Prostate Cancer Molecule Identified as Potential Target for Novel Therapies

Scientists at the University of North Carolina at Chapel Hill have identified a molecule called Ack1 that plays a significant role in the aggressive growth of prostate cancer. Ack1, a member of the growth-promoting tyrosine kinase gene family, stimulates tumor formation by signaling prostate cells to eliminate a tumor-suppressor protein. This protein normally inhibits rapid cell growth by signaling the cell to self-destruct. The study, published in the journal Cancer Research, highlights Ack1 as a potential target for developing novel drugs against prostate cancer.

Key Takeaways:

• Ack1, a molecule identified by UNC Chapel Hill scientists, stimulates the aggressive growth of prostate cancer by signaling prostate cells to eliminate a tumor-suppressor protein.
• The study finds that Ack1 is more active in advanced prostate tumors, suggesting it could be a target for novel drug development.
• The team discovered that Ack1 binds to a protein called Hsp90, which associates with many oncogenic signaling proteins, and that the inhibition of Hsp90 with the experimental drug geldanamycin can dramatically decrease Ack1 activity and slow tumor formation.
• The study suggests that targeting Ack1 could provide a novel approach to treating prostate cancer, as demonstrated by the profound effects on tumor growth in experimental systems.
• The team's earlier work identified Mer, a cell surface tyrosine kinase, as being expressed at reasonably high levels in prostate cancer cells, which led them to investigate the potential role of Mer in prostate cancer growth signaling.
• The study's senior author, Dr. Shelton Earp, directs the UNC Lineberger Comprehensive Cancer Center and is Lineberger professor of cancer research and a professor of pharmacology and medicine.

Statistics:

• The study found that Ack1 activity was much higher in advanced prostate tumors compared to benign prostatic hypertrophy tissue.
• The inhibition of Ack1 activity with geldanamycin completely blocked experimental tumor growth, demonstrating its potential as a target for novel therapeutics.
• The study utilized the university's Michael Hooker Proteomics Core Facility to conduct experiments that led to the discovery of the Ack1-Mer interaction.

Sources:

• Cancer Research, a journal in which the study was published.
• Health & Medicine Week, a publication that reported on the study.
• NewsRx.com, a website that provided the study's information.
• UNC Lineberger Comprehensive Cancer Center, the institution where Dr. Shelton Earp and his team conducted the research.