相关实验视频
Updated: Jun 20, 2025

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In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
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[circ_BACH2通过调节miR-370-3p影响乳头甲状腺癌的恶性生物行为]
1Departemnt of Otolaryngology, the Fourth Central Hospital of Tianjin, Tianjin 300140, China.
Zhonghua zhong liu za zhi [Chinese journal of oncology]
|July 22, 2024
概括
沉默circ_BACH2通过向miR-370-3p和GIT1来抑制乳头甲状腺癌的进展,减少扩散,迁移和入侵,同时促进体外和体内细胞灭绝.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
背景情况:
- 乳头甲状腺癌 (PTC) 是最常见的甲状腺癌类型.
- 了解推动PTC进展的分子机制对于开发有效疗法至关重要.
研究的目的:
- 研究循环RNA BACH2 (circ_BACH2) 在乳头甲状腺癌恶性行为中的作用.
- 阐明涉及miR-370-3p和G蛋白结合受体激酶相互作用因子1 (GIT1) 的分子机制.
主要方法:
- 通过RT-qPCR和西白斑来评估基因和蛋白质的表达.
- 细胞检测包括流细胞计,CCK-8,Transwell和克隆形成,以评估增殖,亡,迁移和入侵.
- 双 luciferase 记者测定以确认目标关系.
- 在裸体小鼠的体内瘤形成实验中.
主要成果:
- 在PTC组织和细胞中,circ_BACH2和GIT1被上调,而miR-370-3p被下调.
- circ_BACH2与GIT1正相关,与miR-370-3p负相关.
- 沉默circ_BACH2抑制了PTC细胞的增殖,迁移,入侵和瘤生长,同时促进了亡.
- miR-370-3p抑制或GIT1过度表达可以逆转这些效应.
结论:
- circ_BACH2通过海绵化miR-370-3p促进PTC进展,导致GIT1表达的增加.
- 针对circ_BACH2/miR-370-3p/GIT1轴为乳头甲状腺癌提供了一个潜在的治疗策略.
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