PMID- 31938018 OWN - NLM STAT- PubMed-not-MEDLINE LR - 20220412 IS - 1475-2867 (Print) IS - 1475-2867 (Electronic) IS - 1475-2867 (Linking) VI - 20 DP - 2020 TI - LINC00908 negatively regulates microRNA-483-5p to increase TSPYL5 expression and inhibit the development of prostate cancer. PG - 10 LID - 10.1186/s12935-019-1073-x [doi] LID - 10 AB - BACKGROUND: Accumulating evidence has associated aberrant long non-coding RNAs (lncRNAs) with various human cancers. This study aimed to explore the role of LINC00908 in prostate cancer (PCa) and its possible underlying mechanisms. METHODS: Microarray data associated with PCa were obtained from the Gene Expression Omnibus (GEO) to screen the differentially expressed genes or lncRNAs. Then, the expression of LINC00908 in PCa tissues and cell lines was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The localization of LINC00908 in PCa cells was examined by fluorescence in situ hybridization (FISH). The relationship among LINC00908, microRNA (miR)-483-5p, and TSPYL5 was detected by bioinformatics analysis, dual-luciferase reporter assay, RNA pull-down, RNA binding protein immunoprecipitation (RIP), and FISH assays. Cell biological behaviors were assessed after the expression of LINC00908, miR-483-5p, and TSPYL5 was altered in PCa cells. Lastly, tumor growth in nude mice was evaluated. RESULTS: Poorly expressed LINC00908 was witnessed in PCa tissues and cells. LINC00908 competitively bound to miR-483-5p to up-regulate the TSPYL5 expression. Overexpression of LINC00908 resulted in reduced PCa cell proliferation, migration and invasion, and promoted apoptosis. Additionally, the suppression on PCa cell proliferation, migration and invasion was induced by up-regulation of TSPYL5 or inhibition of miR-483-5p. In addition, in vivo experiments showed that overexpression of LINC00908 inhibited tumor growth of PCa. CONCLUSION: Overall, LINC00908 could competitively bind to miR-483-5p to increase the expression of TSPYL5, thereby inhibiting the progression of PCa. Therefore, LINC00908 may serve as a novel target for the treatment of PCa. CI - (c) The Author(s) 2020. FAU - Fan, Li AU - Fan L AD - Department of Urology, China-Japan Union Hospital of Jilin University, No. 126, Xiantai Street, Changchun, 130033 Jilin People's Republic of China. ISNI: 0000 0004 1771 3349. GRID: grid.415954.8 FAU - Li, Hai AU - Li H AD - Department of Urology, China-Japan Union Hospital of Jilin University, No. 126, Xiantai Street, Changchun, 130033 Jilin People's Republic of China. ISNI: 0000 0004 1771 3349. GRID: grid.415954.8 FAU - Zhang, Yun AU - Zhang Y AD - Department of Urology, China-Japan Union Hospital of Jilin University, No. 126, Xiantai Street, Changchun, 130033 Jilin People's Republic of China. ISNI: 0000 0004 1771 3349. GRID: grid.415954.8 LA - eng PT - Journal Article DEP - 20200109 PL - England TA - Cancer Cell Int JT - Cancer cell international JID - 101139795 PMC - PMC6953146 OTO - NOTNLM OT - Apoptosis OT - Invasion OT - LINC00908 OT - Migration OT - Proliferation OT - Prostate cancer OT - TSPYL5 OT - microRNA-483-5p COIS- Competing interestsThe authors declare that they have no competing interests. EDAT- 2020/01/16 06:00 MHDA- 2020/01/16 06:01 PMCR- 2020/01/09 CRDT- 2020/01/16 06:00 PHST- 2019/08/14 00:00 [received] PHST- 2019/12/13 00:00 [accepted] PHST- 2020/01/16 06:00 [entrez] PHST- 2020/01/16 06:00 [pubmed] PHST- 2020/01/16 06:01 [medline] PHST- 2020/01/09 00:00 [pmc-release] AID - 1073 [pii] AID - 10.1186/s12935-019-1073-x [doi] PST - epublish SO - Cancer Cell Int. 2020 Jan 9;20:10. doi: 10.1186/s12935-019-1073-x. eCollection 2020.