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当代肿瘤药物靶点

Editor-in-Chief

ISSN (Print): 1568-0096
ISSN (Online): 1873-5576

Research Article

ZIP14通过调控P38 MAPK通路影响宫颈癌细胞的增殖、凋亡和迁移

卷 24, 期 8, 2024

发表于: 21 November, 2023

页: [779 - 790] 页: 12

弟呕挨: 10.2174/0115680096250711231024063841

价格: $65

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摘要

背景:子宫颈癌(CC)仍然是一个主要的公共卫生问题,也是全世界女性死亡的主要原因。了解其发病机制的分子基础对于开发新的治疗策略至关重要。在这项研究中,我们旨在剖析一个特定的分子ZIP14在CC的发生和发展中的作用。 方法:我们使用基因表达Omnibus来鉴定靶基因,而使用KEGG来描述cc相关途径。分别使用CCK8、Transwell和流式细胞术评估CC细胞的增殖、迁移和凋亡水平。目的基因对CC细胞体内肿瘤发生的影响采用皮下肿瘤发生试验。 结果:在CC样品中发现ZIP14 (SLC39A14)表达过低。我们的KEGG通路分析揭示了P38丝裂原活化蛋白激酶(MAPK)通路在CC发病机制中的潜在参与。HeLa和Caski细胞中ZIP14过表达增加p38磷酸化,抑制细胞生长和迁移,促进细胞凋亡。相反,ZIP14敲低产生相反的效果。重要的是,ZIP14过表达诱导的生物效应可以被p38 MAPK通路抑制剂SB203580抵消。体内实验进一步证实了ZIP14对CC细胞迁移的影响。 结论:我们的研究首次阐明了ZIP14在CC发病机制中的关键作用,揭示了其通过激活p38 MAPK信号通路的抑制作用。这一发现不仅提供了对CC分子基础的更深入了解,而且突出了ZIP14作为一个有前途的治疗靶点。由于ZIP14具有显著的治疗干预潜力,我们的研究结果为进一步的研究奠定了坚实的基础,并为探索宫颈癌的新治疗方式铺平了道路。

关键词: 宫颈癌,ZIP14, P38 MAPK, GEO,发病机制,细胞凋亡,水平。

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