睡眠丧失诱导的瘤性途径通过神经元特异的互白素-1受体辅助蛋白 (AcPb) 进行介导
Yool Lee1, Erika L English2, Catherine M Schwartzmann3
1Department of Translational Medicine and Physiology, Elson S. Floyd College of Medicine, Washington State University, Spokane, WA 99202, USA; Sleep and Performance Research Center, Washington State University, Spokane, WA 99202, USA; Steve Gleason Institute for Neuroscience, Washington State University, Spokane, WA 99202, USA.
睡眠障碍通过AcPb通路调节癌症相关基因,促进促瘤的大脑环境. 这种效应在AcPb无值小鼠中减弱,表明AcPbbb.
科学领域:
- 神经科学是一个神经科学.
- 在瘤学瘤学.
- 免疫学 免疫学 免疫学
背景情况:
- 互乐金-1β (IL1) 是睡眠调节,免疫反应和瘤发育中的关键细胞因子.
- IL1受体辅助蛋白 (AcP) 和其神经元特异的异型AcPb介导IL1信号传递.
- 在此之前,AcPb在睡眠和神经网络中的作用已经在AcPb无细胞小鼠中得到证实.
研究的目的:
- 为了研究急性睡眠障碍 (SD) 对脑癌相关途径的影响.
- 为了比较野生型 (WT) 和AcPb无 (AcPb-/-) 小鼠中的这些效应.
主要方法:
- 利用RNA测序分析睡眠中断后从WT和AcPb-/-小鼠的脑组织.
- 进行了转录组和通路丰富分析.
- 结合发现与癌症基因组图谱 (TCGA) 数据库.
主要成果:
- 睡眠障碍在WT小鼠中增加了AcPb mRNA,但不是AcP mRNA.
- 在SD后的WT小鼠中观察到癌症,免疫和病毒途径的显著变化.
- 这些SD诱导的途径改变在AcPb-/-小鼠中被减弱,包括减少了Src酸化依赖基因.
结论:
- 睡眠障碍促进了由AcPb调节的亲瘤性大脑环境.
- 依赖AcPb的途径与癌症的进展和转移有关.
- 通过TCGA识别的与睡眠相关的基因对LGG和GBM等脑瘤的患者预后产生影响.
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