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KDM6A促进肝细胞癌的进展,并通过上调FGFR4表达的调节来决定伦瓦替尼的疗效

Wenyun Guo¹, Songling Li², Yifei Qian¹

¹State Key Laboratory of Systems Medicine for Cancer, Department of Liver Surgery, Renji-Med-X Clinical Stem Cell Research Center, RenJi Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P. R. China.

Clinical and translational medicine

|October 17, 2023

概括

通过激活FGFR4.4,KDM6A促进肝细胞癌 (HCC) 的进展. 向KDM6A可能会提高lenvatinib治疗在HCC患者的有效性,提供新的治疗策略.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
癌症研究癌症研究

背景情况:

肝细胞癌 (HCC) 的预后不好,治疗选择有限.
伦瓦提尼布在晚期HCC中表现出有限的疗效,需要新的治疗点.

研究的目的:

调查KDM6A在HCC进展中的作用及其对伦瓦提尼布敏感性的影响.
阐明KDM6A在HCC中的潜在分子机制.

主要方法:

使用了DEN-CCL4和异种移植小鼠模型,以及HCC细胞系.
在机理学研究中使用RNA测序和ChIP测定.
评估KDM6A在HCC扩散,迁移和药物敏感性中的作用.

主要成果:

在HCC中,KDM6A被上调,并与预后不佳有关.
通过KDM6A的淘汰,抑制了HCC细胞的增殖,迁移和肝脏瘤发生.
KDM6A激活FGFR4,抑制PI3K-AKT-mTOR通路并重新编程新陈代谢.
在HCC模型中,KDM6A knockdown降低了lenvatinib的疗效.

结论:

通过FGFR4激活,KDM6A促进了HCC的进展.
KDM6A是HCC预后和伦瓦替尼治疗疗效的潜在生物标志物.

关键词:

在FGFR4中.在KDM6A中,KDM6A是肝细胞癌是肝细胞癌.伦瓦提尼布 (Lenvatinib) 是一种药物.脂质新陈代谢脂质新陈代谢

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