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长期间歇性 Estradiol 暴露会在 MCF10A 细胞中诱导表皮-介质酶过渡类可塑性

Kana Sakiyama¹, Kohei Kumegawa², Liying Yang³

¹Division of Cancer Epigenomics, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan; Department of Breast and Endocrine Surgery, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.

Biochemical and biophysical research communications

|March 13, 2026

概括

经期较长可能会增加乳腺癌的风险. 波动性雌激醇暴露,而不是累积量,可以将乳腺上皮细胞重新编程成更为可塑的状态,从而影响细胞转变.

科学领域:

内分泌学在内分泌学.
细胞生物学细胞生物学
癌症研究癌症研究

背景情况:

流行病学研究表明,月经持续时间长和乳腺癌风险增加之间存在联系.
这种关联背后的精确生物机制在很大程度上是未知的.
雌激素水平在月经周期期间自然波动,这表明时间暴露模式可能至关重要.

研究的目的:

调查持续或间歇性雌激素暴露对乳腺上皮细胞的长期影响.
识别与波动激素信号相关的细胞变化和分子通路.
了解雌二醇暴露模式如何影响上皮细胞可塑性和潜在的癌症发展.

主要方法:

使用了非瘤源的乳腺上皮细胞系MCF10A.
应用连续和间歇性雌激醇刺激40周.
进行了转录组分析 (RNA-seq) 和ATAC-seq,以评估基因表达和染色质可访问性.

主要成果:

间歇性 Estradiol 暴露诱导了一个独特的细胞群 (ELITE 细胞) 与螺旋状形态,减少粘附和持续的增殖.
这些表型变化在激素戒断后是部分可逆的.
精英细胞表现出表皮-介质细胞转换 (EMT) 程序 (ZEB1/2) 的上调和相关的染色体重塑.
在这种ERα/ERβ阴性模型中,雌激素的影响可能涉及非正规的途径,如GPER.

结论:

长期的,波动的雌激醇信号可以重编程乳腺上皮细胞,增加它们的可塑性.
激素暴露的模式,而不仅仅是累积剂量,对于驱动细胞状态过渡至关重要.
这些发现提供了有关月经特征与乳腺癌风险相关的潜在机制的见解.

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