持久性有机污染物促进前列腺癌的攻击性
Julio Buñay1,2,3, Myriam Kossai2,4, Christelle Damon-Soubeyrant1,2,3
1Université Clermont Auvergne, iGReD, CNRS UMR 6293, INSERM U1103, 28, place Henri Dunant, BP38, 63001, Clermont-Ferrand, France.
Oncogene
|August 16, 2023
概括
暴露于像二氧化和PCB-153这样的持久性有机污染物 (POPs) 会促进前列腺癌的生长和转移. 这项研究确定了Acetyl-CoA乙转移酶-1 (ACAT1) 放松调节作为推动这些效应的关键机制.
科学领域:
- 环境健康 环境健康
- 在瘤学瘤学.
- 生物化学 生物化学
背景情况:
- 持久性有机污染物 (POP),包括二氧化和PCB-153,与癌症发病率和攻击性增加有关.
- 虽然已知二氧化在某些癌症中的作用,但其对前列腺癌的影响需要进一步调查.
- 前列腺癌的进展可能受到二氧化和PCB-153暴露的影响.
研究的目的:
- 为了研究低剂量二氧化和PCB-153暴露对前列腺癌进展的影响,在体外和体内模型.
- 为了确定POP诱导的前列腺癌攻击性背后的分子机制.
- 为了验证人类前列腺癌数据集和患者样本中的发现.
主要方法:
- 前列腺癌细胞和Ptenpc-/-小鼠暴露于低剂量的二氧化和PCB-153.
- 评估癌细胞生长,转移和组织病理学变化.
- 对乙-CoA乙转移酶-1 (ACAT1) 表达的分析及其在二氧化物中介作用中的作用.
- 检查公开的前列腺癌数据集和一组暴露于色剂的退伍军人.
主要成果:
- 暴露于二氧化物和PCB-153增强了前列腺癌细胞的生长和转移 ex vivo 和 in vivo.
- 在暴露在Ptenpc-/-的小鼠中观察到类似于组织病变性癌症的模式.
- 确定ACAT1上调作为二氧化物对细胞迁移影响的调解者.
- 在高级人类前列腺癌和暴露于色剂的退伍军人中证实了ACAT1和体通路酶放松调节.
结论:
- 暴露于二氧化物和PCB-153会在前列腺瘤中促进前列腺扩散的计划.
- 在二氧化碳诱导的前列腺癌进展中,ACAT1放松调控是关键事件.
- 这项研究强调了POPs作为侵袭性前列腺癌的环境风险因素.
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