These findings suggest for the first time that Camkk2 and Ampk have opposing effects in prostate cancer progression. In contrast, deletion of AMP-activated protein kinase (Ampk) β1 resulted in earlier onset of adenocarcinoma development. Here we show that Camkk2 deletion or pharmacological inhibition protects against prostate cancer development in a pre-clinical mouse model that lacks expression of prostate-specific phosphatase and tensin homologue (Pten). Previous studies reported that calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK2) expression is increased in human prostate cancer. New targets are required for treating prostate cancer, particularly castrate-resistant disease.
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