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Updated: Apr 18, 2026

MicroRNA Detection in Prostate Tumors by Quantitative Real-time PCR qPCR
Published on: May 16, 2012
MiR-203 down-regulates Rap1A and suppresses cell proliferation, adhesion and invasion in prostate cancer
Jun Xiang1, Cuidong Bian2, Hao Wang3
1Department of Urology, Tongji Hospital, Tongji University School of Medicine, NO 389 Xinchun road, Shanghai, 200065, China. zhuxufifa2007@163.com.
Objective:
Evidence supports an important role for miR-203 in the regulation of the proliferation, migration and invasion of prostate cancer (PCa) cells. However, the exact mechanisms of miR-203 in PCa are not entirely clear.
Methods:
We examined the expression of miR-203 in prostate cancer tissues, adjacent normal tissues, PCa cell lines and normal prostate epithelial cells by qRT-PCR. Then, the effects of miR-203 or Rap1A on proliferation, adhesion and invasion of PCa cells were assayed using CKK-8, adhesion analysis, and transwell invasion assays. Luciferase reporter assay was performed to assess miR-203 binding to Rap1A mRNA. Tumor growth was assessed by subcutaneous inoculation of cells into BALB/c nude mice.
Results:
Here, we confirmed that the expression of miR-203 was significantly downregulated in prostate cancer specimens compared with matched adjacent normal prostate specimens. Mechanistic dissection revealed that miR-203 mediated cell proliferation, adhesion and invasion in vitro, and tumor growth in vivo, as evidenced by reduced RAC1, p-PAK1, and p-MEK1 expression. In addition, we identified Rap1A as a direct target suppressed by miR-203, and there was an inverse relationship between the expression of miR-203 and Rap1A in PCa. Knockdown of Rap1A phenocopied the effects of miR-203 on PCa cell growth and invasion. Furthermore, Rap1A over-expression in PCa cells partially reversed the effects of miR-203-expression on cell adhesion and invasion.
Conclusions:
These findings provide further evidence that a crucial role for miR-203 in inhibiting metastasis of PCa through the suppression of Rap1A expression.
Insights
MicroRNA-203 (miR-203) inhibits prostate cancer (PCa) metastasis by targeting Rap1A. Downregulation of miR-203 promotes PCa cell proliferation, adhesion, and invasion, underscoring its tumor-suppressive role.
Area of Science:
- Molecular Biology
- Oncology
- Gene Regulation
Background:
- MicroRNA-203 (miR-203) is implicated in regulating prostate cancer (PCa) cell proliferation, migration, and invasion.
- The precise molecular mechanisms of miR-203 in PCa progression remain incompletely understood.
Purpose of the Study:
- To elucidate the role and underlying mechanisms of miR-203 in prostate cancer.
- To investigate the regulatory relationship between miR-203 and its potential targets in PCa.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) to assess miR-203 expression in PCa tissues and cell lines.
- In vitro assays (CCK-8, adhesion, transwell invasion) to evaluate the functional impact of miR-203 and Rap1A on PCa cells.
- Luciferase reporter assay to confirm direct binding of miR-203 to Rap1A mRNA.
- In vivo tumor growth assessment in nude mice.
Main Results:
- miR-203 expression was significantly downregulated in prostate cancer specimens.
- miR-203 suppressed PCa cell proliferation, adhesion, invasion, and tumor growth in vitro and in vivo.
- Rap1A was identified as a direct target of miR-203, with an inverse expression correlation in PCa.
- Rap1A knockdown mimicked miR-203's suppressive effects, while Rap1A overexpression partially reversed them.
Conclusions:
- miR-203 acts as a tumor suppressor in prostate cancer by inhibiting metastasis.
- Suppression of Rap1A expression by miR-203 is a key mechanism underlying its anti-metastatic effects in PCa.
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