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诺基诺可以提高胰岛素样生长因子结合蛋白3的调节,抑制细胞生长和胰岛素样生长因子信号传递

Chih-Ling Chung¹, Chun-Lin Chen²

¹Department of Biological Sciences, National Sun Yat-Sen University, Kaohsiung, 80424, Taiwan.

European journal of pharmacology

|February 29, 2024

概括

诺基诺 (FQs) 促进胰岛素样生长因子结合蛋白3 (IGFBP-3) 的产生,通过p53依赖的途径抑制癌细胞生长. 这揭示了FQ和相关化合物的新型抗癌机制.

科学领域:

药理学药理学是指药理学的学科.
在瘤学瘤学.
分子生物学分子生物学

背景情况:

诺基诺 (FQs) 具有已知的抗生素特性和对癌细胞的新兴抗增殖作用.
在FQ抗癌活性和免疫调节反应的基础上的精确机制在很大程度上仍未被阐明.
胰岛素样生长因子结合蛋白3 (IGFBP-3) 参与调节细胞增殖和存活.

研究的目的:

研究诺 (FQs) 对类似胰岛素的生长因子结合蛋白3 (IGFBP-3) 生产的生物学影响.
阐明p53瘤抑制蛋白在调解FQ诱导的IGFBP-3生产和抗增殖作用中的作用.
通过新的机制探索FQs作为抗癌剂的潜力.

主要方法:

用FQs对培养细胞和小鼠模型进行治疗.
量化IGFBP-3的mRNA表达和蛋白质分泌.
在p53-依赖和p53-独立的环境中评估细胞增殖,细胞亡和瘤生长,包括p53-无和倒置模型.
采用一种同源性小鼠肝细胞癌 (HCC) 模型进行体内验证.

主要成果:

在培养细胞和小鼠模型中,FQs显著增加了IGFBP-3mRNA表达和蛋白质分泌.
由FQ诱导的IGFBP-3通过抑制IGF-I信号和通过IGF独立的途径来抑制细胞生长.
FQs的抗增殖作用依赖于p53;抑制在p53-null和淘汰细胞中被逆转.
齐普罗夫洛克萨在小鼠HCC模型中证明了瘤细胞亡诱导和瘤生长衰减.

结论:

FQs以p53依赖的方式诱导IGFBP-3的产生,从而抑制细胞增殖.
这项研究揭示了FQs作为抗增殖剂的新型作用机制.
研究结果表明,FQ或其衍生物在癌症治疗和预防策略中的潜在治疗应用.

关键词:

氨基氨基 (Fluoroquinolone) 是一种可以在 IGFBP-3 中.胰岛素类生长因子胰岛素类生长因子瘤是一个瘤.在 p53 里,p53 是一个 p53 的代码.

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