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通过抑制FGF19/FGFR4/PRL来恢复由布罗姆克里普丁诱导的耐药性益生菌瘤中的布罗姆克里普丁敏感性

Z Zhu¹, B Hu², D Zhu²

¹Department of Histology and Embryology, Zhongshan School of Medicine, Sun Yat-Sen University, No.74 Zhongshan Road 2, Guangzhou, 510080, Guangdong, China.

Journal of endocrinological investigation

|June 26, 2024

概括

通过向FGF19/FGFR4通路,可以克服益生菌瘤的耐药性. 与FGFR4抑制剂结合布罗莫克里普丁的治疗显示出治疗耐药性益生菌瘤的前景.

科学领域:

内分泌学在内分泌学.
在瘤学瘤学.
分子生物学分子生物学

背景情况:

甲状腺瘤是常见的垂体瘤,通常用烯胺 (BRC) 治疗.
对BRC的耐药性是治疗益生菌瘤的一个重大临床挑战.
了解BRC耐药性的机制对于开发有效疗法至关重要.

研究的目的:

为了研究基底的分子机制 BRC耐药性在prolactinomas.
确定克服BRC耐药性的潜在治疗点.
评估涉及BRC和FGFR4抑制的组合治疗的疗效.

主要方法:

已确立的BRC诱导的耐药益生菌瘤细胞模型.
利用RNA测序和生物信息学进行基因查.
使用CCK-8,殖民地形成和流细胞计,评估细胞活力,增殖和亡.
通过qRT-PCR,西式涂抹,IHC,IF和Co-IP分析了分子变化.
评估了体外和体外异种移植模型中的组合疗法.

主要成果:

在耐药细胞和瘤中观察到纤维细胞生长因子19 (FGF19) 的表达升高.
沉默FGF19增加了BRC的灵敏度,并减少了FGFR4的酸化.
FGF19与FGFR4结合,通过ERK1/2和JNK通路调节益乳素 (PRL) 合成.
结合BRC和FGFR4抑制剂费索加提尼布 (FISO),协同抑制瘤生长,促进亡,并降低PRL水平.

结论:

确定了FGF19/FGFR4信号作为BRC抗性益生菌瘤中的新机制.
针对FGF19/FGFR4通路提供了一个克服耐药性的潜在策略.
结合BRC和FGFR4抑制剂的联合治疗显示出对抗性益生菌瘤的治疗潜力.

关键词:

布罗莫克里普提因 (bromocriptine) 是一种蛋白质.药物耐药性药物耐药性药物耐药性联邦财政基金19年这是一种FGFR4抑制剂.孕产腺瘤是什么? 孕产腺瘤是什么孕产腺瘤是什么

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