【摘 要】
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LncRNA has been considered to play a crucial role in the progression of several diseases by affecting cell proliferation.However,its role in benzene toxicity remains unclear.Our study showed that the
【机 构】
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Department of Occupational Health and Environmental Health,School of Public Health,Capital Medical U
【出 处】
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首都医科大学公共卫生学院第六届研究生学术论坛
论文部分内容阅读
LncRNA has been considered to play a crucial role in the progression of several diseases by affecting cell proliferation.However,its role in benzene toxicity remains unclear.Our study showed that the expression of lncRNA-OBFC2A increased accompanied with the change of cell proliferation related-genes in benzene-exposed workers.In vitro experiments,1,4-Benzoquinone dose-dependently inhibited cell proliferation and simultaneously caused the decrease of NOTCH1 expression and the increase of KLF15 in AHH-1 cell lines.Meanwhile,1,4-Benzoquinone obviously increased the expression of lncRNA-OBFC2A,which was consistent with our previous population results.Therefore,we propose that lncRNA-OBFC2A is involved in benzene toxicity by regulating cell proliferation.Further,we successfully constructed a lentivirus model of interfering the expression of lncRNA-OBFC2A After interfering lncRNA-OBFC2A,the cell proliferation inhibition and the expression of NOTCH1 and KLF15 induced by 1,4-Benzoquinone were reversed.Subsequently,RNA fluorescence in situ Hybridization assay showed that lncRNA-OBFC2A was located in cell nuclei.These results suggest that benzene and its metabolite decreases cell proliferation via LncRNA-OBFC2A-mediated anti-proliferation effect involving NOTCH1 and KLF15.LncRNA-OBFC2A can be a potential biomarker for benzene toxicity.
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