Arsenite Increases Linc-ROR in Human Bronchial Epithelial Cells that Can Be Inhibited by Antioxidant Factors.

Abstract

Oxidative stress is the main mechanism of arsenite toxicity. Long intergenic non-coding RNA regulator of reprogramming is a newly found stress-response long non-coding RNA that is activated in various stress conditions. However, whether long intergenic non-coding RNA, regulator of reprogramming (linc-ROR) is involved in arsenite-induced oxidative stress has not been explored. In this study, we found that arsenite dose responsively increased the expression of linc-ROR in human bronchial epithelial (HBE) cells, along with elevated oxidative stress demonstrated by increased intracellular reactive oxygen species (ROS) and DNA damage, as well as decreased antioxidant glutathione and superoxide dismutase. We further found that the pre-treatment with N-acetylcysteine, a widely used ROS scavenger, and the over-expression of antioxidant NRF2 protein, both significantly reduced arsenite-induced oxidative stress in arsenite-treated HBE cells, and the linc-ROR over-expression was also inhibited, suggesting that oxidative stress is a key factor for the increase of linc-ROR in arsenite-treated HBE cells. Moreover, our results of bio-informatic analysis showed that arsenite-induced oxidative stress might modulate linc-ROR expression via 3 genes and the up-regulated linc-ROR in arsenite-induced oxidative stress may get involved in cellular processes such as cellular stress response, RNA metabolism, and DNA repair. Collectively, our study demonstrates that oxidative stress plays the key role in arsenite-induced over-expression of linc-ROR, and linc-ROR may be a new clue for exploring the mechanism of arsenite toxicity.