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KMID : 0811720160200010025
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Korean Journal of Physiology & Pharmacology
2016 Volume.20 No. 1 p.25 ~ p.33
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Activation of K+ channel by 1-EBIO rescues the head and neck squamous cell carcinoma cells from Ca2+ ionophore-induced cell death
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Yin Ming-Zhe
Park Seok-Woo
Kang Tae-Wook
Kim Kyung-Soo
Yoo Hae-Young
Lee Jun-Ho
Hah J.-Hun
Sung Myung-Hun
Kim Sung-Joon
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Abstract
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Ion channels in carcinoma and their roles in cell proliferation are drawing attention. Intracellular Ca2+ ([Ca2+]i)-dependent signaling affects the fate of cancer cells. Here we investigate the role of Ca2+-activated K+ 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 Ca2+-activated Cl? channels (Ano-1) and Ca2+-activated nonselective cation channels (CAN). 1-EBIO, an activator of SK4, induced outward K+ 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 Ca2+ overloaded condition. Pharmacological modulation of SK4 might provide an intriguing novel tool for the anti-cancer strategy in HNSCC.
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KEYWORD
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Ca2+-activated K+ channel, Ionomycin, Proliferation, Squamous cell cancer, 1-EBIO
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