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向ONECUT2通过降低调节ZKSCAN3/VEGFA来抑制瘤血管生成

Ligang Zhang¹, Cunjie Li², Xinran Song²

¹Guangdong Province Engineering Research Center for Antibody Drug and Immunoassay, Department of Biology, Jinan University, Guangzhou 510632, China; School of Medicine, Foshan University, Foshan 528225, China.

Biochemical pharmacology

|May 26, 2024

概括

通过激活ZKSCAN3来增加VEGFA表达,OC-2促进瘤生长和血管生成. 抑制OC-2 (OC-2 KD) 抑制了瘤进展和血管生成,揭示了OC-2作为潜在的抗癌药物标.

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:

OC-2与瘤生长,转移和血管生成有关.
OC-2调节血管生成因子的精确分子机制尚不清楚.

研究的目的:

阐明OC-2在调节血管生成因子中的分子机制.
研究OC-2在瘤生长,转移和血管生成中的作用.
确定OC-2作为抗血管生成癌症药物的潜在治疗标.

主要方法:

在癌症细胞系和组织中分析OC-2的表达.
在体外和体内进行OC-2敲击 (KD) 实验.
染色体免疫沉降测序 (ChIP-Seq) 用于识别OC-2向基因.
路西法酶记者测定以确认基因点和调节途径.
对血管生成因子和信号通路的分析 (ERK1/2,Smad1).

主要成果:

在HepG2,COLO,MCF-7,SKOV3细胞和直肠癌组织中,OC-2表达高,与血管生成因子水平呈正相关性.
OC-2 KD显著抑制了瘤生长,转移和血管生成.
ChIP-Seq确定了228个OC-2点基因,这些基因参与了瘤进展和信号转导.
OC-2直接与ZKSCAN3结合,通过ZKSCAN3转录程序促进VEGFA的表达.
OC-2 KD降低了VEGFA分泌,抑制了HUVECs中的瘤血管生成.
OC-2与血管新生因子HIF-1α,FGF2,EGFL6和HGF相关.
ERK1/2和Smad1信号通路与OC-2在瘤攻击性中的作用有关.

结论:

OC-2驱动瘤生长,转移和血管生成,部分通过激活ZKSCAN3-VEGFA通路.
OC-2通过ERK1/2和Smad1信号调节瘤的攻击性.
OC-2是开发新型抗血管生成药物的有前途的治疗标.

关键词:

血管新生的产生.在OC-2中,它是OC-2.目标疗法目标疗法瘤是一个瘤.在VEGFA中,VEGFA是VEGFA.在ZKSCAN3中,我们可以看到:

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