2023-06-19 03:30:24
The therapy of castration-resistant prostate cancer represents a challenge. Researchers may now have found a new approach.
Prostate cancer is the most commonly diagnosed malignancy and the second leading cause of cancer death in men in the United States. The stubborn disease can continue to grow even when the amount of testosterone in the body is reduced to very low levels, earning it the awkward name of castration-resistant prostate cancer (CRPC). This poses a major clinical challenge as the androgen receptor (AR) lags behind as a critical actor in cancer and changes its behavior in CRPCs.
Many patients develop CRPC
Androgen deprivation therapy is the first-line treatment for locally advanced or metastatic prostate cancer. Despite the initial response to therapy, almost all patients develop CRPC within a few years. It is now known that CRPC remains dependent on AR signaling. “Understanding the triggers that lead to changes in AR activity is important for developing better treatments for CRPC,” said Ping Yi, assistant professor of biology and biochemistry. The research work was carried out in PNAS published.
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“We found a specific chemical modification of the AR protein that occurs under certain conditions when the amount of male hormones is reduced to castration conditions. This modification affects another protein called TRAF4, which is often overexpressed in advanced prostate cancer. We have shown that overexpression of TRAF4 results in the conversion of androgen-sensitive prostate cancer cells into castration-resistant cells, both in laboratory experiments and in living samples,” Yi said. “We also found that the TRAF4 protein concentration is higher in androgen-insensitive prostate lymph node carcinoma cells.”
Important basis for new therapies
The results also suggest that TRAF4 promotes the spread of cancer to other parts of the body. For this study, Yi examined cells from patients with metastatic cancer who had previously undergone androgen deprivation therapy. The researchers also observed that the TRAF4 protein is higher in cancer cells that are no longer androgen-responsive than in cells that are still androgen-responsive.
The researchers believe their findings provide an important basis for identifying a cohort of CRPC patients who may respond well to treatment that targets the specific molecular changes caused by the AR alteration, and thus a possible treatment option for this patient group.
This article is based on a press release the University of Houston. We have the original publication for you here and linked in the text.
Image source: Daesun Kim, Unsplash
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