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暴露于甲酸盐会诱导前列腺癌中的微RNA-5010/Nrf2-EGR1/GDF15信号表达

Yuh-Shyan Tsai¹, Yeong-Chin Jou², Ian Seng Cheong³

¹Department of Urology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.

Ecotoxicology and environmental safety

|January 21, 2025

概括

暴露于甲酸盐,特别是DEHP代谢物,与前列腺癌的攻击性增加有关. 这通过微RNA调节发生,激活Nrf-2信号和下游基因,如GDF15,影响瘤进展.

科学领域:

环境健康环境健康
在瘤学瘤学.
分子生物学分子生物学

背景情况:

甲酸盐暴露与通过荷尔蒙变化和氧化压力导致前列腺扩大有关.
甲酸在前列腺癌的发展和进展中的确切作用和机制尚未完全理解.

研究的目的:

调查甲酸盐暴露与前列腺癌之间的关联.
阐明潜在的分子机制,包括microRNA和信号通路的参与.

主要方法:

使用HPLC-MS和ELISA在前列腺活检和前列腺切除患者队列中的尿甲酸代谢物 (DEHP) 的分析.
小RNA测序以识别与甲酸暴露和癌症阶段有关的microRNA表达变化.
在前列腺癌细胞中进行体外研究,以评估DEHP对Nrf-2信号和GDF15表达的影响.

主要成果:

与良性病例相比,前列腺癌患者的尿中MEOHP和 ΣDEHP代谢物水平显著更高.
在前列腺癌中,MIR-5010是上调的,MIR-205是下调的,MIR-5010与Nrf-2通路激活有关.
在体外,DEHP暴露增加了Nrf-2信号,EGR-1和GDF15的表达,以及与甲酸盐代谢物和攻击性标志物相关的尿液GDF15.

结论:

暴露于甲酸盐,特别是DEHP,可能会导致前列腺癌的攻击性.
该机制涉及Nrf-2/EGR-1/GDF15信号通路的微RNA介导调节.
尿液中的GDF15水平可以作为甲酸诱导前列腺癌进展的潜在生物标志物.

关键词:

这是GDF-15的GDF-15.在 Nrf-2 中.这是一个微型RNA.甲酸 Ester 是一种甲酸.前列腺癌是前列腺癌.

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