Abstract
Breast cancer is the most diagnosed cancer in woman worldwide and leads to over 600,000 deaths annually. The vast majority of breast cancer-related deaths are attributed to metastasis to visceral organs or the brain. Therefore, understanding how these cells achieve metastasis is vital.
Ion channels, such as the epithelial sodium channel (ENaC), are emerging as new targets for cancer research due to their role in regulating cell functions such as the process that allows cancer cells to undergo phenotypic chances necessary for metastasis. Our research examines the influence of overexpressing the pore-forming subunit of ENaC, alpha-ENaC, in breast cancer cells on their cell migration and proliferation. We hypothesise that increasing expression of ENaC will restore the cells to a more epithelial state thus reducing cell migration and proliferation.