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环境相关的双甲暴露通过调节microRNA生物发生促进卵巢癌的发展

Sophia S N Lam^1,2, Zeyu Shi^1,2, Carman K M Ip³

¹School of Biological Sciences, University of Hong Kong, Hong Kong, China.

Journal of cellular and molecular medicine

|August 23, 2023

概括

对双A (BPA) 的环境暴露通过增加癌症干细胞 (CSCs) 来促进卵巢癌. 这通过G蛋白结合受体30 (GPR30) 和microRNA-21 (miR-21) 途径发生,独立于经典雌激素受体.

科学领域:

内分泌学在内分泌学.
环境健康环境健康
在瘤学瘤学.

背景情况:

双A (BPA) 是一种广泛存在的环境污染物.
怀疑BPA有助于卵巢致癌,但机制尚不清楚.
癌症干细胞 (CSCs) 驱动瘤的开始和进展.

研究的目的:

调查BPA在卵巢CSC中的作用.
为了确定特定的分子途径介导BPA对卵巢CSC的影响.
探索BPA诱导的卵巢癌的潜在治疗点.

主要方法:

用纳米BPA治疗卵巢癌细胞 (ER阳性和ER缺陷) 的方法.
评估CSC的形成和扩张.
使用siRNA和对抗剂对G蛋白结合受体30 (GPR30) 和Exportin-5参与的分析.
评估微RNA (miRNA) 生物发生,特别是miR-21.

主要成果:

环境相关的BPA度显著增加了卵巢CSC的形成和扩张.
BPA的作用是由非经典的雌激素受体GPR30介导的,而不是经典的ER.
由于BPA失调了EXPORTIN-5,导致了改变的微RNA生物发生 (miR-21).
抑制GPR30或出口蛋白-5可以逆转CSC表型.

结论:

非经典的雌激素受体GPR30和microRNA失调是BPA在卵巢CSC中的前瘤源作用的新媒体.
低,生理水平的BPA可以通过CSCs促进卵巢癌.
向GPR30或Exportin-5可能为BPA诱导的卵巢癌提供治疗策略.

关键词:

双 A 是一种双 A.癌症干细胞是癌症干细胞.这是一个微型RNA.雌激素受体的受体卵巢癌是发生在卵巢的癌症.

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