Activation of K+ channel by 1-EBIO rescues the head and neck squamous cell carcinoma cells from Ca2+ ionophore-induced cell deathopen access
- Authors
- Yin, Ming Zhe; Park, Seok-Woo; Kang, Tae Wook; Kim, Kyung Soo; Yoo, Hae Young; Lee, Junho; Hah, J. Hun; Sung, Myung Hun; Kim, Sung Joon
- Issue Date
- Jan-2016
- Publisher
- KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
- Keywords
- Ca2+-activated K+ channel; Ionomycin; Proliferation; Squamous cell cancer; 1-EBIO
- Citation
- KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY, v.20, no.1, pp 25 - 33
- Pages
- 9
- Journal Title
- KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
- Volume
- 20
- Number
- 1
- Start Page
- 25
- End Page
- 33
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/7413
- DOI
- 10.4196/kjpp.2016.20.1.25
- ISSN
- 1226-4512
2093-3827
- Abstract
- 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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