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Updated: Jun 8, 2025

Overexpressing Long Noncoding RNAs Using Gene-activating CRISPR

Overexpressing Long Noncoding RNAs Using Gene-activating CRISPR

Published on: March 1, 2019

DOK1促进了ccRCCCC的发展

Wei Xie¹, Yuanfeng Zhang², Bian Shu³

¹The Affiliated Chongqing General Hospital of Chongqing University, School of Medicine, Chongqing University, Chongqing, China, zip code: 401147.

Journal of Cancer

|November 8, 2024

概括

接蛋白1 (DOK1) 通过增强增殖和迁移,促进清细胞细胞癌 (ccRCC) 的进展. DOK1可以作为ccRCC治疗的生物标志物和治疗点.

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:

细胞癌 (RCC),特别是透明细胞亚型 (ccRCC),占全球癌症负担的重要部分.
目前尚不完全了解ccRCC瘤发生的分子驱动因素.
作为潜在的瘤抑制剂的对接蛋白1 (DOK1) 在ccRCC病变发生过程中的作用目前尚不清楚.

研究的目的:

研究DOK1在清细胞细胞癌中的预后意义和功能作用.
阐明DOK1影响ccRCC进展的分子机制.

主要方法:

对患者数据的生物信息分析,以将DOK1表达与预后相关联.
定量聚合酶连锁反应 (qPCR) 和西部涂抹来评估ccRCC中的DOK1mRNA和蛋白质水平.
试验室试验评估DOK1对ccRCC细胞行为的影响.

主要成果:

在ccRCC组织和细胞中,DOK1在mRNA和蛋白质水平上显著过度表达.
高DOK1表达与较差的患者存活率和晚期瘤阶段有关.
过度表达DOK1加速了ccRCC细胞的增殖,迁移,入侵和上皮-介质细胞过渡 (EMT).
DOK1似乎通过PI3K/AKT/GSK3β信号通路来调节ccRCC的进展.

结论:

过度表达DOK1促进ccRCC的进展,并与患者的不良结果有关.
DOK1通过PI3K/AKT/GSK3β信号通路作用,推动ccRCC的发展.
DOK1代表了ccRCC的潜在诊断生物标志物和治疗点.

关键词:

DOK1 是一个DOK1 这就是KIRC.这就是PI3K-AKTT.ccRCC ccRCC 在线观看表皮细胞-介质细胞过渡.

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