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微小RNA-373-3p通过淀粉样前体蛋白促进肺腺癌细胞增殖。

miR-373-3p promotes lung adenocarcinoma cell proliferation via APP.

作者信息

Fan Xiaoxi, Xu Shun, Yang Chunlu

机构信息

Department of Thoracic Surgery, First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.

出版信息

Oncol Lett. 2018 Jan;15(1):1046-1050. doi: 10.3892/ol.2017.7372. Epub 2017 Nov 8.

DOI:10.3892/ol.2017.7372
PMID:29387243
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5768135/
Abstract

Previous studies have indicated that lung adenocarcinoma (LUAD) is one of the common human malignancies, and its incidence keeps rising. With the help of microarray technology, downregulation of miR-373-3p was observed in LUAD tissues compared with normal lung tissues. Notably, the present study demonstrated that the expression of amyloid precursor protein (APP) mRNA in LUAD tissues was overexpressed compared with adjacent tissues. Bioinformatic analysis demonstrated that miR-373-3p may interact with the 3' untranslated region of APP mRNA, and then western blot and dual-luciferase reporter gene assays were employed to verify the interaction. Finally, CCK-8 assays were used to measure the tumor-suppressing effect of miR-373-3p on A549 and it was demonstrated that overexpression of miR-373-3p may more effectively inhibit the proliferation of A549 compared with APP si-RNA. Overall, the findings suggest that miR-373-3p downregulation partly accounts for APP overexpression and leads to a promotion of cell growth in LUAD. miR-373-3p may therefore act as a valuable target in potential anticancer strategies to treat LUAD.

摘要

先前的研究表明,肺腺癌(LUAD)是常见的人类恶性肿瘤之一,其发病率持续上升。借助微阵列技术,与正常肺组织相比,在LUAD组织中观察到miR-373-3p表达下调。值得注意的是,本研究表明,与相邻组织相比,LUAD组织中淀粉样前体蛋白(APP)mRNA的表达上调。生物信息学分析表明,miR-373-3p可能与APP mRNA的3'非翻译区相互作用,随后采用蛋白质免疫印迹法和双荧光素酶报告基因测定法来验证这种相互作用。最后,使用CCK-8测定法来检测miR-373-3p对A549细胞的肿瘤抑制作用,结果表明,与APP小干扰RNA相比,miR-373-3p的过表达可能更有效地抑制A549细胞的增殖。总体而言,研究结果表明,miR-373-3p表达下调部分导致APP表达上调,并促进LUAD细胞生长。因此,miR-373-3p可能成为治疗LUAD潜在抗癌策略中的一个有价值靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfe0/5768135/667c1b98801c/ol-15-01-1046-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfe0/5768135/6e65c660914d/ol-15-01-1046-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfe0/5768135/d14ba77e4e6f/ol-15-01-1046-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfe0/5768135/53fdc69bd2c7/ol-15-01-1046-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfe0/5768135/c3c7cd1735f0/ol-15-01-1046-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfe0/5768135/667c1b98801c/ol-15-01-1046-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfe0/5768135/6e65c660914d/ol-15-01-1046-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfe0/5768135/d14ba77e4e6f/ol-15-01-1046-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfe0/5768135/53fdc69bd2c7/ol-15-01-1046-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfe0/5768135/c3c7cd1735f0/ol-15-01-1046-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfe0/5768135/667c1b98801c/ol-15-01-1046-g04.jpg

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