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Updated: Oct 12, 2025

MicroRNA Detection in Prostate Tumors by Quantitative Real-time PCR qPCR
Published on: May 16, 2012
miR-33b-3p Acts as a Tumor Suppressor by Targeting DOCK4 in Prostate Cancer
Yu Mei1, Kai Li1, Zhicheng Zhang2
1School of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Abstract:
Despite that androgen-deprivation therapy results in long-lasting responses, the disease inevitably progresses to metastatic castration-resistant prostate cancer. In this study, we identified miR-33b-3p as a tumor suppressor in prostate cancer. miR-33b-3p was significantly reduced in prostate cancer tissues, and the low expression of miR-33b-3p was correlated with poor overall survival of prostate cancer patients. Overexpression of miR-33b-3p inhibited both migration and invasion of highly metastatic prostate cancer cells whereas inhibition of miR-33b-3p promoted those processes in lowly metastatic cells. The in vivo results demonstrate that miR-33b-3p suppresses metastasis of tail vein inoculated prostate cancer cells to lung and lymph nodes in mice. DOCK4 was validated as the direct target of miR-33b-3p. miR-33b-3p decreased the expression of DOCK4 and restoration of DOCK4 could rescue miR-33b-3p inhibition on cell migration and invasion. Moreover, downregulation of miR-33b-3p was induced by bortezomib, the clinically used proteasome inhibitor, and overexpression of miR-33b-3p enhanced the insufficient inhibition of bortezomib on migration and invasion as well as metastasis of prostate cancer cells. In summary, our findings demonstrate that miR-33b-3p suppresses metastasis by targeting DOCK4 in prostate cancer. Our results suggest that enhancing miR-33b-3p expression may provide a promising therapeutic strategy for overcoming that proteasome inhibitor's poor efficacy against metastatic prostate cancer.
Insights
MicroRNA miR-33b-3p acts as a tumor suppressor in prostate cancer, inhibiting metastasis by targeting DOCK4. Enhancing miR-33b-3p may improve treatment for metastatic prostate cancer.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Prostate cancer often progresses to metastatic castration-resistant prostate cancer despite androgen-deprivation therapy.
- Identifying novel therapeutic targets is crucial for managing advanced prostate cancer.
Purpose of the Study:
- To investigate the role of miR-33b-3p in prostate cancer metastasis.
- To identify the molecular targets and therapeutic potential of miR-33b-3p.
Main Methods:
- Analysis of miR-33b-3p expression in prostate cancer tissues and correlation with patient survival.
- In vitro studies on prostate cancer cell migration and invasion.
- In vivo metastasis models in mice.
- Validation of DOCK4 as a direct miR-33b-3p target.
- Investigation of bortezomib's effect on miR-33b-3p expression and prostate cancer cell behavior.
Main Results:
- miR-33b-3p expression is significantly reduced in prostate cancer tissues and correlates with poor survival.
- Overexpression of miR-33b-3p inhibits prostate cancer cell migration and invasion, while inhibition promotes these processes.
- miR-33b-3p suppresses lung and lymph node metastasis in vivo.
- DOCK4 is a direct target of miR-33b-3p, and its restoration rescues miR-33b-3p's inhibitory effects.
- Bortezomib downregulates miR-33b-3p, and miR-33b-3p overexpression enhances bortezomib's efficacy against metastasis.
Conclusions:
- miR-33b-3p functions as a tumor suppressor in prostate cancer by inhibiting metastasis through targeting DOCK4.
- Enhancing miR-33b-3p expression represents a potential therapeutic strategy to improve treatment outcomes for metastatic prostate cancer, particularly in combination with proteasome inhibitors.
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