Sympathetic β2-Adrenergic Receptor Blockade Overcomes Docetaxel Resistance in Prostate Cancer

Scientists examined whether pharmacological inhibition of β2-adrenergic receptor (β2-AR) increased cell sensitivity to docetaxel in castration-resistant prostate cancer cells and the possible regulation of β2-AR in cell autophagy and apoptosis and the several molecular mechanisms, which may suggest a promising therapeutic strategy for overcoming docetaxel resistance in CRPC.