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Updated: May 28, 2026

miRNA Expression Analyses in Prostate Cancer Clinical Tissues
Published on: September 8, 2015
[Inhibition of SRC-1 expression in prostate cancer cells by RNAi and its significance]
Bo Peng1, Si-Qi Wang, Hong-Jun Zhao
1Department of Urology, The First Affiliated Hospital of Wenzhou Medicine College, Wenzhou, Zhejiang 325000, China.
Objective:
To investigate the inhibition of the expression of steroid receptor coactivator-1 (SRC-1) in the LNCap cell line through RNA interference (RNAi) and the effect of the silenced SRC-1 gene on LNCap cells.
Methods:
The experiment included four groups: siRNA transfection, siRNA negative control, bland vehicle (with Lipofectamine 2000 but no siRNA), and blank control (with neither Lipofectamine 2000 nor siRNA). LNCap cells were transfected with designed siRNA using the liposomes method, the expressions of SRC-1 determined by Q-PCR and Western blot, and the proliferation of the LNCap cells detected by the CCK-8 method.
Results:
The expression of SRC-1 mRNA in the transfected LNCap cells was decreased by 35% at 24 hours and 77% at 48 hours, with statistically significant differences from the blank control group (P < 0.05). The SRC-1 protein expression of the transfected group was 0.359 +/- 0.034 at 24 hours and 0.257 +/- 0.065 at 48 hours, markedly decreased as compared with that of the negative control (0.782 +/- 0.078 and 0.766 +/- 0.043) , bland vehicle (0.840 +/- 0.013 and 0.786 +/- 0.051), and blank control group (0.816 +/- 0.065 and 0.805 +/- 0.107) (P < 0.05). The LNCap cell growth inhibition rates were 25%, 52%, 55% and 60% at 24, 48, 72 and 96 hours, respectively.
Conclusion:
The expression of SRC-1 is correlated with the growth of LNCap cells; its high expression in androgen-independent prostate cancer cells may be involved in the progression to androgen-independence. Inhibiting the expression of SRC-1 may be an option for the treatment of androgen-dependent prostate cancer.
Insights
Steroid receptor coactivator-1 (SRC-1) inhibition using RNA interference significantly reduced LNCap cell growth. Silencing SRC-1 may offer a therapeutic strategy for androgen-dependent prostate cancer.
Area of Science:
- Molecular Biology
- Cancer Research
- Gene Expression Regulation
Context:
- Steroid receptor coactivator-1 (SRC-1) is implicated in various cellular processes.
- Prostate cancer progression, particularly to androgen-independence, may involve SRC-1.
- LNCap cells are a human prostate cancer cell line model.
Purpose:
- To investigate the inhibition of SRC-1 expression in LNCap cells via RNA interference (RNAi).
- To evaluate the impact of silenced SRC-1 on LNCap cell proliferation.
- To explore SRC-1 as a potential therapeutic target in prostate cancer.
Summary:
- RNAi successfully reduced SRC-1 mRNA and protein expression in LNCap cells by up to 77% and significantly, respectively.
- LNCap cell proliferation was inhibited in a time-dependent manner following SRC-1 silencing, reaching 60% inhibition by 96 hours.
- Quantitative PCR and Western blot confirmed successful gene silencing, while CCK-8 assays measured cell growth inhibition.
Impact:
- Demonstrates a direct correlation between SRC-1 expression levels and LNCap cell growth.
- Suggests that high SRC-1 expression contributes to androgen-independent prostate cancer.
- Highlights the potential of SRC-1 inhibition as a therapeutic approach for androgen-dependent prostate cancer.
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