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LINC00894抑制了神经元细胞亡,并调节了激活转录因子3的表达
Hanjing Hu1, Yuxiao Liu1, Cheng Qiu1
1Department of Biochemistry and Molecular Biology, School of Medicine, Key Laboratory of Neuroregeneration and Ministry of Education of Jiangsu, Co-innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Nantong University, Nantong, Jiangsu, China.
Gene
|June 10, 2024
概括
长非编码RNA LINC00894促进神经元细胞的增殖,并抑制细胞亡. 这项研究揭示了LINC008944.
科学领域:
- 神经科学是一个神经科学.
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
背景情况:
- 在神经细胞中LINC00894的生物功能在很大程度上是未知的.
- 长非编码RNAs (lncRNAs) 越来越多地被认为是它们在细胞过程中的角色.
研究的目的:
- 研究LINC00894在神经元细胞增殖和亡中的作用.
- 阐明LINC00894在神经母细胞瘤细胞中的功能背后的分子机制.
主要方法:
- 细胞活力测试 (MTT,CCK-8) 进行.
- 亡测定 (附录V-FITC,激活的Caspase3) 测定
- 反应性氧物种 (ROS) 测量测量
- RNA测序 (RNA-seq) 是指RNA的测序.
- 定量逆转录聚合酶连锁反应 (RT-qPCR) 是一种
- 免疫阻塞是指免疫阻塞.
主要成果:
- LINC00894 knockdown 降低了细胞增殖和活力,同时增加了细胞亡和ROS水平.
- LINC00894 保护细胞免受过氧化诱导的亡.
- 发现LINC00894可以调节激活转录因子3 (ATF3) 的表达.
- 宫外ATF3表达在LINC00894下调细胞中挽救了增殖缺陷和亡.
- ATF3的淘汰加剧了LINC00894的淘汰对细胞活力和细胞亡的影响.
结论:
- LINC00894促进神经元细胞的增殖,并抑制细胞亡.
- 该机制涉及调节ATF3表达的机制.
- LINC00894在神经母细胞瘤细胞中起着保护作用.
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