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Gene. 2019 Apr 11. pii: S0378-1119(19)30386-5. doi: 10.1016/j.gene.2019.04.033. [Epub ahead of print]

LncRNA SNHG15 acts as an oncogene in prostate cancer by regulating miR-338-3p/FKBP1A axis.

Author information

1
Department of Urology, Zhejiang Provincial People's Hospital, Hangzhou Medical College, Hangzhou, Zhejiang 310014, China.
2
Department of Urology, Zhejiang Provincial People's Hospital, Hangzhou Medical College, Hangzhou, Zhejiang 310014, China. Electronic address: Zhang123_Q@163.com.

Abstract

Long non-coding RNAs (lncRNAs) are crucial regulators in the progression of various diseases. Although the role of lncRNAs in prostate cancer (PCa) has been studied in recent years, there are still numerous lncRNAs need to be elucidated. This study aims to detect the role of lncRNA small nucleolar RNA host gene 15 (SNHG15) in human prostate cancer. Using qRT-PCR analysis, we identified the upregulation of SNHG15 in PCa cell lines. Loss-of function assays were conducted to determine the regulatory effect of SNHG15 on PCa cell proliferation, migration and epithelial-mesenchymal transition (EMT). According to the results of functional assays, we found that knockdown of SNHG15 impaired cell viability, suppressed cell proliferation, inhibited cell migration and invasion, reversed EMT progress. All these findings revealed the oncogenic function of SNHG15 in PCa. Mechanism investigation revealed that SNHG15 was located in the cytoplasm of PCa cells and acted as a molecular sponge of microRNA-338-3p (miR-338-3p). Moreover, FKBP prolyl isomerase 1A (FKBP1A) was a target of miR-338-3p. This investigation demonstrated that SNHG15 may serve as a competing endogenous RNA (ceRNA) to regulate miR-338-3p and FKBP1A. Finally, the involvement of miR-338-3p and FKBP1A in SNHG15-mediated biological function was demonstrated by performing rescue assays. In summary, our study revealed the function of a novel pathway in PCa.

KEYWORDS:

FKBP1A; Proliferation; Prostate cancer; SNHG15; miR-338-3p

PMID:
30981837
DOI:
10.1016/j.gene.2019.04.033

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