Researchers at the University of North Carolina at Chapel Hill have discovered a molecule that triggers aggressive prostate tumors. The molecule, labeled as Ack1is a part of the tyrosine kinase gene family and triggers aggressiveness in prostate tumors by messing up with their signals and directing cells to dump a tumor-suppressor protein.
This protein usually fights cancer growth by signaling that the cell destroy itself. Researchers say that Ack1 could be a new target for drug companies to target anti-cancer drugs. 'It's a remarkable effect. Tumors grew more rapidly and invaded as if they were converted to advanced prostate cancer,' said Dr. Shelton Earp, director of the UNC Lineberger Comprehensive Cancer Center and lead author of the study. It was found that in experimental systems Ack1 had a significant role in promoting tumor growth. The study also found that a drug developed by the National Cancer Institute was able to inhibit the growth of Ack1. The drug called geldanamycin inhibited Ack1 through interference with its molecular interactions, 'If you add geldanamycin to the prostate cancer cell, the drug knocks Hsp90 off oncogenic signaling molecules. This dramatically decreases Ack1 activity and slows tumor formation,' Earp added. The team also found that Ack1 levels were much higher in benign prostatic hypertrophy, or non-cancerous prostate enlargement than in advanced prostate cancer. "Because we found Ack1 is more active in advanced prostate tumors, and its inhibition blocks experimental tumor growth, we believe Ack1 should be a target for novel drug development," the researchers concluded in the study, the report of which is published in the November 15 issue of the journal Cancer Research.
L. H. Lang
University of North Carolina School of Medicine