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KCI등재 학술저널

Activation of K<sup>+</sup> channel by 1-EBIO rescues the head and neck squamous cell carcinoma cells from Ca<sup>2+</sup> ionophore-induced cell death

Activation of K<sup>+</sup> channel by 1-EBIO rescues the head and neck squamous cell carcinoma cells from Ca<sup>2+</sup> ionophore-induced cell death

Ion channels in carcinoma and their roles in cell proliferation are drawing attention. Intracellular Ca<sup>2+</sup> ([Ca<sup>2+</sup>]<sub>i</sub>)-dependent signaling affects the fate of cancer cells. Here we investigate the role of Ca<sup>2+</sup>-activated K<sup>+</sup> channel (SK4) in head and neck squamous cell carcinoma cells (HNSCCs) of dif-ferent cell lines; SNU-1076, OSC-19 and HN5. Treatment with 1 μM ionomycin induced cell death in all the three cell lines. Whole-cell patch clamp study suggested common expressions of Ca<sup>2+</sup>-activated Cl<sup>&#8722;</sup> channels (Ano-1) and Ca<sup>2+</sup>-activated nonselective cation channels (CAN). 1-EBIO, an activator of SK4, induced outward K<sup>+</sup> current (ISK4) in SNU-1076 and OSC-19. In HN5, ISK4 was not observed or negligible. The 1-EBIO-induced current was abolished by TRAM-34, a selective SK4 blocker. Interestingly, the ionomycin-induced cell death was effectively prevented by 1-EBIO in SNU-1076 and OSC-19, and the rescue effect was annihilated by combined TRAM-34. Con-sistent with the lower level of ISK4, the rescue by 1-EBIO was least effective in HN5. The results newly demonstrate the role of SK4 in the fate of HNSCCs under the Ca<sup>2+</sup> overloaded condition. Pharmacological modulation of SK4 might provide an intriguing novel tool for the anti-cancer strategy in HNSCC.

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