Report Identifies Proteins That Drive Spread in Castration-resistant PC

Report Identifies Proteins That Drive Spread in Castration-resistant PC
Inhibiting the protein BRD4 can stop the migration of castration-resistant prostate cancer cells, regardless of the mechanism causing resistance to treatment, new research has shown. This suggests that BRD4 might be a therapeutic target to prevent metastasis (spread) in prostate cancer patients who have become resistant to androgen-deprivation therapies. The study, "BRD4 regulates metastatic potential of castration-resistant prostate cancer through AHNAK," was published in the journal Molecular Cancer Research. Most prostate cancers are — or at least start off — driven by signaling from androgens, the so-called "male hormones." This is why one of the mainstays of prostate cancer treatment is hormone-based therapy aimed at reducing the amount of these hormones and/or making their signals weaker. However, some cancers develop resistance to these therapies. At this point, such tumors are called castration-resistant prostate cancers (CRPCs) because they are able to grow even if there aren't androgens around. Thus, researchers are ever on the hunt for the mechanisms that drive CRPC to grow and metastasize. In most cases, patients start producing an androgen receptor that no longer needs androgens to become active, but researchers have also found cases of people who stop producing any forms of the androgen receptor. Looking at non-androgen molecules that could drive cancer spread, investigators focused on the BET family of proteins, which includes BRD2, BRD3, and BRD4. Using a
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