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假基因OCT4-pg5通过与miR-145-5p竞争,上调OCT4B的表达,促进膀癌的进展

Wuer Zhou¹, Yue Yang^1,2, Wei Wang^1,2

¹The Department of Urology, General Hospital of Southern Theater Command, PLA, Guangzhou, China.

Cell cycle (Georgetown, Tex.)

|June 6, 2024

概括

通过促进EMT和激活Wnt/β-catenin通路,OCT4-pg5/miR-145-5p/OCT4B网络推动了膀癌 (BC) 的进展和对西斯普拉丁的耐药性. 这个轴是BC的潜在治疗目标.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
生物化学生物化学

背景情况:

膀癌 (BC) 是全球流行的一种恶性瘤.
竞争的内源性RNA (ceRNA) 网络为BC进展和预后提供了潜在的生物标志物.
在BC中OCT4-pg5/miR-145-5p/OCT4B ceRNA网络的作用需要阐明.

研究的目的:

研究OCT4-pg5/miR-145-5p/OCT4B ceRNA网络在膀癌 (BC) 进展中的作用.
探索这种网络影响BC细胞行为和化学抵抗的潜在机制.
评估这个网络作为BC的治疗目标的潜力.

主要方法:

对BC细胞系中的OCT4-pg5和OCT4B表达的分析与正常膀细胞的分析.
评估OCT4-pg5,OCT4B和miR-145-5p对BC细胞增殖和入侵的影响.
使用3'UTR试验,研究OCT4-pg5和miR-145-5p之间的相互作用.
通过Wnt/β-catenin通路和下游目标 (MMPs,ZEB1/2) 评估OCT4-pg5对上皮质-介质酶过渡 (EMT) 的影响.
确定OCT4-pg5和OCT4B对BC细胞对西斯普拉丁敏感性的影响,包括细胞亡和细胞周期分析.

主要成果:

在BC细胞中,OCT4-pg5表达升高,与OCT4B表达和晚期瘤等级相关.
过度表达OCT4-pg5和OCT4B增强了BC细胞的增殖和入侵,而miR-145-5p抑制了这些效应.
OCT4-pg5与miR-145-5p竞争结合,导致OCT4B的表达增加.
OCT4-pg5通过Wnt/β-catenin通路诱导EMT,从而上调MMP和ZEB因子.
升高的OCT4-pg5和OCT4B通过抑制细胞亡和促进G1细胞循环停止来降低西斯普拉丁的敏感性.

结论:

在OCT4-pg5/miR-145-5p/OCT4B轴通过Wnt/β-catenin通路诱导EMT促进BC进展.
这一轴增强了BC细胞对西斯的抵抗力.
OCT4-pg5/miR-145-5p/OCT4B网络代表了膀癌的一个有希望的治疗点.

关键词:

其他CTOS4-pg5 其他国家/地区CT4B 膀癌:膀癌是一种癌症.竞争的内源性RNA.在 miR-145-5p 中使用.

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