New Study Reveals Target for Aggressive Prostate Cancer Treatment

A recent study from researchers at McGill University has identified a potential new approach for treating neuroendocrine prostate cancer, a rare and aggressive form of the disease. The findings, published in the journal Genes & Development, reveal that the loss of the protein ERRγ intensifies the malignancy of prostate tumors in mice. Restoring ERRγ in human cancer cells effectively reversed this aggressive behavior, highlighting its significance as a therapeutic target.

Prostate cancer is the most commonly diagnosed cancer among men in Canada. Research indicates that approximately 15 percent of patients whose tumors stop responding to hormone therapy will develop neuroendocrine prostate cancer. Once this transition occurs, the average life expectancy falls below 18 months. Addressing therapy resistance is a critical challenge in cancer treatment, and the study emphasizes ERRγ’s potential role in overcoming this issue.

Uncovering the Mechanism Behind Aggression

Lead author and professor at McGill’s Department of Biochemistry, Vincent Giguère, stated, “Our findings highlight ERRγ as a promising new therapeutic target.” The research team employed advanced genetic and metabolic analyses to understand the implications of ERRγ loss on tumor growth. They discovered that two genes linked to cancer become overly active when ERRγ is absent.

Notably, the researchers tested existing drugs that inhibit these genes. In their trials with both mouse and human prostate cancer cells, the combination of two drugs demonstrated a significantly greater effect in slowing cancer growth compared to when each drug was used separately. This combination therapy could pave the way for new treatment options for patients currently facing limited alternatives.

Implications for Future Cancer Treatment

Giguère emphasized the clinical importance of these findings, stating, “By targeting the genes that take over when ERRγ activity is low or lost, we open the door to new treatment strategies for patients who currently have few options.” The ongoing research seeks to further understand why ERRγ function becomes impaired, which is crucial for developing effective therapies.

ERRγ has previously been recognized for its role in energy metabolism, but its protective function against tumor progression is now coming to the forefront. Preclinical research led by post-doctoral fellow Ting Li showed that neuroendocrine prostate cancers exhibit significantly lower levels of ERRγ compared to other prostate tumor types. Removing ERRγ in mice accelerated tumor growth, while reactivating the protein in human prostate cancer cells reversed this process, confirming its protective capacity.

The implications of this research extend beyond the laboratory, offering hope for improved treatment strategies for patients grappling with one of the deadliest forms of prostate cancer. As the medical community continues to explore the role of ERRγ, there is optimism that these findings will contribute to better outcomes for individuals diagnosed with neuroendocrine prostate cancer.