Targeting CEP55 in triple-negative breast cancer

Suitable for Honours or PhD students.

Breast cancer in females has now passed lung cancer as the most common diagnosed cancer and affects over 10% of women before age 85, placing an enormous burden on our healthcare system. Despite some spectacular recent successes in fighting breast cancer with new treatments (e.g. immune checkpoint inhibitors, antibody-drug conjugates, PARP inhibitors) and surgical procedures, many patients do not respond long term or at all. Consequently, there is an urgent need for new drugs that can target newly discovered pathways that initiate progress or spread cancer. New therapies are especially needed for difficult-to-treat cancers, such as triple negative breast cancer (TNBC) and certain drug-resistant metastatic breast cancers, with about one third of breast cancers spreading to other tissues such as lungs and brain even after surgery. There is a pressing need to develop a new approach to treating TNBC.

AIM

To devise a new type of therapy to seek out and destroy a key protein called CEP55 that is highly expressed in a wide range of solid human cancers. This protein plays a crucial role in regulating cancer cell division but is silent in normal cells of adult tissues. Studies have shown that both cancer cells and tumours require CEP55 to survive and grow, and that mice overexpressing it spontaneously induce blood and solid tumours. We aim to chemically silence CEP55 by developing a novel therapy that binds to it and signals other proteins to come and destroy it in the body. The project aims to generate preclinical information on the effectiveness of chemically silencing CEP55 in mouse models of metastatic breast cancer.

PROJECT POTENTIAL

The study has the potential to rapidly facilitate translation of a new discovery to the clinic.