由阿尼索米辛驱动的miR-134-3p通过抑制GPR137表达来降低卵巢癌干细胞活性
Lele Ling1, Yichao Wen2, Haiyang Chen2
1Department of Acupuncture and Moxibustion, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200086, China.
Journal of Cancer
|November 29, 2023
概括
一种化合物anisomycin可以通过增加miR-134-3p来降低卵巢癌干细胞活性. 这种微RNA针对GPR137,影响NDEL1/DYNEIN/TUBA1A轴,并可能阻碍癌症的进展.
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:
- 卵巢癌复发和转移与卵巢癌干细胞有关.
- 对人类卵巢癌干细胞 (HuOCSCs) 的安尼索米的调控机制尚未完全理解.
研究的目的:
- 为了研究素如何影响HuOCSCs.
- 为了识别微RNAs (miRNAs) 和它们的基因,这些基因参与了异粒素的作用.
- 阐明卵巢癌中由这些miRNAs调节的分子通路.
主要方法:
- 使用cDNA微阵列,RT-qPCR和TargetScan对miRNA目标的查和验证.
- 功能性检测包括细胞增殖,流细胞计,Transwell,血管生成和体内瘤检测.
- 基因和蛋白质表达的分析通过西方斑点和免疫光学.
- 生物信息分析,以评估目标基因在卵巢癌中的作用.
主要成果:
- anisomycin显著提高了miR-134-3p表达,这是DLK1-DIO3印记miRNA集群中的一个成员.
- 过度表达miR-134-3p抑制了HuOCSC活动,并显著减少了GPR137的表达.
- miR-134-3p通过向GPR137.7来调节NDEL1/DYNEIN/TUBA1A轴,影响细胞骨和迁移.
- 生物信息学表明,GPR137,NDEL1,DYNC1H1,TUBA1A和卵巢癌的发展/预后之间存在很强的相关性.
结论:
- 素可以通过miR-134-3p抑制HuOCSC活性.
- miR-134-3p的机制包括抑制GPR137/NDEL1/DYNEIN/TUBA1A信号通路.
- 这一途径与卵巢癌的进展和患者的治疗结果有关.
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