Long noncoding RNA SNHG1 promotes human prostate cancer progression by sponging miR-383-5p.

Abstract

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.