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Updated: Sep 22, 2025

miRNA Expression Analyses in Prostate Cancer Clinical Tissues
Published on: September 8, 2015
lncRNA MNX1‑AS1 promotes prostate cancer progression through regulating miR‑2113/MDM2 axis
Dong Liang1, Chuanjie Tian2, Xiaowen Zhang3
1Department of Urology Surgery, Binhai County Hospital of TCM, Yancheng, Jiangsu 224500, P.R. China.
Abstract:
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.
Insights
Long non-coding RNA MNX1 Antisense RNA 1 (MNX1-AS1) promotes prostate cancer by regulating the miR-2113/MDM2 axis. Silencing MNX1-AS1 inhibits tumor growth, migration, and invasion, offering a potential therapeutic target for prostate cancer.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in human cancers.
- The specific function and mechanism of lncRNA MNX1 Antisense RNA 1 (MNX1-AS1) in prostate cancer remain largely unexplored.
Purpose of the Study:
- To investigate the role of MNX1-AS1 in prostate cancer development and progression.
- To elucidate the underlying molecular mechanism involving microRNA-2113 (miR-2113) and murine double min 2 (MDM2).
Main Methods:
- Quantitative PCR and Western blotting were used to assess MNX1-AS1, miR-2113, and MDM2 expression in prostate cancer tissues and cell lines.
- In vitro cell assays (proliferation, migration, invasion) and in vivo tumor formation experiments were conducted.
- Dual luciferase reporter assays confirmed interactions between MNX1-AS1, miR-2113, and MDM2.
Main Results:
- MNX1-AS1 expression was significantly upregulated in prostate cancer tissues and cells.
- Knockdown of MNX1-AS1 inhibited cell viability, migration, invasion, and tumor growth.
- MNX1-AS1 was found to target miR-2113, which in turn targets MDM2, indicating an MNX1-AS1/miR-2113/MDM2 regulatory axis.
Conclusions:
- MNX1-AS1 promotes prostate cancer progression by modulating the miR-2113/MDM2 pathway.
- Targeting MNX1-AS1 presents a potential therapeutic strategy for prostate cancer treatment.
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