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Updated: Dec 22, 2025
MicroRNA Detection in Prostate Tumors by Quantitative Real-time PCR qPCR
Published on: May 16, 2012
miR-489-3p Inhibits Prostate Cancer Progression by Targeting DLX1
Peide Bai1, Wei Li1, Zhenghua Wan2
1The Key Laboratory of Urinary Tract Tumors and Calculi, Department of Urology Surgery, The First Affiliated Hospital, School of Medicine, Xiamen University, Xiamen 361003, People's Republic of China.
Purpose:
Prostate cancer (PCa) is the third most common cancer in men and the second leading cause of cancer-related death in men. DLX1 belongs to the DLX homeobox family and exhibits antitumor activity in many kinds of tumors. MicroRNAs (miRNAs) play important roles in the progression of cancer. However, whether miRNAs affect the development of PCa by targeting DLX1 has not been determined. In this study, we aimed to investigate the role of miR-489-3p in the regulation of DLX1 expression and PCa progression and to provide a potential therapeutic target for PCa treatment.
Methods And Materials:
The Cancer Genome Atlas database was used to analyze the divergent expression of DLX1 in carcinomas and adjacent normal tissues. The expression level of DLX1 in malignant and normal prostate cells was also measured using RT-qPCR and Western blotting. A dual-luciferase reporter assay was performed to determine whether miR-489-3p directly targets DLX1. We transfected 22Rv1 and DU145 cells with miR-489-3p mimics to overexpress miR-489-3p and then evaluated its effect on cellular function. MTT, EdU, colony formation and cell cycle assays were used to evaluate cell growth. JC-1 and ROS assays with flow cytometry were performed to indirectly analyze apoptosis. Transwell assays were conducted to investigate metastasis.
Results:
The expression level of DLX1 was upregulated in both PCa tissues and cell lines. MiR-489-3p directly targeted DLX1 and downregulated its expression. Overexpression of miR-489-3p significantly suppressed cell growth. MiR-489-3p induced apoptosis through mitochondrial function impairment. Overexpression of miR-489-3p also inhibited cell migration and invasion. DLX1 overexpression reversed the above effects induced by miR-489-3p.
Conclusion:
We identified the involvement of the miR-489-3p/DLX1 pathway in PCa for the first time. In this pathway, miR-489-3p acts as a tumor suppressor by negatively regulating the expression of DLX1. MiR-489-3p may be a potential therapeutic target for PCa treatment.
Insights
MicroRNA-489-3p suppresses prostate cancer (PCa) by targeting DLX1. This finding reveals a novel miR-489-3p/DLX1 pathway and offers a potential therapeutic target for PCa treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Prostate cancer (PCa) is a leading cause of cancer-related death in men.
- DLX1, a homeobox gene, has shown antitumor activity in various cancers.
- MicroRNAs (miRNAs) are critical regulators in cancer progression, but their role in PCa via DLX1 targeting is unclear.
Purpose of the Study:
- To investigate the role of miR-489-3p in regulating DLX1 expression in PCa.
- To determine the impact of the miR-489-3p/DLX1 pathway on PCa progression.
- To explore miR-489-3p as a potential therapeutic target for PCa.
Main Methods:
- Analysis of DLX1 expression in PCa tissues and cell lines using TCGA, RT-qPCR, and Western blotting.
- Dual-luciferase reporter assay to confirm direct targeting of DLX1 by miR-489-3p.
- Functional assays (MTT, EdU, colony formation, cell cycle, apoptosis, migration, invasion) in PCa cells with miR-489-3p overexpression.
Main Results:
- DLX1 expression is upregulated in PCa tissues and cell lines.
- MiR-489-3p directly targets and downregulates DLX1 expression.
- Overexpression of miR-489-3p inhibits PCa cell growth, induces apoptosis, and suppresses migration and invasion.
- DLX1 overexpression counteracted the tumor-suppressive effects of miR-489-3p.
Conclusions:
- The miR-489-3p/DLX1 pathway is identified in PCa for the first time.
- MiR-489-3p functions as a tumor suppressor in PCa by inhibiting DLX1.
- MiR-489-3p represents a promising therapeutic target for prostate cancer treatment.
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