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揭示人类肺细胞对雷丁的分子反应:转录组学见解和对毒性的影响

Francisco Carlos da Silva Junior¹, Junyi Lin², Markus Hecker³

¹Department of Cell Biology and Genetics, Biosciences Center, Federal University of Rio Grande do Norte, Natal, RN, Brazil; Graduate Program in Biochemistry and Molecular Biology, Biosciences Center, Federal University of Rio Grande do Norte, Natal, RN, Brazil.

Environmental toxicology and pharmacology

|September 28, 2025

概括

森林火灾中的污染物雷 (RET) 破坏细胞能量,通过改变基因表达来促进细胞入侵. 低剂量的RET具有悖论性的刺激细胞生长和ATP水平,表明复杂的hormesis效应.

科学领域:

环境毒理学环境毒理学
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

雷 (RET) 是一种在森林火灾发生后普遍存在的多环芳化合物.
在RET生态毒性背后的分子机制尚不清楚.
了解RET的细胞效应对于评估与环境污染物相关的风险至关重要.

研究的目的:

为了研究在BEAS-2B细胞中雷丁 (RET) 毒性的分子机制.
分析RET对细胞活力,能量代谢和细胞与细胞相互作用的影响.
探索RET对细胞迁移,入侵和潜在诱导上皮质-介质细胞过渡 (EMT) 的影响.

主要方法:

全转录组 (RNA-seq) 分析以确定基因表达变化.
细胞活力测试和ATP水平测量.
细胞粘附,迁移 (伤口愈合) 和入侵 (穿透) 测试.

主要成果:

RNA-seq揭示了显著的转录失调,包括长非编码RNA (lncRNA),microRNA (miRNA) 和伪基因.
路径分析表明脂肪酸代谢和线粒体功能受损,导致能量失衡.
低RET剂量表现出hormesis,刺激增殖和ATP水平,而高剂量影响细胞粘附,迁移和侵入性,表明一种类似EMT的表型.

结论:

代谢适应和转录调节是驱动RET对细胞增殖和侵入性影响的关键机制.
暴露于RET会诱导复杂的细胞反应,包括能量失衡和改变基因表达.
这些发现突出了对多环芳相关呼吸道疾病和致癌的潜在影响.

关键词:

在BEAS-2B细胞中,多环芳香碳化合物多环芳香碳化合物在RNA-seqqq.呼吸系统的结果雷毒性雷毒性雷毒性

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