Deregulated Progenitors Express Altered Acid Sensing Ion Channels

Deregulated progenitors may dictate heterogeneity of breast cancer types between patients, as well as treatment resistance, making targeted therapies crucial to preventing their survival, without effecting normal cells. Acid Sensing Ion Channels (ASIC) can affect neoplastic cell physiology and different channel types can regulate cancer progression. They are sodium selective and somewhat calcium permeable channels that sense physiological pH changes. Important in metastasis and apoptosis, ASIC increased expression correlates with deregulated telomerase activity and neoplastic cell physiology. We used western analysis with dual immunofluorescent staining to identify expression levels and subcellular localization patterns for ASIC1a/1b and ASIC3 in deregulated breast epithelial progenitors. These progenitors were derived from a human breast epithelial cell model (HME50‐8) comprised of mortal progenitor cells (p53 heterozygous) and immortal deregulated progenitor cells (mutant p53) that overexpress endogenous hTERT due to resveratrol treatment and certain tumor markers. Our results will provide better predictability of deregulation of renewal pathways in progenitors that have immortalized and acquire naturally occurring oncogenic events.