The Chinese and American research team led by the Roswell Park Cancer Institute s has linked the development of castration-resistant prostate cancer to the lack of androgen receptor expression in prostate cancer cells, identifying new therapeutic targets.

Prostate cancer is one of the most common cancers in men and the second leading cause of cancer death in men, as patients with advanced prostate cancer still develop or relapse after treatment.

For men with advanced cancer or who are unable to surgically remove the tumor, the standard treatment regimen is to use drugs to target and block the androgen receptor (AR), a protein that binds to androgen. AR targeted therapy prevents or inhibits the growth of cancer cells, but somehow their effects are always short-lived. After one or two years of treatment, many patients develop castration-resistant prostate cancer, a form of invasive and drug-resistant disease.

To unravel the mechanisms of prostate cancer resistance and development, the researchers examined AR expression patterns in 89 castration-resistant prostate cancer patients and found three different types: AR in the nucleus (nuc-AR), AR It is in the nucleus and cytoplasm (nuc/cyto-AR), and AR has low or no expression (AR−/lo).

Further studies later confirmed that cancer cells lacking AR did not respond to the treatment of the prostate cancer drug enzalutamide (trade name Xtandi). These cells are more likely to grow, regenerate, and proliferate than other AR-containing cells. Through deep RNA-Seq analysis, the researchers found that BCL-2 is a key regulator and is also expected to be a therapeutic target for castration-resistant prostate cancer.

"In order to survive under chemical castration and antiandrogen therapy, prostate cancer cells overexpress, redistribute or lose androgen receptors," the researchers said. "Our research provides a new proof of treatment strategy that not only treats advanced and metastatic prostate cancer, but also prevents castration resistance."

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