Protein discovery could help solve prostate cancer drug resistance
Blocking CHRM1 with dicyclomine restored docetaxel’s ability to kill cells and stop tumor growth in prostate cancer models.
Researchers at Washington State University discovered that the muscarinic M1 receptor (CHRM1) contributes to docetaxel resistance in prostate cancer. Blocking CHRM1 with the clinically available drug dicyclomine restored docetaxel’s cytotoxicity in resistant cell lines and in an animal model derived from patient‑resistant tissue, suggesting a combination therapy that may improve outcomes for castration‑resistant prostate cancer and potentially other docetaxel‑treated cancers.
Docetaxel resistance limits treatment options for advanced prostate cancer. By identifying CHRM1 as a driver of resistance and showing that an existing drug can reverse it, this study provides a clear, actionable path toward more effective combination therapies that could extend survival and reduce side effects.
Evidence level: Állatkísérletes. Állatmodellben vizsgálták.
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