Li Teng, Xing Yi, Yang Fan, Sun Yangyang, Zhang Shaojin, Wang Qingwei, Zhang Weixing
Department of Urology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Department of Opthalmology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Cancer Med. 2020 Jun;9(11):3852-3862. doi: 10.1002/cam4.2992. Epub 2020 Apr 5.
Prostate cancer remains one of the most prevalent cancers and the main causes of cancer-related deaths in males. Various articles introduced that long noncoding RNAs (lncRNAs) are found in vital functions in the development and progression of cancers. Although SNHG3 (small nucleolar RNA host gene 3) has been investigated in many cancers, now researches on the role and mechanism of SNHG3 in prostate cancer are lacked. In this work, SNHG3 exerted high expression in prostate cancer cell lines. Suppression of SNHG3 inhibited cell proliferation, migration, EMT (epithelial-mesenchymal transition) process and promoted cell apoptosis. Additionally, it was found that SNHG3 could bind with miR-577. Subsequently, SMURF1 (Smad ubiquitination regulatory factor 1) was identified as a downstream target of miR-577 and had a negative correlation with miR-577. SNHG3 was found to positively regulate SMURF1 expression. Furthermore, rescue assays demonstrated that co-transfection of pcDNA3.1/SMURF1 reversed the effects of SNHG3 knockdown in cell proliferation, migration, EMT process and cell apoptosis. SNHG3 also promoted tumorigenesis in vivo. All the results above explained that SNHG3 accelerated prostate cancer progression by sponging miR-577 to up-regulate SMURF1 expression, suggesting that SNHG3 may act as a biomarker for prostate cancer patients.
前列腺癌仍然是最常见的癌症之一,也是男性癌症相关死亡的主要原因。各种文章介绍,长链非编码RNA(lncRNAs)在癌症的发生和发展中发挥着重要作用。尽管SNHG3(小核仁RNA宿主基因3)已在多种癌症中得到研究,但目前关于SNHG3在前列腺癌中的作用和机制的研究尚缺乏。在这项研究中,SNHG3在前列腺癌细胞系中高表达。抑制SNHG3可抑制细胞增殖、迁移、上皮-间质转化(EMT)过程并促进细胞凋亡。此外,研究发现SNHG3可与miR-577结合。随后,SMURF1(Smad泛素化调节因子1)被鉴定为miR-577的下游靶点,且与miR-577呈负相关。研究发现SNHG3可正向调节SMURF1的表达。此外,挽救实验表明,共转染pcDNA3.1/SMURF1可逆转SNHG3敲低对细胞增殖、迁移、EMT过程和细胞凋亡的影响。SNHG3在体内也促进肿瘤发生。上述所有结果表明,SNHG3通过海绵吸附miR-577上调SMURF1表达,从而加速前列腺癌进展,提示SNHG3可能作为前列腺癌患者的生物标志物。