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Updated: Feb 8, 2026
miRNA Expression Analyses in Prostate Cancer Clinical Tissues
Published on: September 8, 2015
Expression of p53 and its mechanism in prostate cancer
Jiukai Wan1, Jun Zhang1, Junqiang Zhang1
1Department of Urology, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou, Henan 450007, P.R. China.
Abstract:
The present study aimed to investigate the expression of tumor protein p53 (p53), and its mechanism of function, in prostate cancer (PC). Small interfering RNA (siRNA) was used to interfere with p53 expression in the PC cell line, DU145. Cell viability and p53 expression were analyzed using cell counting kit-8 (CCK-8) and western blotting. The effects of p53 expression on the proliferation, migration and adhesion abilities of PC cells were analyzed using Cell Counting kit-8, Transwell and adhesion assays. Changes in cell proliferation, migration and adhesion ability were observed following treatment with extracellular signal-regulated kinase (ERK) inhibitor, PD184352, and janus kinase (JNK) inhibitor, SP60012. The expression level of p53 declined 24 h after siRNA transfection (P<0.05). Furthermore, JNK and ERK, downstream proteins of the focal adhesion kinase (FAK)-Src proto-oncogene, non-receptor tyrosine kinase (Src) signaling pathway, were activated. These effects were associated with reduced proliferation, migration and adhesion abilities of PC cells compared with untransfected control cells (P<0.05). PD184352 and SP600125 treatments also resulted in reduced proliferation, migration and adhesion abilities of PC cells (P<0.05). In conclusion, PC cells exhibited low p53 expression, and the proliferation, migration and adhesion abilities of PC cells were promoted by inhibiting the activation of JNK and ERK. Together, these results suggest that p53 has potential as a therapeutic target in PC.
Insights
Prostate cancer cells show low tumor protein p53 (p53) expression. Inhibiting JNK and ERK signaling pathways reduced cancer cell proliferation, migration, and adhesion, suggesting p53 as a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Prostate cancer (PC) is a significant health concern.
- The role of tumor protein p53 (p53) in PC progression requires further elucidation.
- Understanding p53's functional mechanisms is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate p53 expression and its functional mechanisms in prostate cancer.
- To analyze the impact of p53 modulation on PC cell behavior.
- To explore the involvement of specific signaling pathways in p53-mediated effects.
Main Methods:
- Utilized small interfering RNA (siRNA) to reduce p53 expression in the DU145 PC cell line.
- Assessed cell viability, proliferation, migration, and adhesion using CCK-8, Transwell, and adhesion assays.
- Analyzed protein expression via western blotting and investigated pathway modulation using ERK and JNK inhibitors (PD184352 and SP600125).
Main Results:
- siRNA-mediated p53 knockdown led to a significant decrease in p53 expression.
- Reduced p53 levels correlated with decreased proliferation, migration, and adhesion of PC cells.
- Inhibition of JNK and ERK signaling pathways mimicked the effects of p53 reduction, decreasing PC cell aggressiveness.
Conclusions:
- Prostate cancer cells exhibit diminished p53 expression.
- The focal adhesion kinase (FAK)-Src pathway, involving JNK and ERK, plays a role in PC cell proliferation, migration, and adhesion.
- Targeting p53 or inhibiting JNK/ERK signaling pathways presents a promising therapeutic strategy for prostate cancer.
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