Long noncoding RNAs (lncRNAs) have been reported to play vital roles in the development of human cancers, but our understandings of most lncRNAs in cancers are still limited. Recently, accumlating evidences have showed that many RNA transcripts could function as competing endogenous RNAs (ceRNAs) by competitively binding common microRNAs. In this study, we demonstrated that a lncRNA, Small Nucleolar RNA Host Gene 1 (SNHG1), as a ceRNA for miR-199a-3p, played a critical role in prostate cancer cell proliferation. We found that SNHG1 was aberrantly up-regulated in prostate carcinoma tissues; while, miR-199a-3p was abnormally down-regulated. The level of SNHG1 in prostate cancer was significantly negatively correlated with that of miR-199a-3p. Our data indicated that SNHG1 could interact with miR-199a-3p and inhibit the activity of miR-199a-3p in prostate cancer cells. In addition, miR-199a-3p could target the 3' UTR of CDK7 and suppress CDK7 expression. More importantly, SNHG1 increased CDK7 expression by competitively binding miR-199a-3p, and then promoted cell proliferation and cell cycle progression in prostate cancer. Taken together, these findings elucidated a novel mechanism of prostate cancer progression. Thus, SNHG1 might serve as a potential target for prostate cancer therapies.
Keywords: CDK7; Proliferation; Prostate cancer; SNHG1; miR-199a-3p.
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