通过靶向 CCND1,上调 miR-519d-3p 可抑制口腔鳞状细胞癌细胞的活力、增殖和 G1/S 细胞周期转换。

IF 2.4 4区 医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL
Cancer Biotherapy and Radiopharmaceuticals Pub Date : 2024-03-01 Epub Date: 2020-10-14 DOI:10.1089/cbr.2020.3984
Wenjie Zhang, Wei Hong
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引用次数: 0

摘要

背景:微RNA(miR)-519d-3p可抑制肿瘤的发展,但它在口腔鳞状细胞癌(OSCC)中的作用还有待进一步确定。材料与方法:收集 OSCC 和邻近组织(邻近组织 n = 45;I-II 期 OSCC n = 21;III-IV 期 OSCC n = 24)。分别采用细胞计数试剂盒-8(CCK-8)、集落形成试验和流式细胞术评估 OSCC 的细胞活力、增殖和细胞周期。细胞周期调控蛋白(细胞周期蛋白 D1 [CCND1]、CDK4 和 CDK6)和 miR-519d-3p 的相对表达量根据需要用 Western 印迹法和定量实时聚合酶链反应法进行测定。为了验证 TargetScan 预测的 miR-519d-3p 和 CCND1 共享潜在结合位点,进行了双荧光素酶报告实验。miR-519d-3p 与 CCND1 之间的相关性分析采用 Pearson 相关性检验。结果在 OSCC 组织中,miR-519d-3p 表达下调与肿瘤分级较高有关。上调 miR-519d-3p 可抑制 OSCC 细胞的活力和增殖,增加 G0/G1 期细胞的数量,减少 S/G2 期细胞的数量,并下调细胞周期相关蛋白(CDK4、CDK6)的表达。CCND1是miR-519d-3p的靶基因,过表达CCND1可逆转miR-519d-3p上调对OSCC细胞活力、增殖和细胞周期的抑制作用。结论:miR-519d-3p上调通过靶向CCND1抑制了OSCC的细胞活力、增殖和G1/S细胞周期转换。目前的研究结果为治疗 OSCC 提供了一种可能的临床选择。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Upregulation of miR-519d-3p Inhibits Viability, Proliferation, and G1/S Cell Cycle Transition of Oral Squamous Cell Carcinoma Cells Through Targeting CCND1.

Background: MicroRNA (miR)-519d-3p suppresses tumor development, however, its role in oral squamous cell carcinoma (OSCC) has yet to be determined. Materials and Methods: OSCC and adjacent tissues were collected (n = 45 for adjacent; n = 21 for Stage I-II OSCC; n = 24 for Stage III-IV OSCC). The cell viability, proliferation, and cell cycle of OSCC were, respectively, assessed by the Cell Counting Kit-8 (CCK-8), colony formation assay, and flow cytometry. Relative expressions of cell cycle-regulated proteins (Cyclin D1 [CCND1], CDK4, and CDK6) and miR-519d-3p were measured with Western blot and quantitative real-time polymerase chain reaction as needed. Dual-luciferase reporter assay was performed to verify the prediction of TargetScan that miR-519d-3p and CCND1 shared potential binding sites. Correlation analysis between miR-519d-3p and CCND1 was performed with Pearson's correlation test. Results: In OSCC tissues, downregulating miR-519d-3p expression correlated with a higher tumor grade. Upregulating miR-519d-3p expression inhibited OSCC cell viability and proliferation, increased cells in G0/G1 phase and reduced those in S/G2 phase, and downregulated the expressions of cell cycle-related protein (CDK4, CDK6). CCND1 was the target gene of miR-519d-3p, and overexpressed CCND1 reversed the effects of upregulation of miR-519d-3p on suppressing the viability, proliferation, and cell cycle of OSCC cells. Conclusions: miR-519d-3p upregulation suppressed the cell viability, proliferation, and G1/S cell cycle transition of OSCC through targeting CCND1. The current findings provide a possible clinical option for OSCC treatment.

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来源期刊
CiteScore
7.80
自引率
2.90%
发文量
87
审稿时长
3 months
期刊介绍: Cancer Biotherapy and Radiopharmaceuticals is the established peer-reviewed journal, with over 25 years of cutting-edge content on innovative therapeutic investigations to ultimately improve cancer management. It is the only journal with the specific focus of cancer biotherapy and is inclusive of monoclonal antibodies, cytokine therapy, cancer gene therapy, cell-based therapies, and other forms of immunotherapies. The Journal includes extensive reporting on advancements in radioimmunotherapy, and the use of radiopharmaceuticals and radiolabeled peptides for the development of new cancer treatments.
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