Department of Urology, The Fourth Affiliated Hospital Zhejiang University School of Medicine, Yiwu.
Department of Urology, The Second Hospital of Jiaxing, Jiaxing.
Anticancer Drugs. 2021 Mar 1;32(3):286-295. doi: 10.1097/CAD.0000000000000916.
Prostate cancer is the most common urinary malignancy in males. Long noncoding RNA small nucleolar RNA host gene 1 (lncRNA SNHG1) has been reported to play a crucial role in the development of various cancers. However, the understanding of SNHG1 in prostate cancer is still limited and needs further investigation. In this study, we found the level of SNHG1 was significantly upregulated in prostate cancer tissues and cells. Knockdown of SNHG1 significantly suppressed proliferation, migration and invasion and promoted cell apoptosis in prostate cancer cells. In addition, knockdown of SNHG1 significantly downregulated proliferating cell nuclear antigen and upregulated cleaved caspase-3. MiR-383-5p was identified to be a target of SNHG1 by bioinformatics analysis, dual-luciferase reporter assay, RNA immunoprecipitation assay and RNA pull-down assay. MiR-383-5p was significantly downregulated in prostate cancer tissues and cells. Inhibition of miR-383-5p could partially restore the effects of SNHG1 knockdown on prostate cancer cell proliferation, apoptosis, migration and invasion. Furthermore, murine xenograft models were established to investigate the effects of SNHG1 and miR-383-5p in tumorigenesis in vivo. We found SNHG1 knockdown or miR-383-5p overexpression repressed tumor growth in vivo. In conclusion, SNHG1 contributed to prostate cancer progression by targeting miR-383-5p, elucidating that SNHG1 might be a target for prostate cancer therapy.
前列腺癌是男性最常见的泌尿系统恶性肿瘤。长链非编码 RNA 小核仁 RNA 宿主基因 1（lncRNA SNHG1）已被报道在各种癌症的发展中发挥关键作用。然而，SNHG1 在前列腺癌中的作用仍知之甚少，需要进一步研究。在本研究中，我们发现 SNHG1 在前列腺癌组织和细胞中的水平显著上调。SNHG1 的敲低显著抑制了前列腺癌细胞的增殖、迁移和侵袭，并促进了细胞凋亡。此外，SNHG1 的敲低显著下调了增殖细胞核抗原并上调了 cleaved caspase-3。生物信息学分析、双荧光素酶报告实验、RNA 免疫沉淀实验和 RNA 下拉实验鉴定 miR-383-5p 是 SNHG1 的一个靶基因。miR-383-5p 在前列腺癌组织和细胞中显著下调。抑制 miR-383-5p 可以部分恢复 SNHG1 敲低对前列腺癌细胞增殖、凋亡、迁移和侵袭的影响。此外，建立了小鼠异种移植模型来研究 SNHG1 和 miR-383-5p 在体内肿瘤发生中的作用。我们发现 SNHG1 的敲低或 miR-383-5p 的过表达抑制了体内肿瘤的生长。总之，SNHG1 通过靶向 miR-383-5p 促进前列腺癌的进展，表明 SNHG1 可能是前列腺癌治疗的一个靶点。
