lncRNA MNX1-AS1 promotes prostate cancer progression through regulating miR-2113/MDM2 axis

A growing number of dysregulated long non-coding (lnc)RNAs have been verified to serve an essential role in human prostate cancer. However, the underlying mechanisms of lncRNA MNX1 Antisense RNA 1 (MNX1-AS1) in prostate cancer has not been explored. Therefore, the present study aimed to explore the function of MNX1-AS1 in prostate cancer tumorigenesis and investigate the in-depth mechanism. The expression of MNX1-AS1, microRNA (miR)-2113 and murine double min 2 (MDM2) in prostate cancer tissues and corresponding normal tissues were assessed by reverse transcription-quantitative PCR. The protein expression levels of MDM2 were detected by western blotting. LNCaP and PC-3 cells were transfected with short hairpin (sh)-MNX1-AS1, miR-2113 mimics, miR-2113 inhibitor and pCDH-MDM2 vector using Lipofectamine(®) 3000. Cell proliferation, migration and invasion abilities were assessed by CCK-8 assay, colony formation and Transwell assay, respectively. Dual luciferase reporter assay was carried out to confirm the putative targets of MNX1-AS1 and miR-2113. Tumor formation experiment in nude mice was applied to evaluate the tumor growth effect of MNX1-AS1 in vivo. The expression of MNX1-AS1 was significantly upregulated in the prostate cancer tissues and cell lines. MNX1-AS1 knockdown suppressed the abilities of cell viability and migration and invasion in vitro and inhibited tumor growth in vivo. Additionally, luciferase reporter assay revealed that MNX1-AS1 could target miR-2113 and negatively interacted with miR-2113 in prostate cancer cells. miR-2113 directly targeted to MDM2 and negatively modulated the expression of MDM2. Rescue assays suggested that the viability, migration and invasion of impaired cells triggered by transfection with sh-MNX1-AS1 alone could be recovered by co-transfection with sh-MNX1-AS1 + miR-2113 inhibitor or sh-MNX1-AS1 + pCDH- MDM2 vector. The present study demonstrated that MNX1-AS1 promoted prostate cancer progression through regulating miR-2113/ MDM2 axis.