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含有4抑制的布罗莫多因通过调节巨细胞极化来对抗胃癌前病变

Lei Zhu¹, Qingxin Cai², Gang Li¹

¹Department of Gastrointestinal Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, China.

|October 13, 2024

概括

odomain 4 (BRD4) 上调促进胃癌前病变 (GPL) 通过影响巨细胞极化和上皮细胞癌变. 抑制BRD4可能是预防胃癌进展的新策略.

科学领域:

胃肠道学和瘤学
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

胃癌前期病变 (GPL),包括肠道甲增生和不增生,是胃癌的关键前体.
了解推动GPL进展的分子机制对于开发有效的癌症预防策略至关重要.

研究的目的:

研究odomain 4 (BRD4) 在胃癌前病变 (GPL) 的发展中的作用.
评估BRD4淘汰对病变进展,巨细胞极化和上皮细胞恶性表型的影响.

主要方法:

胃癌前病变 (GPL) 的老鼠模型是使用1-甲基-3-酸-1-酸瓜尼丁 (MNNG) 诱导的.
在体内和体外 (人类胃上皮细胞GES-1细胞) 中,BRD4被击败.
分析了巨分化和上皮细胞恶性表型,使用病理学部分,免疫组织化学,西部斑点和免疫光.

主要成果:

在老鼠模型中,MNNG诱导导致BRD4水平增加.
降低BRD4 Knockdown降低了GPL的严重程度,抑制了上皮细胞-介质细胞过渡,并抑制了M2巨细胞两极分化.
在GES-1细胞和THP-1衍生的M2巨细胞中,BRD4的淘汰减弱了恶性表型.

结论:

BRD4上调与胃癌前病变 (GPL) 的发展有关.
在GPL期间,BRD4会影响巨细胞极化和上皮细胞癌化.
向BRD4抑制是一种潜在的治疗策略,可以在癌前阶段预防胃癌.

关键词:

胃癌是什么?胃癌是什么?胃癌前的病变是胃癌前的病变.基因调节基因调节在MNNG中,MNNG是MNNG.巨细胞的两极分化

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