatically lower in both cancer cell lines and tumor tissues compared to controls. Accordingly, defects in the regulation of the ADP-ribosylation factor-like tumor suppressor gene 1 gene seems have key tumor suppressive effects in the formation and development of human cancers including lung cancer. Moreover, microRNAs regulating the expression of ADP-ribosylation factor-like tumor suppressor gene 1 have not been described previously. Accordingly, the present study aimed to reveal the influence of miR-16-5p on the regulation of ADP-ribosylation factor-like tumor suppressor gene 1 gene.A549 lung adenocarcinoma cells were used. For the overexpression and silencing experiments of miR-16-5p synthetic microRNA mimics and inhibitors were used, respectively. Gene expression analyses were achieved with the help of quantitative real-time polymerase chain reaction.MiR-16-5p was identified to be predictive target of ADP-ribosylation factor-like tumor suppressor gene 1 and directly targets the expression of ADP-ribosylation factor-like tumor suppressor gene 1 as revealed by the overexpression and silencing experiments. Specifically, it was found that miR-16-5p-overexpressed A549 cells showed a decrease in ADP-ribosylation factor-like tumor suppressor gene 1 gene expression, whereas miR16-5p-suppressed cells showed an increase in expression. These findings possibly suggest that miR-16-5p is the direct regulatory microRNA that posttranscriptionally regulates the expression of ADP-ribosylation factor-like tumor suppressor gene 1.Collectively, miR-16-5p seems to be a key regulatory molecule involved in the posttranscriptional regulation of the ADP-ribosylation factor-like tumor suppressor gene 1, and it might be responsible for the downregulation of this gene in lung cancer.