Abstract
Long non-coding RNAs (lncRNAs) play critical roles in tumorigenesis and cancer progression. The c-Myc upregulated lncRNA MYU (VPS9D1 antisense RNA1, annotated as VPS9D1-AS1) has been reported in several common types of human cancers, which has revealed that lncRNA MYU could function as either an oncogene or a tumor-suppressor gene in different cancer types. However, the function of lncRNA MYU in prostate cancer remains unknown. In the present study, we demonstrated that lncRNA MYU is significantly upregulated in prostate cancer tissues. MYU knockdown impaired prostate cancer cell growth and migration as shown from cell viability, colony formation, Transwell and wound healing assays. In contrast, MYU overexpression displayed opposite effects. No correlation was noted between MYU and its cognate VPS9D1 expression level. Moreover, lncRNA MYU did not regulate the expression of VPS9D1 either at the mRNA or protein level as detected using qRT-PCR and western blotting assays. Furthermore, lncRNA MYU was able to be transported into the extracellular milieu by means of exosomes, and then promoted adjacent cell proliferation and migration. Mechanistically, lncRNA MYU upregulated c-Myc by competitively binding miR-184 and then induced the proliferation of prostate cancer. Thus, this study demonstrated that lncRNA MYU functions as an oncogene in prostate cancer at least in part through the miR-184/c-Myc axis, and may serve as a potential diagnostic biomarker and therapeutic target.