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Updated: Jun 2, 2026
An Orthotopic Murine Model of Human Prostate Cancer Metastasis
Published on: September 18, 2013
Inhibition of prostate cancer using RNA interference-directed knockdown of platelet-derived growth factor receptor
Yong Hyun Park1, Su Yeon Seo, Minju Ha
1Department of Urology, Seoul National University College of Medicine, Seoul, Korea.
Objectives:
To determine whether platelet-derived growth factor receptor (PDGFR) plays a role in the tumorigenicity of prostate cancer cells.
Methods:
PC3 prostate cancer cells were transfected with small interfering (si)PDGFR-α and siPDGFR-β, constructed according to the conventional small interfering RNA design standard. Reverse transcriptase polymerase chain reaction, Western blot analysis, and cell growth were studied to determine the characteristics of PDGFR-α and PDGFR-β in vitro. The prostate cancer xenograft model was established to investigate whether knockout of PDGFR-α and PDGFR-β decreases prostate cancer tumor growth in vivo. The experimental groups were defined as group 1 (PC3 cells only), group 2 (PC3 cells transfected with small interfering green fluorescent protein), group 3 (PC3 cells transfected with siPDGFR-α), group 4 (PC3 cells transfected with siPDGFR-β), and group 5 (PC3 cells transfected with siPDGFR-α and siPDGFR-β).
Results:
Western blot analysis revealed that siPDGFR-α and siPDGFR-β significantly blocked PDGFR-α and PDGFR-β protein expression. After 48 hours of transfection of the PC3 cells with siPDGFR-α and siPDGFR-β, the relative fractions of viable cells were reduced to 47.7% (P = .007) and 38.5% (P = .010). In vivo, mice treated with siPDGFR-α or siPDGFR-β and siPDGFR-α plus siPDGFR-β had significant tumor cell growth arrest compared with the mice in groups 1 and 2 (P = .001). In addition, a significant reduction in the microvessel density was observed in tumors from the mice treated with siPDGFR-α or siPDGFR-β and siPDGFR-α plus siPDGFR-β (P < .001).
Conclusions:
The results of the present study suggest that siPDGFR-α and siPDGFR-β might inhibit prostate cancer cell growth by the suppression of angiogenesis.
Insights
Targeting platelet-derived growth factor receptor (PDGFR) with small interfering RNA (siRNA) significantly inhibited prostate cancer cell growth and tumor progression in vivo. This suggests PDGFR inhibition is a potential therapeutic strategy for prostate cancer by suppressing angiogenesis.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Prostate cancer remains a leading cause of cancer-related deaths worldwide.
- The role of platelet-derived growth factor receptor (PDGFR) in prostate cancer tumorigenicity is not fully understood.
- Identifying novel therapeutic targets is crucial for improving patient outcomes.
Purpose of the Study:
- To investigate the role of PDGFR-α and PDGFR-β in prostate cancer cell tumorigenicity.
- To evaluate the efficacy of inhibiting PDGFR-α and PDGFR-β in preclinical models of prostate cancer.
- To determine if PDGFR inhibition affects tumor growth and angiogenesis.
Main Methods:
- PC3 prostate cancer cells were transfected with small interfering RNA (siRNA) targeting PDGFR-α and PDGFR-β.
- In vitro studies assessed PDGFR expression and cell viability using RT-PCR and Western blot.
- In vivo efficacy was evaluated in a prostate cancer xenograft mouse model, assessing tumor growth and microvessel density.
Main Results:
- siPDGFR-α and siPDGFR-β effectively reduced PDGFR-α and PDGFR-β protein expression in PC3 cells.
- Inhibition of PDGFR-α and PDGFR-β significantly decreased prostate cancer cell viability in vitro.
- In vivo, PDGFR inhibition led to significant tumor growth arrest and reduced microvessel density in xenograft models.
Conclusions:
- PDGFR-α and PDGFR-β play a significant role in prostate cancer cell tumorigenicity.
- siPDGFR-α and siPDGFR-β demonstrate potential as therapeutic agents for prostate cancer.
- Inhibition of PDGFR signaling suppresses angiogenesis, contributing to reduced tumor growth.
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