Caveolin‑1 facilitated KCNA5 expression, promoting breast cancer viability.

Potassium voltage‑gated channel subfamily A member 5 (KCNA5) is a voltage‑gated potassium channel protein encoded by the KCNA5 gene. A large number of studies have shown that KCNA5 is associated with the survival of malignant tumors, including breast cancer, but the detailed mechanism remains inconclusive. Our previous study found that KCNA5 is co‑expressed with a scaffolding protein, caveolin‑1 in MCF‑10A‑neoT non‑tumorigenic epithelial cell. In the present study, KCNA5 and caveolin‑1 were expressed in breast cancer tissues and cell lines. Exposing MCF‑10A‑neoT to 2 mM of methyl‑β‑cyclodextrin, an agent to disrupt caveolae and lipid rafts led to a downregulation of caveolin‑1 that reduced the expression of KCNA5. Furthermore, following caveolin‑1 knockdown, the expression of KCNA5 was decreased in MDA‑MB‑231 human breast cancer and MCF‑10A‑neoT non‑tumorigenic epithelial cell lines. In subsequent experiments, the MTT assay showed that increased caveolin‑1 and KCNA5 expression promoted the survival of MCF‑7 human breast cancer cells, but cell survival was not affected following KCNA5 overexpression alone. Using small interfering RNA technology, KCNA5‑silenced MCF‑10A‑neoT cells were established and a decreased level of phosphorylated‑AKT serine/threonine kinase (AKT) was observed in the cells compared with the parental cells. Overall, these results suggested that caveolin‑1 facilitated KCNA5 expression and may be associated with AKT activation. [ABSTRACT FROM AUTHOR]