Title : Dual effects of arsenic trioxide on tumor cells and the potential underlying mechanisms.

Pub. Date : 2018 Sep

PMID : 30127993






6 Functional Relationships(s)
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1 The data demonstrated that low-dose arsenic trioxide (0.1 microM) enhanced the viability and apoptosis of tumor cells expressing hERG channels following long-term incubation. Arsenic Trioxide ETS transcription factor ERG Homo sapiens
2 Therefore, we hypothesized that this hormesis effect of low-dose arsenic trioxide on tumor cells may be associated with the hERG channel. Arsenic Trioxide ETS transcription factor ERG Homo sapiens
3 Furthermore, low dose arsenic trioxide promoted the hERG-channel current by changing the kinetics of channel gating and prolonging the open-channel stage. Arsenic Trioxide ETS transcription factor ERG Homo sapiens
4 Simultaneously, high-dose As2O3 (1 or 10 microM) significantly reduced the expression of hERG in tumor cells compared with the control group, which resulted in reduced proliferation rate and promotion of apoptotic rate. Arsenic Trioxide ETS transcription factor ERG Homo sapiens
5 The results of the present study demonstrate that the dual effects of arsenic trioxide on hERG channels vary according to concentration, resulting in the dual effects on tumor cells. Arsenic Trioxide ETS transcription factor ERG Homo sapiens
6 This provides a theoretical basis for the potential clinical application of arsenic trioxide, suggesting that hERG channels are an important target in preventing and treating tumorigenesis during arsenicosis. Arsenic Trioxide ETS transcription factor ERG Homo sapiens