Downregulation of the Ca(2+)-activated K(+) channel KC a3.1 by histone deacetylase inhibition in human breast cancer cells.

ABSTRACT: The intermediate-conductance Ca(2+)-activated K(+) channel KC a3.1 is involved in the promotion of tumor growth and metastasis, and is a potential therapeutic target and biomarker for cancer. Histone deacetylase inhibitors (HDACis) have considerable potential for cancer therapy, however, the effects of HDACis on ion channel expression have not yet been investigated in detail. The results of this study showed a significant decrease in KC a3.1 transcription by HDAC inhibition in the human breast cancer cell line YMB-1, which functionally expresses KCa3.1. A treatment with the clinically available, class I, II, and IV HDAC inhibitor, vorinostat significantly downregulated KC a3.1 transcription in a concentration-dependent manner, and the plasmalemmal expression of the KC a3.1 protein and its

SUBMITTER: Ohya S 

PROVIDER: S-EPMC4804315 | biostudies-literature | 2016 Apr

REPOSITORIES: biostudies-literature