Cairo: Hani Kamal El-Din
Scientists at Weill Cornell Medical Center have discovered a new mechanism that explains how prostate cancer “resists” treatment. Their study revealed that the absence of the PKCλ/ι protein in prostate cancer cells allows the enzyme EZH2 to stimulate aggressive tumor growth. The findings of the research were published in Nature Communications.
Prostate cancer remains one of the leading causes of cancer-related deaths among men, claiming over 30,000 lives annually in the United States. While the disease is treatable in its early stages through therapies aimed at blocking androgen receptors (male sex hormones), some tumors eventually become resistant to treatment. This form of the disease, known as neuroendocrine prostate cancer, is highly aggressive and loses its dependence on androgens, which makes it much harder to treat.
The researchers studied the tissues of prostate cancer patients and identified a key mechanism that contributes to the aggressiveness of the disease. They found that the absence of PKCλ/ι in cancer cells activates an alternative form of the EZH2 enzyme, which, even under therapy conditions, suppresses androgen receptors. This modified form of EZH2 stimulates the production of specific proteins and activates tumor growth factors such as TGF-β.
Experiments conducted on mice confirmed that targeting the alternative functions of EZH2 opens new avenues for treatment. The researchers found that blocking the TGF-β signaling pathway eliminated the resistance of tumor cells, restoring sensitivity to drugs such as enzalutamide. This could also enhance the effectiveness of immunotherapy, which has not yet met expectations in treating prostate cancer.
This discovery offers a deeper understanding of how prostate cancer resists treatment and provides scientists with the opportunity to develop new therapeutic strategies that could improve treatment outcomes, especially in cases characterized by high aggressiveness and resistance to traditional therapies.
