芳烃受体(AhR)激活介导苯并(a)芘诱导的HaCaT细胞AQP3和Notch1的过表达。

IF 2.3 4区 医学 Q3 ENVIRONMENTAL SCIENCES Environmental and Molecular Mutagenesis Pub Date : 2023-11-20 DOI:10.1002/em.22580
Claudia I. Almendarez-Reyna, Carlos Gabriel de la Trinidad Chacón, Ángeles C. Ochoa-Martínez, Luis A. Rico-Guerrero, Iván N. Pérez-Maldonado
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引用次数: 0

摘要

本研究的目的有两个:1)评估苯并[a]芘(BaP)对体外暴露HaCaT细胞中AQP3和Notch1基因表达水平的影响;2)通过生物信息学方法探讨被评估基因可能的生物学作用。细胞暴露于浓度逐渐增加的BaP (0.0 ~ 4.0 μM)中1 ~ 4天。处理后,检测细胞活力及AhR、CYP1A1、AQP3、Notch1基因表达水平。利用生物信息学工具评估被评估基因可能的生物学作用。BaP对HaCaT细胞的细胞毒性较低。一个显著的过度表达(p
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The aryl hydrocarbon receptor (AhR) activation mediates benzo(a)pyrene-induced overexpression of AQP3 and Notch1 in HaCaT cells

The aim of this study was twofold: (1) evaluate the effect of benzo[a]pyrene (BaP) on expression levels of AQP3 and Notch1 genes in HaCaT cells exposed “in vitro” and (2) investigate the possible biological role of assessed genes by bioinformatics methods. Cells were exposed to increasing concentrations of BaP (0.0–4.0 μM) for 1–4 days. After treatments, cell viability and expression levels of AhR, CYP1A1, AQP3, and Notch1 genes were evaluated. The possible biological role of assessed genes was evaluated using bioinformatics tools. Low cytotoxicity in HaCaT cells dosed with BaP was detected. A significant overexpression (p < .05) of CYP1A1, AQP3, and Notch1 was found in exposed HaCaT cells. The gene expression upregulation was dependent on AhR activation. The bioinformatics analysis showed that these genes were enriched in related cancer signaling pathways. The findings suggest that AQP3 and Notch1 are upregulated by AhR activation in HaCaT cells exposed to BaP.

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来源期刊
CiteScore
5.40
自引率
10.70%
发文量
52
审稿时长
12-24 weeks
期刊介绍: Environmental and Molecular Mutagenesis publishes original research manuscripts, reviews and commentaries on topics related to six general areas, with an emphasis on subject matter most suited for the readership of EMM as outlined below. The journal is intended for investigators in fields such as molecular biology, biochemistry, microbiology, genetics and epigenetics, genomics and epigenomics, cancer research, neurobiology, heritable mutation, radiation biology, toxicology, and molecular & environmental epidemiology.
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