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多酶补偿在头部和部状细胞癌细胞系模型中拯救了EGFR淘汰

Megan L Ludwig¹, Nicole L Michmerhuizen², Jiayu Wang²

¹Department of Otolaryngology - Head and Neck Surgery, University of Michigan Medical School, Ann Arbor, MI 48109, United States; Program in Cellular and Molecular Biology, University of Michigan Medical School, Ann Arbor, MI 48109, United States.

Archives of oral biology

|October 16, 2023

概括

研究人员探索了对表皮生长因子受体 (EGFR) 抑制剂的耐药性,用于头部和部状细胞癌 (HNSCC). 与EGFR一起向多个激酶,包括FGFR,XIAP和IGF-1R,显示出克服治疗耐药性的希望.

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:

头部和部状细胞癌 (HNSCC) 的存活率很低.
针对EGFR的抗体塞图西马布由于耐药性而具有有限的疗效.
在HNSCC中EGFR抑制剂耐药性的机制尚未完全理解.

研究的目的:

在没有EGFR活性的情况下研究细胞生存机制.
确定HNSCC中的分子变化和抵抗途径.
发现潜在的组合疗法,以克服EGFR抑制剂耐药性.

主要方法:

使用CRISPR/Cas9.9生成了一个EGFR淘汰HNSCC细胞系.
执行RNA测序以分析转录组变化.
使用激酶抑制剂进行细胞活力测试.
在野生型和耐药HNSCC模型中测试了联合抑制剂的协同效应.

主要成果:

EGFR淘汰细胞表现出减少的增殖和增强的介质细胞表型,具有上调的EMT基因.
EGFR淘汰细胞对单个FGFR抑制剂具有抗性,但对与XIAP或IGF-1R抑制剂的组合敏感.
联合抑制EGFR,FGFR和XIAP或IGF-1R在野生类型和耐塞图西马布的HNSCC细胞中都显示出有效性.

结论:

对EGFR抑制剂的耐药性涉及到复杂的激酶网络.
一个表皮细胞到介质酶转换 (EMT) 现型和多酶耐药性与EGFR淘汰有关.
需要对患者瘤进行进一步的研究,以验证这些发现的临床应用.

关键词:

这种药物是Cetuximab.欧洲农业基金会 (EGFR) 是一个.一个FGFR1.在IGF1R中,IGF1R是指IGF1R.一个XIAP一个XIAP.

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