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NKX3.1表达有助于前列腺癌细胞的上皮-半细胞过渡

Iroda Saydullaeva¹, Bilge Debelec Butuner², Kemal Sami Korkmaz¹

¹Faculty of Engineering, Department of Bioengineering, Cancer Biology Laboratory, Ege University, Izmir 35040, Turkey.

|September 18, 2023

概括

炎症通过改变瘤抑制剂NKX3.1的表达来推动前列腺癌的进展,促进细胞迁移和转移. 这项研究揭示了表皮细胞到介质酶过渡 (EMT) 和介质酶到表皮细胞过渡 (MET) 现型之间的动态转变.

科学领域:

在瘤学瘤学.
细胞生物学细胞生物学
分子生物学分子生物学

背景情况:

炎症与侵袭性前列腺癌和转移有关,但机制尚不清楚.
之前的研究表明,受条件介质 (CM) 诱导LNCaP细胞迁移,与NKX3.1损失有关.
这项研究研究了炎症在前列腺癌细胞迁移和NKX3.1的功能中的作用.

研究的目的:

综合分析炎症介导的前列腺癌细胞迁移.
阐明瘤抑制剂NKX3.1在这个过程中的作用.
了解动态的表型变化,包括上皮细胞转化为介质细胞 (EMT) 和介质细胞转化为上皮细胞 (MET).

主要方法:

利用了瘤微环境中炎症的优化模型.
研究了CM暴露和NKX3.1表达变化的时间依赖性影响.
使用CRISPR/Cas9消耗NKX3.1并分析暴露于炎性细胞因子的迁移细胞.
进行了定量蛋白质组分析和KEGG通路分析.

主要成果:

炎症诱导的迁移包括可逆的E-cadherin损失和改变的维门丁表达,表明EMT.
NKX3.1 枯竭加剧了迁移和EMT表型.
雌激素受体 (AR) 介导的转录在前列腺癌进展期间有助于MET.
定量蛋白质组学揭示了具有明显表型的亚种群,过度表达参与新陈代谢和RNA处理的蛋白质;ABC载体是显著的.

结论:

炎症驱动前列腺癌细胞迁移和异质性通过动态的EMT/MET过渡.
在调节这些迁移和表型变化方面,NKX3.1起着至关重要的作用.
瘤微环境的变化会影响细胞的可塑性,影响前列腺癌的侵袭性和进展.

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