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Updated: Apr 28, 2026

Working with Auditory HEI-OC1 Cells
Published on: September 3, 2016
AP-1 activation attenuates the arsenite-induced apoptotic response in human bronchial epithelial cells by
Aodengqimuge1, Shasha Liu, Sanyue Mai
1Department of New Drug Screening Center, China Pharmaceutical University, No. 24 Tongjiaxiang, Nanjing, 210009, People's Republic of China.
Abstract:
Arsenite is a cytotoxic reagent that has been used clinically to treat certain cancers. Although the cytotoxic mechanisms of arsenite have been investigated, the cellular mechanisms that act against arsenite damage are poorly understood. Heme oxygenase 1 (HO-1) has been implicated in cellular survival under other multiple stress conditions. Here, we show that a significant induction of HO-1 expression is present in human bronchial epithelial cells (Beas-2B) treated with lethal doses of arsenite treatment. This induction depends on the known ERK/AP1 signaling pathway. As expected, HO-1 RNAi knockdown, or ERK/AP1 inhibition, renders the Beas-2B cells more sensitive to arsenite damage. Our data thus suggest that transcriptional upregulation of HO-1 expression via a putative ERK/AP-1 pathway constitutes an inherent mechanism by which arsenite-induced apoptosis is attenuated.
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