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Activation of K(+) Channel by 1-EBIO Rescues the Head and Neck Squamous Cell Carcinoma Cells From Ca(2+) Ionophore-Induced Cell Death

Ming Zhe Yin, Seok-Woo Park, Tae Wook Kang, Kyung Soo Kim, Hae Young Yoo, Junho Lee, J Hun Hah, Myung Hun Sung, Sung Joon Kim

Korean J Physiol Pharmacol. 2016 Jan;20(1):25-33.

PMID: 26807020

Abstract:

Ion channels in carcinoma and their roles in cell proliferation are drawing attention. Intracellular Ca(2+) ([Ca(2+)]i)-dependent signaling affects the fate of cancer cells. Here we investigate the role of Ca(2+)-activated K(+) channel (SK4) in head and neck squamous cell carcinoma cells (HNSCCs) of different 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(2+)-activated Cl(-) channels (Ano-1) and Ca(2+)-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. Consistent 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(2+) overloaded condition. Pharmacological modulation of SK4 might provide an intriguing novel tool for the anti-cancer strategy in HNSCC.

Chemicals Related in the Paper:

Catalog Number Product Name Structure CAS Number Price
AP10045451 1-EBIO 1-EBIO 10045-45-1 Price
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