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miR-4731-5p通过靶向RPLP0增强非小细胞肺癌细胞凋亡并减轻上皮-间质转化

miR-4731-5p Enhances Apoptosis and Alleviates Epithelial-Mesenchymal Transition through Targeting RPLP0 in Non-Small-Cell Lung Cancer.

作者信息

Chang Chang, Xu Meilin

机构信息

Department of Pathology, The First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang 471003, China.

Department of Pathology, Tianjin Chest Hospital, Tianjin Province 300222, China.

出版信息

J Oncol. 2022 Mar 17;2022:3793318. doi: 10.1155/2022/3793318. eCollection 2022.

DOI:10.1155/2022/3793318
PMID:35342398
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8947863/
Abstract

/. MircoRNA-4731-5p (miR-4731-5p) is a new miRNA involved in different human cancers, but its function has not been clarified in non-small-cell lung cancer (NSCLC). The present study attended to resolve the role of miR-4731-5p in NSCLC. . The expression level of miR-4731-5p or ribosomal protein large P0 (RPLP0) and NSCLC clinicopathologic characteristics were analyzed. The binding between miR-4731-5p and RPLP0 was confirmed by TargetScan prediction and luciferase reporter experiment. Also, the probable role of miR-4731-5p in NSCLC via RPLP0 was elaborated by the MTT, western blotting, immunofluorescence, transwell, flow cytometry, and TUNEL assays. Moreover, verification was conducted in xenografted nude mice. . The level of miR-4731-5p was notably declined and , which was involved in the prognosis of lung cancer patients. The miR-4731-5p mimic could remarkably restrain cell viability, invasion, and the translational expression level of vimentin and e-cadherin, with promoted cell apoptosis in NSCLC, which were notably reversed by RPLP0 overexpression. . miR-4731-5p/RPLP0 axis might be an underlying therapeutic target for NSCLC.

摘要

微小RNA-4731-5p(miR-4731-5p)是一种参与多种人类癌症的新型微小RNA,但它在非小细胞肺癌(NSCLC)中的功能尚未明确。本研究旨在阐明miR-4731-5p在NSCLC中的作用。分析了miR-4731-5p或核糖体蛋白大P0(RPLP0)的表达水平与NSCLC临床病理特征之间的关系。通过TargetScan预测和荧光素酶报告基因实验证实了miR-4731-5p与RPLP0之间的结合。此外,通过MTT、蛋白质印迹、免疫荧光、Transwell、流式细胞术和TUNEL分析阐述了miR-4731-5p通过RPLP0在NSCLC中可能发挥的作用。此外,还在异种移植裸鼠中进行了验证。miR-4731-5p的水平显著下降,且与肺癌患者的预后有关。miR-4731-5p模拟物可显著抑制NSCLC细胞的活力、侵袭以及波形蛋白和E-钙黏蛋白的翻译表达水平,并促进细胞凋亡,而RPLP0的过表达可显著逆转这些作用。miR-4731-5p/RPLP0轴可能是NSCLC的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36c7/8947863/30d087354322/JO2022-3793318.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36c7/8947863/5d98b0c71b32/JO2022-3793318.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36c7/8947863/e220886c81ec/JO2022-3793318.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36c7/8947863/86119f9d9c57/JO2022-3793318.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36c7/8947863/73b63a9c2534/JO2022-3793318.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36c7/8947863/30d087354322/JO2022-3793318.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36c7/8947863/5d98b0c71b32/JO2022-3793318.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36c7/8947863/e220886c81ec/JO2022-3793318.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36c7/8947863/86119f9d9c57/JO2022-3793318.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36c7/8947863/73b63a9c2534/JO2022-3793318.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36c7/8947863/30d087354322/JO2022-3793318.005.jpg

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