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Updated: Aug 15, 2026

miRNA Expression Analyses in Prostate Cancer Clinical Tissues
Published on: September 8, 2015
Stable suppression of tumorigenicity by Pin1-targeted RNA interference in prostate cancer
Akihide Ryo1, Hiroji Uemura, Hitoshi Ishiguro
1Department of Pathology, Yokohama City University School of Medicine, Yokohama, Japan. aryo@yokohama-cu.ac.jp
Purpose:
The peptidyl-prolyl isomrase Pin1 plays a catalytic role in oncogenesis in solid cancers, including prostate cancer. In the present study, we sought to determine the potential of Pin1-targeted gene silencing in inhibiting cellular growth and tumorigenicity in prostate cancer.
Experimental Design:
A retrovirus-mediated RNA interference targeting Pin1 was expressed in PC3 and LNCaP cells, and cell growth and several transformed properties were investigated.
Results:
The stable expression of Pin1-specific small interfering RNA constructs in PC3 and LNCaP cells significantly reduced cellular proliferation, colony formation, migration, and invasion but strongly enhanced the apoptotic response induced by serum depletion or treatment with anticancer agents. Furthermore, Pin1 depletion significantly suppressed tumorigenic potential in athymic mice, resulting in the inhibition of both tumor growth and angiogeneisis.
Conclusions:
These results strongly suggest that Pin1 plays an important role not only in tumorigenesis but also in the maintenance of the transformed phenotype in prostate cancer cells. Hence, Pin1 may serve as a promising therapeutic target, particularly for recurrent prostate tumors.
Insights
Targeting peptidyl-prolyl isomerase (Pin1) with gene silencing inhibits prostate cancer growth and tumorigenicity. Pin1 depletion suppressed tumor growth, angiogenesis, and enhanced apoptosis, indicating its therapeutic potential.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genetics
Background:
- The peptidyl-prolyl isomerase Pin1 is implicated in oncogenesis across various solid tumors.
- Pin1's role in prostate cancer progression and tumorigenicity warrants further investigation.
Purpose of the Study:
- To evaluate the efficacy of Pin1-targeted gene silencing in inhibiting prostate cancer cell growth and tumorigenicity.
- To explore Pin1 as a potential therapeutic target for prostate cancer, especially recurrent forms.
Main Methods:
- Retrovirus-mediated RNA interference was employed to silence Pin1 expression in PC3 and LNCaP prostate cancer cell lines.
- Cellular proliferation, colony formation, migration, invasion, and apoptosis were assessed.
- Tumorigenic potential was evaluated in vivo using athymic mouse models.
Main Results:
- Pin1 gene silencing significantly reduced prostate cancer cell proliferation, colony formation, migration, and invasion.
- Pin1 depletion enhanced apoptosis induced by serum depletion or anticancer agents.
- In vivo studies demonstrated that Pin1 suppression inhibited tumor growth and angiogenesis in athymic mice.
Conclusions:
- Pin1 is crucial for both the tumorigenesis and the maintenance of the transformed phenotype in prostate cancer cells.
- Pin1 represents a promising therapeutic target for prostate cancer, with potential benefits for recurrent tumors.
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