Journal
KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
Volume 20, Issue 1, Pages 25-33Publisher
KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
DOI: 10.4196/kjpp.2016.20.1.25
Keywords
Ca2+-activated K+ channel; Ionomycin; Proliferation; Squamous cell cancer; 1-EBIO
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Funding
- Basic Science Research Program through the National Research Foundation of Korea - Ministry of Education, Science, and Technology [NRF 2011-0017370, NRF 2012-0000809]
- Seoul Na-tional University Hospital
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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 mu M 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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