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miR-193b-3p通过PRNP向抑制肺癌细胞迁移和入侵

Hsiang-Ling Ho^1,2, Shin-Chih Lin¹, Chao-Wei Chiang¹

¹Department of Pathology and Laboratory Medicine, Taipei Veterans General Hospital, Taipei, 112201, Taiwan.

Journal of biomedical science

|February 19, 2025

概括

这项研究揭示了一条新的途径,即c-Jun抑制miR-193b-3p,增加PrPc并促进肺癌转移. 针对这一轴为肺癌提供了潜在的新疗法.

科学领域:

分子瘤学分子瘤学
癌症转移的机制癌症转移的机制
通过RNA介导的基因调节.

背景情况:

肺癌转移导致~90%的死亡.
细胞蛋白 (PrPc) 增强了肺癌的侵袭性.
关于PRNP转录后调节的研究有限.

研究的目的:

研究PRNP在肺癌中的转录后调节.
阐明微RNA在控制PRNP表达中的作用.
确定影响肺癌细胞迁移和入侵的调节途径.

主要方法:

双露西法酶记者测定和RNA免疫沉 (RIP) 确定了miRNA-PRNP相互作用.
染色体免疫沉 (ChIP) 试验确定了c-Jun作为miR-193b-3p的调节者.
在实验室 (基于细胞) 和体内 (老鼠异种移植) 模型中评估了功能角色.

主要成果:

miR-193b-3p直接准PRNP 3'-UTR,降低PrPc的表达,抑制肺癌细胞的迁移,入侵和增殖.
c-Jun作为miR-193b-3p的转录抑制剂.
高的PrPc或c-Jun表达和低的miR-193b-3p表达与较差的患者存活率相关.
在小鼠模型中,miR-193b-3p模仿注射减少了瘤体积.

结论:

一个新的c-Jun-miR-193b-3p-PrPc调节轴促进了肺癌转移.
这一途径涉及c-Jun抑制miR-193b-3p,导致PRNP上调.
这个轴介绍了使用RNA向策略的肺癌治疗的潜在治疗点.

关键词:

在此期间,PRNP PRNP.细胞的质蛋白质是细胞的质蛋白质.这是入侵的入侵.肺癌是一种肺癌.转移转移转移转移移民移民移民转录后的监管转录后的监管在 miR-193b-3p 中.

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