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环境的PFOS和6:2Cl-PFESA重塑了肝癌中铁灭的脆弱性

Jiawei Hong^1,2,3,4, Keyi Du^1,4,5, Tong Wu^1,4,5

¹Division of Hepatobiliary and Pancreatic Surgery, Department of Surgery, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China.

Environmental science & technology

|February 17, 2026

概括

和多醇基物质 (PFAS) 在正常细胞中促进细胞死亡,但在肝癌细胞中防止细胞死亡. 这通过STAT3-GPX4信号循环发生,突出显示PFAS替代品的风险.

科学领域:

环境毒理学环境毒理学
癌症生物学癌症生物学
细胞死亡研究细胞死亡研究

背景情况:

铁,细胞死亡途径涉及铁和脂质过氧化,对于健康和癌症抑制至关重要.
像PFAS这样的环境污染物对肝癌中铁亡的影响尚不清楚.

研究的目的:

为了研究PFAS对肝细胞癌 (HCC) 和正常肝细胞中铁的作用.
阐明在HCC中PFAS诱导的铁化调节的潜在分子机制.

主要方法:

使用了长期体外和体内暴露模型,使用了环境相关的PFAS剂量.
采用多组学分析来了解分子反应.
研究了STAT3-GPX4信号轴的作用.

主要成果:

PFAS在正常肝细胞中促进铁亡,但在HCC中诱导耐药性.
长期暴露于PFOS和6:2 Cl-PFESA可以增强HCC中铁灭菌的抵抗力.
PFAS激活STAT3,调节GPX4并创建一个自我维持的循环,抑制脂质过氧化和HCC中的铁.
6:2 Cl-PFESA 显示效果比 PFOS 强,质疑其安全性.

结论:

PFAS具有双重效应:诱导正常细胞中的铁亡,同时通过STAT3-GPX4通路重编程促进HCC的耐药性.
这凸显了与PFAS及其替代品相关的潜在健康风险.
STAT3-GPX4轴代表了HCC的潜在治疗目标.

关键词:

在HCC中,HCC是HCC,HCC是HCC.在STAT3-GPX4中使用.细胞类型的二元性.铁灭的耐药性铁灭的耐药性这就是Pfass.

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