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拜卡莱因促进KDM4E诱导BICD1并通过阻断PAR1信号传递来抑制三阴性乳腺癌的进展

Yun Dong¹, Gaojian He², Kun Chen³

¹Department of Traditional Chinese Medicine, Dazhou Vocational College of Chinese Medicine, Dazhou, Sichuan, China.

Molecular carcinogenesis

|April 12, 2024

概括

拜卡莱因通过增强KDM4E蛋白来对抗三阴性乳腺癌 (TNBC),这增加了BICD1的表达. 这一途径通过阻断PAR1信号来抑制TNBC的进展,提供了一种新的治疗策略.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
生物化学生物化学

背景情况:

三阴性乳腺癌 (TNBC) 仍然是一个具有挑战性的恶性瘤,治疗选择有限.
拜卡莱因是一种天然的黄类化合物,显示出克服TNBC化学抵抗的潜力.
贝卡莱因在TNBC中的作用背后的精确分子机制需要阐明.

研究的目的:

阐明贝卡莱因通过哪种分子途径发挥其抗TNBC作用.
为了识别和表征TNBC细胞中baicalein的蛋白标.
为了研究KDM4E,BICD1和PAR1在Baicalein介导的TNBC抑制中的作用.

主要方法:

在用baicalein治疗的TNBC细胞中分析KDM4E的蛋白质表达.
基因淘汰和过度表达研究,以评估KDM4E和BICD1.1的功能作用.
在BICD1促进体中进行质子修饰分析 (H3K9me3).
研究BICD1和PAR1.1之间的蛋白质-蛋白质相互作用.
评估TNBC细胞的移动性,活力,亡以及对血栓激活的反应.

主要成果:

拜卡莱因增强了TNBC细胞中氨酸特异性脱甲基酶4E (KDM4E) 的表达和稳定性.
降低KDM4E降低了Baicalein对TNBC细胞增殖和亡抵抗的抑制作用.
KDM4E通过降低H3K9me3在其促进物上升调 Bicaudal D同源1 (BICD1).
BICD1与蛋白酶激活受体-1 (PAR1) 相互作用,促进其内细胞分裂并阻断PAR1信号传递.
拜卡林诱导的KDM4E/BICD1通路激活抑制了血栓刺激的TNBC进展.

结论:

拜卡莱因通过涉及KDM4E和BICD1.1的新型分子途径抑制了TNBC的进展.
贝卡莱因-KDM4E-BICD1轴抑制了PAR1信号传递,这是TNBC的一个关键驱动因素.
这项研究确定了针对KDM4E和BICD1的有希望的治疗策略,用于TNBC治疗.

关键词:

在BICD1中,它是BICD1.这就是KDM4E.在 PAR1 信号传输中.巴伊卡莱因 (Baicalein) 是一种植物.三重阴性乳腺癌是什么?

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