Research uncovers how prostate cancer cells resist treatment

Researchers at Texas A&M Health have identified a molecular mechanism that increases cholesterol levels inside prostate cancer cells—an important process that may help explain how some tumours progress and become resistant to treatment. 

The study, led by Ziying Liu, a former student in the lab of Fen Wang, at the Institute of Biosciences and Technology and the Naresh K Vashisht College of Medicine, found that a cell signalling receptor called fibroblast growth factor receptor 1 (FGFR1) helps prostate cancer cells increase their internal supply of cholesterol. 

When the research team removed FGFR1 from prostate cancer cells, cholesterol levels dropped. Genes responsible for taking up low-density lipoprotein (LDL) and producing cholesterol within the cell became less active. 

The standard first-line treatment for prostate cancer is androgen deprivation therapy (ADT). Although many patients initially respond to this therapy, most cases progress within one to three years to a more aggressive form known as castration-resistant prostate cancer. 

One of the biological processes contributing to this transition is steroidogenesis—the production of steroid hormones derived from cholesterol. Because these hormones can fuel tumour growth even when androgen levels are suppressed, understanding how cancer cells obtain and regulate cholesterol has become an important focus of prostate cancer research. 

By clarifying the molecular mechanisms that control cholesterol metabolism in prostate cancer cells, the research may help identify potential targets for future therapies aimed at slowing or preventing disease progression. 

“Cancer cells frequently rewire metabolic pathways to sustain growth, and evade therapeutic treatment,” Wang said. “Our group has previously shown that aberrant FGFR1 signalling drives several metabolic programmes in prostate cancer, including glycolysis, choline metabolism and iron metabolism. This study adds cholesterol metabolism to that list and further highlights FGFR1 as a multifunctional pathway that could be exploited for future immunotherapy strategies.” 

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