阿斯塔山丁通过通过二维基化来向USP39介导的β-catenin稳定,从而抑制肝细胞癌

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Xiaomei Li^1,2, Huiyuan Xu¹, Ruoxi Chen¹

¹School of Basic Medicine, Putian University, Putian, 351100, Fujian, China.

Scientific reports

|November 14, 2025

概括

阿斯丁通过向USP39来抑制肝细胞癌 (HCC),从而导致β-catenin的降解,并阻断Wnt/β-catenin通路. 这揭示了阿斯塔克桑的新奇机制.

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:

在肝细胞癌 (HCC) 中,阿斯丁通过Wnt/β-catenin通路显示出潜在的抗癌作用.
在HCC中调节Wnt/β-catenin通路时,二基酶USP39的作用需要进一步研究.

研究的目的:

阐明阿斯塔丁抗HCC作用的机制,重点关注USP39和Wnt/β-catenin通路.
研究USP39作为HCC治疗中潜在的治疗点.

主要方法:

在体外研究使用HepG2和HuH7细胞系与阿斯塔丁治疗,评估增殖 (CCK-8,殖民地形成,EDU).
分析USP39,β-catenin和Cyclin D1的表达方式,通过Western blot和qPCR.
在裸体小鼠体内异种移植模型以评估瘤生长和分子变化.

主要成果:

阿斯坦丁降低了HCC细胞活力和瘤生长,降低了USP39,β-catenin和Cyclin D1水平.
通过抑制USP39,阿斯丁促进了β-catenin的无处不在和降解,从而阻断了Wnt/β-catenin的信号传输.
过度表达β-catenin部分逆转了USP39的抗瘤作用.

结论:

阿斯塔丁通过准USP39产生抗HCC作用,从而导致β-catenin的无化和降解.
在HCC中,USP39在阿斯塔丁抑制Wnt/β-catenin通路方面发挥着关键作用.
针对USP39,可能与阿斯塔丁结合,为HCC治疗提供了一个有前途的策略.

关键词:

阿斯塔克桑丁是一种阿斯塔克桑丁.肝细胞癌是肝细胞癌.核武器的扩散 USP39 美国39 在Ubiquitination中使用.在B-catenin中.

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