eISSN: 1896-9151
ISSN: 1734-1922
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abstract:
Basic research

Long noncoding RNA SNHG20 promotes prostate cancer progression via upregulating DDX17

Xing-Cheng Wu
,
Wei-Gang Yan
,
Zhi-Gang Ji
,
Guo-Yang Zheng
,
Guang-Hua Liu

Online publish date: 2019/06/06
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Introduction
Accumulating evidence has revealed the critical roles of long noncoding RNAs (lncRNAs) in various cancers. LncRNA SNHG20 has been shown to be a cancer-associated lncRNA in several cancers with diverse mechanisms. However, the clinical references, biological roles, and mechanisms of action of SNHG20 in prostate cancer (PCa) are still unclear.

Material and methods
The expression of SNHG20 in PCa tissues and cell lines was detected by RT-qPCR. The correlations between SNHG20 expression and clinicopathological features were analyzed by 2 test. The roles of SNHG20 in PCa cell proliferation and migration were detected by CCK-8, EdU incorporation, and transwell assays. The regulatory mechanisms of SNHG20 on DDX17 were detected by dual luciferase reporter assay, RT-qPCR, and western blot.

Results
SNHG20 is highly expressed in PCa tissues and cell lines. High expression of SNHG20 is positively correlated with high Gleason score and advanced tumor stage. Functional experiments revealed that overexpression of SNHG20 promotes PCa cell proliferation and migration. SNHG20 knockdown represses PCa cell proliferation and migration. Mechanistically, SNHG20 was verified to act as a competing endogenous RNA (ceRNA) to upregulate DDX17. DDX17 is also highly expressed and has oncogenic roles in PCa. Furthermore, the expression of DDX17 is significantly positively correlated with that of SNHG20 in PCa tissues. Depletion of DDX17 reverses the oncogenic roles of SNHG20 in PCa.

Conclusions
These data showed that SNHG20 promotes PCa cell proliferation and migration via acting as a ceRNA to upregulate DDX17. This study also suggested that SNHG20 may be a potential novel therapeutic target for PCa.

keywords:

prostate cancer, long noncoding RNA, competing endogenous RNA, DDX17, proliferation, migration

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