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胰岛素样生长因子2和mRNA结合蛋白3通过调节AKT1和RELA表达增强了黑色素瘤的迁移

Yi-Shuan Sheen¹, Yan-Jie Syu^1,2, Yu-Chuan Chang³

¹Department of Dermatology, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan.

Experimental dermatology

|January 29, 2024

概括

胰岛素样生长因子2-6受体结合蛋白3 (IMP-3) 通过调节AKT1和RELA促进黑色素瘤细胞迁移. 高水平的IMP-3与黑色素瘤预后不佳以及患者样本中AKT1和RELA表达的增加相关.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

胰岛素样生长因子2曼诺6-酸盐受体结合蛋白3 (IMP-3) 是黑色素瘤的一个不良预后因素.
IMP-3促进黑色素瘤细胞迁移和入侵,部分通过调节HMGA2mRNA表达.

研究的目的:

为了确定IMP-3的额外RNA目标.
阐明IMP-3增强黑色素瘤细胞迁移的分子机制.

主要方法:

配合RNA免疫沉和下一代测序 (RIP-Seq) 来识别IMP-3结合RNAs.
使用细胞系进行过度表达和淘汰研究 (MeWo,A2058).
小干扰RNA (siRNA) 和等离子体转移来调节基因表达.
对人类黑色素瘤样本的分析.

主要成果:

IMP-3直接与AKT1,MAPK3,RB1和RELARNAs进行结合.
IMP-3的过度表达会增加MeWo细胞中的AKT和RELA蛋白水平.
抑制AKT1或RELA可以抑制黑色素瘤细胞迁移.
阻断IMP-3降低了AKT1和RELA的表达,并减少了A2058细胞的迁移.
恢复AKT1或RELA表达可以逆转IMP-3对迁移的抑制作用.
HMGA2不会影响AKT1或RELA的表达.
人类黑色素瘤中的高IMP-3水平与高HMGA2,AKT1和RELA表达相关.

结论:

IMP-3通过调节AKT1和RELA轴来增强黑色素瘤细胞迁移.
IMP-3在黑色素瘤进展中的作用涉及超出HMGA2调节的途径.
针对IMP-3/AKT1/RELA轴可能为黑色素瘤提供治疗策略.

关键词:

一个AKT1一个AKT1 在HMGA2中使用.在IMP-3中,IMP-3是IMP-3.在RELA中,您可以使用RELA.黑色素瘤是一种黑色素瘤.

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