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.

中文翻译：

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LncRNA SNHG3使miR-577上调前列腺癌中SMURF1的表达。

前列腺癌仍然是最普遍的癌症之一，也是男性与癌症相关的死亡的主要原因。各种文章介绍了在癌症的发生和发展中重要的功能中发现了长的非编码RNA（lncRNA）。尽管已经在许多癌症中研究了SNHG3（小核仁RNA宿主基因3），但目前尚缺乏关于SNHG3在前列腺癌中的作用和机制的研究。在这项工作中，SNHG3在前列腺癌细胞系中发挥了高表达。SNHG3的抑制抑制细胞增殖，迁移，EMT（上皮-间质转化）过程并促进细胞凋亡。此外，还发现SNHG3可以与miR-577结合。随后，SMURF1（Smad泛素调节因子1）被确定为miR-577的下游靶标，并且与miR-577呈负相关。SNHG3被发现正调控SMURF1表达。此外，急救试验证明pcDNA3.1 / SMURF1的共转染逆转了SNHG3敲低对细胞增殖，迁移，EMT过程和细胞凋亡的影响。SNHG3还促进体内肿瘤发生。以上所有结果均说明，SNHG3通过使miR-577海绵化以上调SMURF1表达来加速前列​​腺癌的进展，这表明SNHG3可能充当前列腺癌患者的生物标志物。