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通过SNHG15介导的反循环与HNRNPA1/SLC7A11/GPX4通路相互作用,促进胃癌的进展

Yantao Duan^1,2, Yonghao Yan^1,2, Hongbing Fu³

¹Department of Gastric Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.

|May 8, 2024

概括

长非编码RNA SNHG15通过调节铁亡来促进胃癌 (GC). 它增强细胞生长,迁移和入侵,为GC治疗提供了一个新的治疗点.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
遗传学是一个遗传学.

背景情况:

长非编码RNAs (lncRNAs) 与胃癌 (GC) 的启动和进展有关.
在GC中,lncRNA SNHG15的特定作用和调节机制在很大程度上仍未被描述.
了解SNHG15在铁亡中的参与对于新的治疗策略至关重要.

研究的目的:

为了研究SNHG15在胃癌中的生物功能.
阐明SNHG15在GC进展和铁亡中的作用背后的分子机制.
确定SNHG15作为胃癌的潜在治疗点.

主要方法:

对GC组织 (队列和TCGA) 的RNA测序 (RNA-seq) 数据分析.
定量实时PCR (qRT-PCR) 用于SNHG15验证.
在体外和体外的功能增益和丧失测试.
涉及转录因子 (E2F1,MYC),微RNA海绵 (miR-24-3p),RNA结合蛋白 (HNRNPA1) 和铁亡标记物 (SLC7A11,GPX4) 的机制研究.

主要成果:

SNHG15在GC中表达很高,与晚期和不良预后相关.
在体外和体内,SNHG15促进GC细胞生长,迁移和入侵.
SNHG15的表达受到瘤转录因子E2F1和MYC的上调.
SNHG15通过通过HNRNPA1稳定SLC7A11,调节SLC7A11/GPX4轴来抑制铁亡.

结论:

在胃癌中,SNHG15充当致癌性lncRNA,由E2F1和MYC驱动.
SNHG15通过一种依赖于HNRNPA1的机制调节铁,其中包括SLC7A11/GPX4.
SNHG15代表了胃癌治疗的有前途的治疗标.

关键词:

E2F1 E2F1 E2F1 E2F1 E2F1 E2F1 E2F1 E2F1 在HNRNPA1中.我的世界 MYC 在SNHG15中,SNHG15是第15个.铁性化 (ferroptosis) 是一种胃癌胃癌是一种胃癌.

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