[miR-2110通过调控CDT1影响肺腺癌的生物学行为]

Q3 Medicine 四川大学学报(医学版) Pub Date : 2024-09-20 DOI:10.12182/20240960505
Yuan Mi, Xuzhe Li, Cong Wang, Chenxi Lin, Zhichao Zhao, Xiaofei Yan, Ping Shi, Lei Wang
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引用次数: 0

摘要

目的通过细胞和动物实验研究 miR-2110 对肺腺癌(LUAD)细胞增殖、凋亡和转移等生物学行为的影响:方法:利用ENCORI、TargetScan、miRTarBase和Tarbase等生物信息学网站分析miR-2110在LUAD样本中的表达变化,并预测miR-2110的靶点。收集 LUAD 组织样本和细胞,通过 PCR 技术验证 miR-2110 表达的变化。通过 CCK-8 试验、克隆形成试验、Transwell 试验和流式细胞术分析 LUAD 细胞功能的变化。结果:与正常肺组织相比,miR-2110 在 LUAD 组织和细胞中的表达明显降低。miR-2110的过表达抑制了LUAD细胞的增殖和转移,促进了肿瘤细胞的凋亡(与miR-2110过表达组相比,PCDT1基因逆转了miR-2110的增殖、转移和凋亡)(活体实验表明,与对照组相比,miR-2110的过表达显著降低了肿瘤增殖指标Ki67以及两种转移指标vimentin和MMP9的表达。结论:miR-2110 可通过靶向 CDT1 抑制 LUAD 的增殖和转移,为治疗 LUAD 提供了新的理论依据。
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[miR-2110 Affects the Biological Behaviors of Lung Adenocarcinoma by Regulating CDT1].

Objective: To investigate the effect of miR-2110 on the biological behaviors, such as cell proliferation, apoptosis, and metastasis, of lung adenocarcinoma (LUAD) cells by means of cell and animal experiments.

Methods: Bioinformatics websites, including ENCORI, TargetScan, miRTarBase, and Tarbase, were used to analyze the changes in the expression of miR-2110 in LUAD samples and to predict miR-2110 target. LUAD tissue samples and cells were collected and the changes in the expression of miR-2110 were verified through PCR technology. CCK-8 assay, clonogenic assay, Transwell assay, and flow cytometry were conducted to analyze alterations in the functions of LUAD cells. In addition, 10 BALB/c female nude mice aged 6 to 8 weeks were randomly divided into 2 groups, and the effect of miR-2110 on LUAD was investigated by in vivo experiments.

Results: miR-2110 was significantly decreased in LUAD tissues and cells compared with the normal lung tissues. miR-2110 overexpression inhibited the proliferation and metastasis of LUAD cells and promoted the apoptosis of tumor cells (P<0.05). Bioinformatics prediction and dual luciferase reporter gene assay results confirmed that miR-2110 could target and bind to CDT1. In addition, overexpression of CDT1 gene reversed the proliferation, metastasis, and apoptosis of miR-2110 compared with the miR-2110 overexpression group (P<0.05). Nude mice in vivo experiments showed that miR-2110 overexpression significantly decreased the expression of Ki67, a tumor proliferation index, and vimentin and MMP9, two metastasis indices, compared with the control group.

Conclusion: miR-2110 can inhibit proliferation and metastasis of LUAD by targeting CDT1, providing a new rationale for the treatment of LUAD.

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来源期刊
四川大学学报(医学版)
四川大学学报(医学版) Biochemistry, Genetics and Molecular Biology-Molecular Biology
CiteScore
0.70
自引率
0.00%
发文量
8695
期刊介绍: "Journal of Sichuan University (Medical Edition)" is a comprehensive medical academic journal sponsored by Sichuan University, a higher education institution directly under the Ministry of Education of the People's Republic of China. It was founded in 1959 and was originally named "Journal of Sichuan Medical College". In 1986, it was renamed "Journal of West China University of Medical Sciences". In 2003, it was renamed "Journal of Sichuan University (Medical Edition)" (bimonthly). "Journal of Sichuan University (Medical Edition)" is a Chinese core journal and a Chinese authoritative academic journal (RCCSE). It is included in the retrieval systems such as China Science and Technology Papers and Citation Database (CSTPCD), China Science Citation Database (CSCD) (core version), Peking University Library's "Overview of Chinese Core Journals", the U.S. "Index Medica" (IM/Medline), the U.S. "PubMed Central" (PMC), the U.S. "Biological Abstracts" (BA), the U.S. "Chemical Abstracts" (CA), the U.S. EBSCO, the Netherlands "Abstracts and Citation Database" (Scopus), the Japan Science and Technology Agency Database (JST), the Russian "Abstract Magazine", the Chinese Biomedical Literature CD-ROM Database (CBMdisc), the Chinese Biomedical Periodical Literature Database (CMCC), the China Academic Journal Network Full-text Database (CNKI), the Chinese Academic Journal (CD-ROM Edition), and the Wanfang Data-Digital Journal Group.
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