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miR-197-3p 诱导的赖氨酸 63 去泛素化酶下调促进肺腺癌细胞系的细胞增殖并抑制细胞凋亡。

miR‑197‑3p‑induced downregulation of lysine 63 deubiquitinase promotes cell proliferation and inhibits cell apoptosis in lung adenocarcinoma cell lines.

机构信息

Department of Thoracic Surgery, Chest Hospital of Shenyang, Shenyang, Liaoning 110044, P.R. China.

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

出版信息

Mol Med Rep. 2018 Mar;17(3):3921-3927. doi: 10.3892/mmr.2017.8333. Epub 2017 Dec 20.

DOI:10.3892/mmr.2017.8333
PMID:29286108
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5802183/
Abstract

Lung adenocarcinoma (LUAD) is a common cause of cancer-associated mortality. The dysregulation of microRNA (miR) expression has been reported to induce lung carcinogenesis. In the present study, miR‑197‑3p upregulation was detected within LUAD tissues compared with in adjacent noncancerous tissues. The suppression of miR‑197‑3p expression was confirmed to inhibit proliferative ability and induce apoptosis of LUAD cell lines; miR‑197‑3p overexpression within the HBE cell line exhibited opposing effects. Via in silico modeling, western blot analyses and dual‑luciferase assays, it was confirmed that miR‑197‑3p directly targets the lysine 63 deubiquitinase (CYLD) gene. In the present study, the expression of miR‑197‑3p was negatively associated with CYLD mRNA expression within LUAD cell lines. In conclusion, the findings of the present study have provided novel insight into the association of miR‑197‑3p with LUAD proliferation and apoptotic regulation; the miR‑197‑3p/CYLD axis may serve as a novel potential therapeutic target for the treatment of LUAD.

摘要

肺腺癌 (LUAD) 是癌症相关死亡的常见原因。已有研究报道,微小 RNA (miR) 表达失调可诱导肺癌发生。在本研究中,与相邻非癌组织相比,LUAD 组织中 miR-197-3p 的表达上调。抑制 miR-197-3p 的表达被证实可抑制 LUAD 细胞系的增殖能力并诱导其凋亡;而在 HBE 细胞系中过表达 miR-197-3p 则呈现出相反的效果。通过计算机建模、western blot 分析和双荧光素酶报告基因实验,证实 miR-197-3p 可直接靶向赖氨酸 63 去泛素化酶 (CYLD) 基因。本研究还发现,在 LUAD 细胞系中,miR-197-3p 的表达与 CYLD mRNA 表达呈负相关。综上所述,本研究为 miR-197-3p 与 LUAD 增殖和凋亡调控之间的关联提供了新的见解;miR-197-3p/CYLD 轴可能成为 LUAD 治疗的新的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d8/5802183/9b496cbefb34/MMR-17-03-3921-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d8/5802183/4d79747ac141/MMR-17-03-3921-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d8/5802183/2da9bfca286e/MMR-17-03-3921-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d8/5802183/c7ac0cf95385/MMR-17-03-3921-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d8/5802183/45e8b676b266/MMR-17-03-3921-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d8/5802183/9b496cbefb34/MMR-17-03-3921-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d8/5802183/4d79747ac141/MMR-17-03-3921-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d8/5802183/2da9bfca286e/MMR-17-03-3921-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d8/5802183/c7ac0cf95385/MMR-17-03-3921-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d8/5802183/45e8b676b266/MMR-17-03-3921-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d8/5802183/9b496cbefb34/MMR-17-03-3921-g04.jpg

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