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Similar to calcium (Ca 2+ ) and chloride (Cl - ) ion channels/transporters, potassium (K + ) channels have been recognized as a crucial cancer treatment target. Recent studies have provided convincing evidences of positive correlation between elevated expression levels of Ca 2+ -activated K + (K Ca ) channels and cancer proliferation, metastasis, and poor patient prognosis. In cancer cells, K Ca 1.1 and K Ca 3.1 K Ca channels are co-localized with Ca 2+ -permeable Orai/TRP channels to provide a positive-feedback loop for Ca 2+ entry. They are responsible for the promotion of cell growth and metastasis in the different types of cancer, and are therefore potential therapeutic targets and biomarkers for cancer. We determined the epigenetic and post-transcriptional dysregulation of K Ca 3.1 by class I histone deacetylase inhibitors in breast and prostate cancer cells. We further determined the transcriptional repression and protein degradation of K Ca 1.1 by vitamin D receptor agonists and androgen receptor antagonists, which are expected as potential therapeutic drugs for triple-negative breast cancer. The anti-inflammatory cytokine, interleukin-10 (IL-10) is an immunosuppressive factor involved in tumorigenesis, and plays a crucial role in escape from tumor immune surveillance. We determined K Ca 3.1 activators are a possible therapeutic option to suppress the tumor-promoting activities of IL-10. These results may provide new insights into cancer treatment focused on Ca 2+ -activated K + channels.

Ca<sup>2+</sup>-activated K<sup>+</sup> channels as cancer therapeutic targets