索-3在Trp53-null乳腺瘤发生过程中改变了编码血管化和上皮-介质细胞过渡功能的基因表达
Elena Morozova1, Anastasia Kariagina1, Calista Busch1
1Department of Microbiology, Genetics, and Immunology, Michigan State University, East Lansing, MI, USA.
概括
基-3 (oxybenzone) 降低了小鼠瘤中的表皮细胞转变为介质细胞,改变了血管生成和基因表达. 这可能会促进上皮瘤,同时抑制状细胞瘤发病率.
科学领域:
- 内分泌学 在内分泌学.
- 在瘤学瘤学.
- 毒理学 毒理学 毒理学
背景情况:
- 基-3 (oxybenzone) 是一种常见的防晒成分,具有内分泌干扰的潜力.
- 之前的研究表明,三能促进上皮瘤,但在高脂肪饮食的小鼠中,可以预防脊柱细胞瘤.
研究的目的:
- 在上皮瘤中研究基-3对上皮细胞转移到介质细胞转变 (EMT) 的作用.
- 为了确定相-3在瘤类型上的差异性作用的基础分子机制.
主要方法:
- 从先前用二-3治疗的小鼠上皮瘤的分析.
- 基因表达分析以确定与血管生成和EMT相关的变化.
- 使用乳腺瘤细胞系表现出EMT特征的体外研究.
主要成果:
- 二-3在上皮瘤中降低了表皮细胞向介质细胞的转变.
- 观察到相关的基因表达变化,特别是在调节血管生成和EMT的基因中.
- 三抑制了EMT阳性乳腺瘤细胞系中的细胞迁移和Timp1表达.
结论:
- 三抑制EMT可能稳定瘤血管,有助于表皮瘤促进.
- 观察到对EMT和基因表达的影响可以解释基-3在促进上皮瘤和抑制状细胞瘤方面的双重作用.
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