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微RNA-3653-3p通过调节CRIPTO-1来抑制乳头甲状腺癌的进展

Xiaojun Bai¹, Yanjun Xu², Yilun Liu³

¹Department of Ultrasound in Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai Institute of Ultrasound in Medicine, Shanghai, China. 0351016@alumni.sjtu.edu.cn.

Cellular and molecular biology (Noisy-le-Grand, France)

|January 27, 2024

概括

在乳头甲状腺癌 (PTC) 中,microRNA-3653-3p (miR-3653-3p) 的下调. 抑制 miR-3653-3p 通过向 CRIPTO-1 来抑制 PTC 细胞的增殖,迁移和入侵.

科学领域:

内分泌学在内分泌学.
在瘤学瘤学.
分子生物学分子生物学

背景情况:

乳头甲状腺癌 (PTC) 是最常见的内分泌恶性瘤.
在PTC中转移显著恶化了患者的预后.
了解推动PTC进展的分子机制对于开发有效的治疗方法至关重要.

研究的目的:

为了研究miR-3653-3p在乳头甲状腺癌进展中的作用.
为了确定miR-3653-3p是否影响PTC细胞的增殖,迁移和入侵.
为了确定参与PTC病原发生的miR-3653-3p的下游目标.

主要方法:

定量实时聚合酶连锁反应 (qRT-PCR) 用于测量miR-3653-3p表达.
细胞计数工具-8 (CCK-8),殖民地形成,transwell和Matrigel测试以评估细胞行为.
双路西法酶记者测定和西方抹除以识别和验证下游目标.

主要成果:

在PTC组织中发现miR-3653-3p表达显著下调.
在体外,miR-3653-3p的过度表达抑制了PTC细胞的增殖,迁移和入侵.
克里普托-1被确定为miR-3653-3p.的直接下游目标.

结论:

miR-3653-3p在乳头甲状腺癌中充当瘤抑制剂.
在PTC进展上miR-3653-3p的抑制作用是通过CRIPTO-1调节的介导.
miR-3653-3p及其调节途径代表了PTC的潜在生物标志物和治疗点.

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