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LINC01088/miR-22/CDC6 Axis Regulates Prostate Cancer Progression by Activating the PI3K/AKT Pathway
Mediators of Inflammation ( IF 4.6 ) Pub Date : 2023-7-19 , DOI: 10.1155/2023/9207148
Jianwei Li 1 , Xinghua Huang 1 , Haodong Chen 1 , Caifu Gu 2 , Binyu Ni 3 , Jianhua Zhou 1
Affiliation  

Background. Prostate cancer (PCa) harms the male reproductive system, and lncRNA may play an important role in it. Here, we report that the LINC01088/microRNA- (miRNA/miR-) 22/cell division cycle 6 (CDC6) axis regulated through the phosphatidylinositide 3-kinases- (PI3K-) protein kinase B (AKT) signaling pathway controls the development of PCa. Methods. lncRNA/miRNA/mRNA associated with PCa was downloaded and analyzed by Gene Expression Omnibus. The expression and correlation of LINC01088/miR-22/CDC6 in PCa were analyzed and verified by RT-qPCR. Dual-luciferase was used to analyze the binding between miR-22 and LINC01088 or CDC6. Cell Counting Kit-8 and Transwell were used to analyze the effects of LINC01088/miR-22/CDC6 interactions on PCa cell viability or migration/invasion ability. Localization of LINC01088 in cells was analyzed by nuclear cytoplasmic separation. The effect of LINC01088/miR-22/CDC6 interaction on downstream PI3K/AKT signaling was analyzed by Western blot. Results. LINC01088 or CDC6 was upregulated in prostate tumor tissues or cells, whereas miR-22 was downregulated, miR-22 directly targets both LINC01088 and CDC6. si-LINC01088 inhibits the PCa process by suppressing the PI3K/AKT pathway. CDC6 reverses si-linc01088-mediated cell growth inhibition and reduction of PI3K and AKT protein levels. Conclusion. Our results demonstrate that the LINC01088/miR-22/CDC6 axis functions in PCa progression and provide a promising diagnostic and therapeutic target.

中文翻译:

LINC01088/miR-22/CDC6 轴通过激活 PI3K/AKT 通路调节前列腺癌进展

背景。前列腺癌(PCa)危害男性生殖系统,lncRNA可能在其中发挥重要作用。在此,我们报告通过磷脂酰肌醇 3-激酶- (PI3K-) 蛋白激酶 B (AKT) 信号通路调节的 LINC01088/microRNA- (miRNA/miR-) 22/细胞分裂周期 6 (CDC6) 轴控制细胞分裂的发育。前列腺癌。方法。通过 Gene Expression Omnibus 下载并分析与 PCa 相关的 lncRNA/miRNA/mRNA。通过RT-qPCR分析和验证LINC01088/miR-22/CDC6在PCa中的表达和相关性。使用双荧光素酶分析 miR-22 与 LINC01088 或 CDC6 之间的结合。使用 Cell Counting Kit-8 和 Transwell 分析 LINC01088/miR-22/CDC6 相互作用对 PCa 细胞活力或迁移/侵袭能力的影响。通过核细胞质分离分析 LINC01088 在细胞中的定位。通过蛋白质印迹分析 LINC01088/miR-22/CDC6 相互作用对下游 PI3K/AKT 信号传导的影响。结果。LINC01088 或 CDC6 在前列腺肿瘤组织或细胞中上调,而 miR-22 下调,miR-22 直接靶向 LINC01088 和 CDC6。si-LINC01088 通过抑制 PI3K/AKT 通路来抑制 PCa 过程。CDC6 逆转 si-linc01088 介导的细胞生长抑制以及 PI3K 和 AKT 蛋白水平的降低。结论。我们的结果表明,LINC01088/miR-22/CDC6 轴在 PCa 进展中发挥作用,并提供有前景的诊断和治疗靶点。
更新日期:2023-07-19
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