期刊
ONCOLOGY REPORTS
卷 33, 期 2, 页码 533-538出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/or.2014.3617
关键词
BKCa channels; breast cancer; beta-catenin; iberiotoxin
类别
资金
- Biological Sciences Funding Program of the Office of Vice-President for Research of the University of Iowa
- NIH [R01CA99908, R01-CA133114]
- Department of Obstetrics and Gynecology Research Development Fund
In breast cancers, the large conductance Ca2+ and voltage sensitive K+ (BKCa) channels have been hypothesized to function as oncoproteins, yet it remains unclear how inhibition of channel activity impacts oncogenesis. We demonstrated herein that iberiotoxin (IbTX), an inhibitor of BKCa channels, differentially modulated the in vitro tumorigenic activities of hormone-independent breast cancer cells. Specifically, in HER-2/neu-overexpressing UACC893 cells and triple-negative MDA-MB-231 cells, IbTX selectively attenuated anchorage-independent growth with concomitant downregulation of beta-catenin as well as total and phosphorylated Akt and HER-2/neu. By contrast, HER-2/neu-overexpressing SK-BR-3 cells were insensitive to IbTX. Molecular analyses showed an absence of beta-catenin and a dose-dependent upregulation of total and phosphorylated Akt and HER-2/neu in these cells. Taken together, these studies identify beta-catenin as a putative modulator of the inhibitory actions of IbTX in sensitive breast cancer cells.
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