Wang Xiaoyan, Qi Guanbin, Zhang Juanjuan, Wu Jingcan, Zhou Nannan, Li Lei, Ma Jing
Department of Pneumology, Huaihe Hospital of Henan University , Kaifeng, China .
DNA Cell Biol. 2017 Nov;36(11):892-900. doi: 10.1089/dna.2017.3830. Epub 2017 Sep 5.
Small nucleolar RNA host gene 12 (SNHG12) is a novel long noncoding RNA identified to be upregulated and functions as an oncogene in several cancers. However, the function of SNHG12 and its target genes in modulating nonsmall cell lung cancer (NSCLC) development are rarely reported. In the present study, we validated that SNHG12 was overexpressed, while miR-138 was low-expressed, in NSCLC cells compared with normal human lung epithelial cells. SNHG12 harbored the binding site of miR-138 and inversely regulated the expression miR-138. Knockdown of SNHG12 inhibited proliferation and colony-forming ability, induced apoptosis, and increased caspase-3 activity of NSCLC cells, whereas miR-138 downregulation restored these effects. Furthermore, SNHG12 knockdown decreased volumes and weight of xenograft tumors in a NSCLC mouse model. Taken together, these findings suggested that knockdown of SNHG12 suppressed cell growth and induced apoptosis by upregulating miR-138 in NSCLC.
小核仁RNA宿主基因12(SNHG12)是一种新发现的长链非编码RNA,已被证实其在多种癌症中表达上调并发挥癌基因的作用。然而,SNHG12及其靶基因在调节非小细胞肺癌(NSCLC)发生发展中的作用鲜有报道。在本研究中,我们验证了与正常人肺上皮细胞相比,SNHG12在NSCLC细胞中高表达,而miR-138低表达。SNHG12含有miR-138的结合位点,并反向调节miR-138的表达。敲低SNHG12可抑制NSCLC细胞的增殖和集落形成能力,诱导细胞凋亡,并增加caspase-3活性,而miR-138下调可恢复这些作用。此外,在NSCLC小鼠模型中,敲低SNHG12可减小异种移植瘤的体积和重量。综上所述,这些发现表明,敲低SNHG12通过上调miR-138抑制NSCLC细胞生长并诱导细胞凋亡。