ArticleOncology letters2018
Expression of p53 and its mechanism in prostate cancer.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.
- Androgen receptor binding sites enabling genetic prediction of mortality due to prostate cancer in cancer-free subjects.Nature communications · 2023Pooled it
- METTL3 drives malignant progression in TP53-mutant prostate cancer.Molecular biology reports · 2025Article
- RNA-Seq Uncovers Association of Endocrine-Disrupting Chemicals with Hub Genes and Transcription Factors in Aggressive Prostate Cancer.International journal of molecular sciences · 2025Article
- Prognosis, immunological features and potential mechanisms of HKR1 in prostate cancer via single-cell and bulk RNA-sequencing.BMC cancer · 2025Article
- Exosomal AHSG in ovarian cancer ascites inhibits malignant progression of ovarian cancer by p53/FAK/Src signaling.Translational cancer research · 2024Article
- A comparative assessment ofInternational journal of reproductive biomedicine · 2022Article
- Therapeutic Potential of Marine Peptides in Prostate Cancer: Mechanistic Insights.Marine drugs · 2022Review
- Transcription factor p53-mediated activation of miR-519d-3p and downregulation of E2F1 attenuates prostate cancer growth and metastasis.Cancer gene therapy · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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