Volume 15, Issue 4 (July 2013) 15, 439–440; 10.1038/aja.2013.14
PRSS3/mesotrypsin in prostate cancer progression: implications for translational medicine
Evette S Radisky
Department of Cancer Biology, Mayo Clinic Comprehensive Cancer Center, Jacksonville, FL 32224, USA
Correspondence: Dr ES Radisky, (radisky.evette@mayo.edu)
published online 18 March 2013
Abstract |
Prostate cancer morbidity and mortality are caused by metastasis to other vital organs and tissues. Metastatic prostate cancer is a terminal disease in need of improved therapies. Hockla et al. have identified prostate cancer cell upregulation of the digestive protease PRSS3/mesotrypsin in association with metastasis and recurrence. Gene silencing of PRSS3 led to pronounced reductions in invasion and metastasis in cell culture and in an orthotopic mouse model of prostate cancer. Importantly, a recently developed inhibitor of mesotrypsin was equally effective in suppressing invasion. These results identify mesotrypsin as a potential therapeutic target in metastatic prostate cancer.
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