A New Way to Target Resistant Prostate Cancer Cells
Jul 29, 2025
Prostate cancer remains a significant health concern, especially in advanced stages. Researchers are investigating innovative strategies to combat treatment-resistant forms of the disease. One promising approach involves targeting the androgen receptor's interaction with proliferating cell nuclear antigen. New peptide and small molecule strategies could potentially improve treatment outcomes for patients suffering from castration-resistant prostate cancer. This breakthrough could change the landscape of prostate cancer therapies.
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Resistant Prostate Cancer Mechanism
Castration-resistant prostate cancer (CRPC) grows despite low testosterone levels.
The AR-V7 variant keeps driving cancer growth independent of hormone therapy.
insights INSIGHT
PCNA-AR Interaction in Cancer
Proliferating cell nuclear antigen (PCNA) binds androgen receptor (AR) to promote prostate cancer cell growth.
Testosterone strengthens PCNA-AR binding in normal AR but ARV7 binds PCNA constantly.
volunteer_activism ADVICE
Blocking PCNA to Inhibit Cancer
Use small peptides like R9AR-PIP to block PCNA-AR binding and reduce cancer gene activation.
Alternatively, molecules like PCNAI1S prevent PCNA from entering the nucleus to inhibit prostate cancer growth.
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Prostate cancer is the second most diagnosed cancer among men worldwide and remains a leading cause of cancer-related death. While early forms of the disease can usually be treated successfully, advanced cases remain a major challenge. Scientists have now discovered a new potential way to slow the growth of advanced, treatment-resistant prostate cancer. These results were recently published in Volume 16 of Oncotarget by researchers from the University of Cincinnati College of Medicine.
Understanding Advanced Prostate Cancer
Early-stage prostate cancer can often be treated successfully. Most treatments work by lowering testosterone levels or blocking the hormone from activating the androgen receptor (AR), which drives cancer growth.
In some patients, however, the disease progresses to castration-resistant prostate cancer (CRPC). Even with drastic reductions in testosterone levels, the tumors continue to grow at this stage. CRPC is much more difficult to treat, and current therapies such as hormone blockers or chemotherapy typically extend life by only a few months.
One reason for this resistance is that cancer cells often switch to a different form of the androgen receptor called AR-V7. This variant remains permanently active, even without testosterone, making hormone-based drugs less effective. Because of this, new treatment strategies that work independently of hormone levels are needed.
The Study: Targeting a New Weakness in Prostate Cancer Cells
In the study titled “Targeting PCNA/AR interaction inhibits AR-mediated signaling in castration resistant prostate cancer cells,” researchers Shan Lu and Zhongyun Dong from the University of Cincinnati College of Medicine investigated a new way to block CRPC growth.
Full blog - https://www.oncotarget.org/2025/07/29/a-new-way-to-target-resistant-prostate-cancer-cells/
Paper DOI - https://doi.org/10.18632/oncotarget.28722
Correspondence to - Zhongyun Dong - dongzu@ucmail.uc.edu
Video short - https://www.youtube.com/watch?v=fiJWZ_fKxgs
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Keywords - cancer, PCNA, androgen receptor, PCNA inhibitors, AR splicing variants, CRPC
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