Long non-coding RNA VIM-AS1 promotes prostate cancer growth and invasion by regulating epithelial-mesenchymal transition.

Long non-coding RNAs (lncRNAs) have been elucidated to participate in the development and progression of prostate cancer (PCa). Here, we aimed to detect the expression, function and further underlying the mechanisms of lncRNA VIM-AS1 in PCa. A total of 88 PCa and 31 normal prostate tissue samples were collected after surgical resection. Expression of VIM-AS1 in the samples was detected using quantitative real-time polymerase chain reaction (qRT-PCR). Similarly, the relative level of VIM-AS1 in PCa cell lines to normal prostate cell line was also measured. Lentivirus for up- or down-regulating VIM-AS1 was used to establish the experimental cells. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay and colony formation assay were utilized to study the proliferation, and wound-healing, and transwell assay was utilized to study the migration and invasion abilities of established cells. Furthermore, western blot was employed to detect the expression of the related proteins. VIM-AS1 was expressed significantly higher in PCa tissues comparing with normal prostate tissues. Higher VIM-AS1 expression predicted larger tumor size, metastasis and advanced TNM stage. Inhibition of VIM-AS1 reduced cell proliferation, migration and invasion of PC3 cells but overexpression of VIM-AS1 promoted cell growth, migration and invasion. We also found VIM-AS1 promoted the expression of vimentin, which further promoted epithelial-mesenchymal transition (EMT) of PCa cells. lncRNA VIM-AS1 was overexpressed in PCa tissues and cell lines and promoted PCa proliferation and metastasis via EMT through regulating vimentin, which might provide a novel target for the diagnosis and therapy for PCa.