Project 467082

Lung cancer is the deadliest cancer type in Canada, claiming the lives of 21,000 Canadians every year. Current treatments are damaging not only to cancer cells but also healthy cells. This emphasizes the need for new treatments that specifically target cancerous cells. When cells divide, two cellular machines called centrosomes help distribute the DNA equally into daughter cells. Centrosome amplification (CA) is the cancer-specific phenomenon of having extra centrosomes in the cell. This can cause abnormal chromosome imbalances during cell division and loss of vital DNA, resulting in cell death. Despite its potentially lethal effects, many cancer types have CA, making them reliant on coping mechanisms for their survival. One mechanism called centrosome clustering involves grouping extra centrosomes into two clusters to enable equal distribution of DNA during cell division. KIFC1 is a protein involved in the clustering process that is abnormally upregulated in cancer, but its potential as a therapeutic target in lung cancer has not been thoroughly explored. My project addresses this knowledge gap. I will measure KIFC1 expression in lung tumours and assess whether it correlates with CA and clinical factors like disease subtype and tumour mutation status. This will identify patient populations that could benefit from KIFC1-targeted therapy. In parallel, I will inactivate KIFC1 in normal cells and lung cancers with and without CA to determine if this causes cancer-specific cell death. Ultimately, my research will determine whether targeting KIFC1 represents a promising new treatment strategy for lung cancers with CA. My findings could inform future development of KIFC1-targeted therapies that could be translated into the clinic to improve lung cancer survival rates.