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转录因子ATF2通过激活METTL3/cyclin D1通路促进胃癌的进展

Hong Meng¹, Jing Li², Huapeng Sun³

¹Department of Pathology, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, China.

Drug development research

|July 8, 2023

概括

激活转录因子2 (ATF2) 通过激活METTL3/cyclin D1通路,促进胃癌 (GC) 的生长,使ATF2成为GC治疗的潜在治疗标.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
生物化学生物化学

背景情况:

胃癌 (GC) 是全球癌症死亡的主要原因之一.
了解驱动GC进展的分子机制对于开发有效的治疗方法至关重要.

研究的目的:

研究胃癌中激活转录因子2 (ATF2) 的生物功能和潜在机制.
探索ATF2作为GC治疗点的潜力.

主要方法:

使用GEPIA,UALCAN,人类蛋白质图谱和StarBase数据库对GC组织中ATF2表达的生物信息分析.
定量实时聚合酶连锁反应 (qRT-PCR),细胞计数套件-8 (CCK-8),EDU测定和流动细胞计量来评估ATF2在GC细胞增殖和亡中的作用.
双露西法酶记者基因测定和染色体免疫沉定量PCR (ChIP-qPCR) 验证ATF2与METTL3促进体结合.
西方斑块和基因组丰富分析 (GSEA) 阐明METTL3/cyclin D1信号通路.

主要成果:

在GC组织和细胞系中,ATF2表达显著升高,与患者存活时间缩短相关.
过度表达ATF2增强了GC细胞的增殖和抑制了细胞灭亡,而ATF2倒置抑制了细胞增殖和促进了细胞灭亡.
ATF2直接与METTL3促进体结合,促进METTL3转录,随后增加环林D1的表达,从而促进细胞循环的进展.

结论:

通过激活METTL3/cyclin D1信号通路,ATF2促进胃癌细胞的增殖,并抑制细胞灭绝.
ATF2代表了胃癌的一个有前途的治疗标.

关键词:

在ATF2中使用ATF2.在METTL3中,METTL3是METTL3的第一个类型.灭症 (apoptosis) 是一种死亡的过程.胃癌胃癌是一种胃癌.它们的扩散和扩散.

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