Circ_0104700通过向miR-66565来增强MCM2表达,有助于急性髓性白血病的进展
Kang Chen1, Xiaohan Ning1, Xiaohong Yan1
1Department of Hematology, The Affiliated Qingdao Central Hospital of Qingdao University, Qingdao, Shandong, People's Republic of China.
Hematology (Amsterdam, Netherlands)
|June 26, 2023
概括
这项研究表明,circ_0104700通过通过miR-665.5增加MCM2表达来促进急性髓性白血病 (AML) 的进展. 向circ_0104700,miR-665或MCM2可能为AML提供新的治疗策略.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 基因规则 基因规则
背景情况:
- 急性髓性白血病 (AML) 是一种具有不良预后的血液性恶性瘤.
- 识别驱动AML病变的新型分子机制对于开发有效疗法至关重要.
研究的目的:
- 为了研究circ_0104700在AML病变发生中的作用.
- 为了阐明circ_0104700在AML进展中的潜在分子机制.
主要方法:
- 在AML样本和细胞系中分析了Circ_0104700的表达.
- 功能性测试包括甲基纤维素殖民地形成,CCK-8,细胞循环和亡分析.
- 机制探索涉及生物信息学,RT-qPCR,双露西法酶记者测定和西部抹杀.
主要成果:
- Circ_0104700在AML上调并促进细胞活力,同时抑制细胞亡.
- Circ_0104700的耗尽在G0/G1阶段停止了细胞周期.
- Circ_0104700 作为 miR-665 的竞争性内源RNA,调节 MCM2 的上升,并激活 JAK/STAT 信号.
结论:
- Circ_0104700通过通过海绵化miR-665.5增强MCM2表达来促进AML的进展.
- Circ_0104700,miR-665和MCM2代表了AML治疗的潜在治疗点.
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