Studies help explain why some prostate cancers become resistant to hormone therapy

Two new studies led by researchers from the UCLA Jonsson Comprehensive Cancer Center give insight into how cells use energy to influence the way prostate tumors survive and grow — advancements that can help explain why some prostate cancers become resistant to hormone therapy, the most commonly used treatment for men with advanced stages of the disease.

In the first study, published today in Nature Cell Biology, the team of investigators identified a specific process in prostate cells that helps determine how they evolve from one type of cell to another, which plays a crucial role in determining a response to treatment.

Hormone therapy, also known as antiandrogen therapy, plays a crucial role in temporarily halting the growth of prostate cancer cells. Over time, however, the majority of patients eventually see their cancer return and progress, underscoring the pressing need for continued advancements to enhance clinical outcomes.

“Identifying metabolic alterations and understanding patterns in cancer cells could be a critical component to developing new cancer treatments,” said Andrew Goldstein, associate professor of molecular, cell and developmental biology and urology at the David Geffen School of Medicine at UCLA and member of the UCLA Jonsson Comprehensive Cancer Center. “New technological advances are giving us insight into actually how these tumors are breaking down their nutrients — known as cancer metabolism — to help them grow. And we might be able to harness or exploit that biology to make tumors more treatable.”

The team discovered that blocking a specific part of cell metabolism, called the mitochondrial pyruvate carrier, and adding a substance called lactate can change the cell behavior. These changes could potentially affect the success of treatments for prostate cancer, especially those targeting the androgen receptor, a key player in prostate cancer growth.

Reference: Studies help explain why some prostate cancers become resistant to hormone therapy; Nature Cell Biology, DOI: 10.1038/s41556-023-01274-x