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Mint3作为一个分子点,在肝癌发生的早期阶段被激活

Masaki Nishitani¹, Hikari Okada¹, Kouki Nio¹

¹Department of Gastroenterology, Kanazawa University Graduate School of Medical Sciences, Kanazawa 920-8641, Ishikawa, Japan.

International journal of molecular sciences

|February 26, 2025

概括

薄荷3蛋白质通过激活缺氧诱导因子-1 (HIF-1) 信号来促进早期肝癌 (肝细胞癌,HCC) 的发展. 抑制Mint3抑制了瘤生长,这表明它是预防HCC的目标.

科学领域:

分子生物学分子生物学
在瘤学瘤学.
生物化学生物化学

背景情况:

众所周知,Mint3蛋白可以增强有氧ATP的产生,并激活缺氧诱导因子-1 (HIF-1) 信号.
薄荷3在肝癌发生 (肝癌发展) 中的作用及其激活时间尚不清楚.
在瘤发育中,HIF-1激活至关重要,通常与血管生成有关.

研究的目的:

研究Mint3在肝细胞癌 (HCC) 中的表达和作用.
为了确定Mint3是否参与早期肝癌的发展.
评估Mint3作为预防HCC的潜在分子标.

主要方法:

在手术切除的HCC组织中分析了Mint3的表达.
在HCC细胞系和免疫缺陷小鼠中进行了Mint3淘汰实验.
使用Mint3淘汰赛小鼠来评估化学诱导的HCC发育.

主要成果:

在分化良好的HCC中,Mint3被过度表达,即使没有显著的高血管化,也激活了HIF-1向基因.
Mint3 敲除减少了 HIF-1 基因表达,球形形成和皮下瘤生长.
在Mint3淘汰赛小鼠中,化学诱导的HCC发育被显著抑制.

结论:

Mint3通过激活HIF-1在HCC发育的早期阶段发挥关键作用,在高血管化之前,通过激活HIF-1.
在瘤变得缺氧之前,Mint3会激活HIF-1目标基因.
Mint3代表了一个有前途的分子标,用于预防早期HCC发育.

关键词:

肝细胞癌是肝细胞癌.低氧诱导因子-1 诱导因子-1 munc18-1-相互作用蛋白3的使用情况

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