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微小RNA-1247-3p靶向信号转导和转录激活因子5A以抑制肺腺癌细胞迁移和化疗耐药性。

miR-1247-3p targets STAT5A to inhibit lung adenocarcinoma cell migration and chemotherapy resistance.

作者信息

Lin Jiansheng, Zheng Xinyang, Tian Xikun, Guan Jun, Shi Haizhan

机构信息

Department of cardiothoracic surgery, The First Hospital of Putian City, No 449 Nanmen West Road, 351100, Chengxiang District, Putian City, Fujian Province, China.

Chosenmed technology (Beijing) Co., Ltd, No. 156, Jinghai 4th Road, Tongzhou District, Beijing, China.

出版信息

J Cancer. 2022 Mar 28;13(7):2040-2049. doi: 10.7150/jca.65167. eCollection 2022.

DOI:10.7150/jca.65167
PMID:35517418
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9066213/
Abstract

Although several advancements have been achieved in research and treatment of lung adenocarcinoma in the past few years, the mechanism concerning cancerous cell migration and the cause of chemoresistance remains ambiguous. This research aimed to explore the impact of miR-1247-3p in lung adenocarcinoma. The mRNA expression of miR-1247-3p and STAT5A were conducted with qRT-PCR. Lentiviral vectors containing miR-1247-3p mimics and inhibitors were constructed. Cell migration were examined using Transwell assay. To observe chemotherapy resistance, Docetaxel, Doxorubicin, and Gefitinib were used. DIANA, miRDB, and TargetScan databases were applied to detect target genes. The binding sites were verified by double luciferase assay. Low expression of miR-1247-3p was observed in lung adenocarcinoma tissues and cell lines. Its expression was lower in advanced stages. Cell migration of lung adenocarcinoma was inhibited by miR-1247-3p, and it could negatively regulate the process of chemoresistance. miR-1247-3p directly binds to 3' UTR of STAT5A mRNA, and it functions via targeting STAT5A. miR-1247-3p acted as a potential governor monitoring cell migration and chemotherapy resistance of LUAD by interacting with STAT5A. It has the potential to be exploited as novel therapeutic target for LUAD in the future.

摘要

尽管在过去几年中，肺腺癌的研究和治疗取得了一些进展，但癌细胞迁移的机制和化疗耐药的原因仍不明确。本研究旨在探讨miR-1247-3p在肺腺癌中的作用。采用qRT-PCR检测miR-1247-3p和STAT5A的mRNA表达。构建了含有miR-1247-3p模拟物和抑制剂的慢病毒载体。使用Transwell实验检测细胞迁移。为了观察化疗耐药性，使用了多西他赛、阿霉素和吉非替尼。应用DIANA、miRDB和TargetScan数据库检测靶基因。通过双荧光素酶实验验证结合位点。在肺腺癌组织和细胞系中观察到miR-1247-3p低表达。其在晚期表达更低。miR-1247-3p抑制肺腺癌细胞迁移，并可负向调节化疗耐药过程。miR-1247-3p直接与STAT5A mRNA的3'UTR结合，并通过靶向STAT5A发挥作用。miR-1247-3p通过与STAT5A相互作用，作为一种潜在的调控因子监测LUAD的细胞迁移和化疗耐药性。未来它有可能被开发为LUAD的新型治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d189/9066213/95936de4e276/jcav13p2040g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d189/9066213/598ac5813296/jcav13p2040g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d189/9066213/88e482db59da/jcav13p2040g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d189/9066213/94721cad7cc9/jcav13p2040g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d189/9066213/8da026581ba0/jcav13p2040g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d189/9066213/96b51efc4116/jcav13p2040g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d189/9066213/95936de4e276/jcav13p2040g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d189/9066213/598ac5813296/jcav13p2040g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d189/9066213/88e482db59da/jcav13p2040g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d189/9066213/94721cad7cc9/jcav13p2040g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d189/9066213/8da026581ba0/jcav13p2040g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d189/9066213/96b51efc4116/jcav13p2040g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d189/9066213/95936de4e276/jcav13p2040g006.jpg

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