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Updated: Jun 16, 2026
Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients
Published on: November 19, 2019
[Effects of RNA interference upon EGFR and its intracellular effective proteins in prostate cancer]
Hui-min Long1, Wei-guo Chen, Xie-qiao Yang
1Department of Urology, the Affiliated Lihuili Hospital of Ningbo University, Ningbo 315040, China.
Objective:
To investigate the growth of prostate cancer in vitro or in vivo by inhibiting the expression of EGFR and its intracellular effective proteins with small RNA interference ( SiRNA).
Methods:
The hormone independence prostate cancer (HIPC) cell line PC-3 was transfected by EGFR SiRNA synthesized and cloned into a recombinant lentivirus vector. The growth rate of transfected PC-3 cell was measured by MTT. The expression of EGFR and the expression and phosphorylation of its intracellular proteins, such as Akt and MAPK, were detected by fluorescent Real-Time PCR and Western blot respectively. Meanwhile nude mice were transplanted with PC-3 cell to establish the tumor model and the tumor growth was observed.
Results:
The transfection efficiency was stable over 75% in PC-3 cell transfected with the recombinant lentivirus vector carrying EGFR SiRNA and the survival rate of PC-3 cell was only 40%-50%. Such depressant effects might be obtained by inhibiting the expression of EGFR mRNA and protein to only 10% as compared with their untreated levels (P < 0.01); meanwhile, the expression level and phosphorylation of Akt and MAPK also obviously decreased to 76.49% and 47.15% respectively (P < 0.05). Compared with the control group, the proliferation activity of tumors in nude mice was inhibited significantly by 34.83% (P < 0.05).
Conclusion:
Lentivirus-mediated EGFR SiRNA can inhibit the growth of HIPC in vivo and in vitro by effectively suppressing the expression of EGFR and its intracellular proteins. The latter may be a potential candidate for future targeted therapy.
Insights
Small interfering RNA (siRNA) targeting EGFR effectively inhibited prostate cancer growth in cell cultures and animal models. This targeted approach suppressed key signaling proteins, showing promise for future therapies.
Area of Science:
- Oncology
- Molecular Biology
- Gene Therapy
Background:
- Prostate cancer remains a significant health concern, with hormone-independent forms presenting treatment challenges.
- Epidermal Growth Factor Receptor (EGFR) is implicated in prostate cancer progression.
- Targeting EGFR offers a potential therapeutic strategy.
Purpose of the Study:
- To investigate the efficacy of inhibiting EGFR expression using small interfering RNA (siRNA) in prostate cancer.
- To evaluate the impact of EGFR inhibition on cancer cell growth in vitro and in vivo.
- To assess the downstream effects on intracellular signaling proteins.
Main Methods:
- PC-3 hormone-independent prostate cancer cells were transfected with EGFR siRNA delivered via a lentivirus vector.
- Cell viability was assessed using MTT assays.
- EGFR expression, and Akt/MAPK phosphorylation were analyzed by Real-Time PCR and Western blot.
- Tumor xenografts were established in nude mice to evaluate in vivo tumor growth inhibition.
Main Results:
- Lentivirus-mediated EGFR siRNA achieved over 75% transfection efficiency in PC-3 cells, reducing cell survival to 40-50%.
- EGFR mRNA and protein levels were suppressed to approximately 10% of control levels (P < 0.01).
- Downstream signaling proteins Akt and MAPK showed significant reductions in expression and phosphorylation (P < 0.05).
- Tumor growth in nude mice was significantly inhibited by 34.83% compared to controls (P < 0.05).
Conclusions:
- Lentivirus-delivered EGFR siRNA effectively inhibits hormone-independent prostate cancer growth both in vitro and in vivo.
- Suppression of EGFR and its downstream signaling pathways is a key mechanism of action.
- EGFR-targeted siRNA therapy represents a promising candidate for future prostate cancer treatment.
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