Long noncoding RNA LINC00662 functions as miRNA sponge to promote the prostate cancer tumorigenesis through targeting miR-34a.

Abstract

Mounting evidence indicates that long noncoding RNAs (lncRNAs) play a critical role in the tumorigenesis. Up-regulation of lncRNA LINC00662 (LINC00662) has previously confirmed in several tumors. However, the study of LINC00662 in prostate cancer (PCa) is limited. Hence, to determine the expression pattern and function of LINC00662 in PCa. LINC00662 expression was first detected in PCa cell lines and tissue samples by qRT-PCR. Based on follow-up data, correlations of LINC00662 expression and clinicopathological features, including overall survival, in PCa patients were evaluated. Cell proliferation, migration, invasion, and apoptosis were detected by CCK-8 assay, colony-forming assay, Wound-healing assay, transwell assay, and flow cytometry, respectively. Additionally, LINC00662-specific miRNA was further confirmed using the dual-luciferase reporter assay and RT-PCR. LINC00662 was significantly upregulated in PCa tissues and cell lines compared with adjacent normal tissue and a normal prostate epithelial cell line. Higher expression of LINC00662 was positively associated with distant metastasis and shorter overall survival. In addition, multivariate analysis revealed that tissue LINC00662 expression was confirmed to be an independent prognostic factor for PCa. Furthermore, LINC00662 silencing inhibited the proliferation, migration, and invasion of PC-3 and LNCaP cells, and promoted apoptosis in vitro. Bioinformatics methods and luciferase reporter assay revealed the close link within miR-34a and 3'-untranslated region (UTR) of LINC00662 and further confirmed that LINC00662 could function as a sponge of miR-34a in PCa cells. Also, the results of RT-PCR showed that knockdown of LINC00662 suppressed the expression levels of miR-34a. The current results further enhanced our understanding of the effects of LINC00662 in PCa and may help to provide a new potential target for PCa treatment.