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Updated: Jan 21, 2026
An Orthotopic Murine Model of Human Prostate Cancer Metastasis
Published on: September 18, 2013
miR-214-5p inhibits human prostate cancer proliferation and migration through regulating CRMP5
Chenghao Zheng1, Kai Guo2, Binshen Chen2
1The Second Clinical Medical School (Zhujiang Hospital), Southern Medical University, Guangzhou, Guangdong, China.
Objectives:
In men, human prostate cancer (PCa) has become the second most common cancer. miRNAs are short non-coding RNAs that can inhibit target gene mRNAs. Studies have showed that the alternation of miRNAs expression in cancer is relevant to pathogenesis of tumor. In present study, we aimed to investigate functions of miR-214-5p in PCa.
Materials And Methods:
10 paired human prostate tumor tissues and homologous para-tumor tissues were recruited, and the levels of miR-214-5p and CRMP5 were respectively determined by qRT-PCR assay. Luciferase activity analysis was performed to explore the regulation of CRMP5 mRNA 3'UTR by miR-214-5p. Then, cell experiments, including cell proliferation, apoptosis, cell cycle, migration and colony formation ability, were performed after proper plasmids or RNAs transfection.
Results:
In PCa tissues and cell lines, expression of miR-214-5p was decreased compared with para-tumor tissues or normal prostate epithelial cell lines. Luciferase activity assay showed a direct combination of miR-214-5p and CRMP5 mRNA 3'UTR, and indicated that the absence of miR-214-5p in PCa cells may contributes to a high level of CRMP5. Cell experiments showed that miR-214-5p can induce inhibition of tumor cell growth, migration and colony forming efficiency, promotion of apoptosis and G1-phase arrest, on the other hand, co-expression of CRMP5 somewhat counteracted these phenotype induced by miR-214-5p.
Conclusion:
Taken together, miR-214-5p shows tumor suppression effects in PCa cells. Loss expression of miR-214-5p in PCa increase levels of CRMP5 through regulating CRMP5 3'UTR, which could be a potential therapy target for PCa.
Insights
Reduced miR-214-5p levels in prostate cancer (PCa) promote tumor growth by increasing CRMP5. Restoring miR-214-5p shows potential for PCa therapy.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- Prostate cancer (PCa) is a leading cancer in men.
- MicroRNAs (miRNAs) are key regulators of gene expression implicated in cancer pathogenesis.
- Dysregulation of miRNA expression is observed in various cancers, including PCa.
Purpose of the Study:
- To investigate the functional role of miR-214-5p in prostate cancer.
- To elucidate the relationship between miR-214-5p and its target gene, CRMP5, in PCa.
- To explore the therapeutic potential of targeting miR-214-5p in PCa.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) to measure miR-214-5p and CRMP5 levels in PCa tissues and cell lines.
- Luciferase reporter assays to confirm direct binding of miR-214-5p to the CRMP5 mRNA 3'UTR.
- In vitro cell-based assays (proliferation, apoptosis, cell cycle, migration, colony formation) following transfection with miR-214-5p mimics/inhibitors and CRMP5 expression vectors.
Main Results:
- miR-214-5p expression was significantly decreased in PCa tissues and cell lines compared to normal controls.
- Luciferase assays confirmed that miR-214-5p directly targets the 3'UTR of CRMP5 mRNA.
- Overexpression of miR-214-5p suppressed PCa cell proliferation, migration, and colony formation, induced apoptosis, and caused G1-phase arrest.
- Conversely, reduced miR-214-5p expression led to increased CRMP5 levels and promoted tumor cell growth.
- CRMP5 partially counteracted the tumor-suppressive effects of miR-214-5p.
Conclusions:
- miR-214-5p acts as a tumor suppressor in prostate cancer.
- Loss of miR-214-5p in PCa contributes to elevated CRMP5 levels via direct targeting of its 3'UTR.
- The miR-214-5p/CRMP5 axis represents a potential therapeutic target for prostate cancer treatment.
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