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hsa-miR-5580-3p 通过抑制 LAMC2 抑制口腔癌细胞活力、增殖和迁移。

hsa‑miR‑5580‑3p inhibits oral cancer cell viability, proliferation and migration by suppressing LAMC2.

机构信息

Department of Gastroenterology, Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430033, P.R. China.

Department of Stomatology, Wuhan Children's Hospital (Wuhan Maternal and Child Healthcare Hospital), Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430015, P.R. China.

出版信息

Mol Med Rep. 2021 Jun;23(6). doi: 10.3892/mmr.2021.12092. Epub 2021 Apr 21.

DOI:10.3892/mmr.2021.12092
PMID:33880581
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8072311/
Abstract

The present study aimed to explore whether and how microRNA‑5580‑3p (miR‑5580‑3p) affected oral cancer (OC) cell phenotypes via regulation of laminin subunit γ2 (LAMC2). Bioinformatics analysis was used to identify miR‑5580‑3p/LAMC2, a novel interactome that, to the best of our knowledge, has not been studied previously in OC. In the present study, the expression levels of miR‑5580‑3p and LAMC2 were detected by reverse transcription‑quantitative PCR, while the protein expression levels of LAMC2 were identified using western blotting. To determine the effects of miR‑5580‑3p and LAMC2 in OC, a number of experiments, including Cell Counting Kit‑8, 5‑bromo‑2'‑deoxyuridine cell proliferation and wound healing migration assays, were performed using OC SCC‑4 and Cal‑27 cell lines. Additionally, luciferase reporter assays were employed to examine the interaction between miR‑5580‑3p and LAMC2 mRNA. The results demonstrated that miR‑5580‑3p expression was downregulated, while LAMC2 expression was upregulated in OC tissues and cell lines. In addition to the observation that miR‑5580‑3p promoted the malignant phenotypes of OC, it was also revealed that miR‑5580‑3p inhibited OC cell viability, proliferation and migration by suppressing LAMC2. Therefore, the present study suggested that miR‑5580‑3p and LAMC2 may be potential biomarkers and therapeutic targets for OC diagnosis and therapies in the future.

摘要

本研究旨在探讨微小 RNA-5580-3p(miR-5580-3p)是否以及如何通过调节层粘连蛋白亚基γ2(LAMC2)来影响口腔癌(OC)细胞表型。生物信息学分析用于鉴定 miR-5580-3p/LAMC2,这是一个新的相互作用组,据我们所知,以前在 OC 中尚未研究过。在本研究中,通过逆转录-定量 PCR 检测 miR-5580-3p 和 LAMC2 的表达水平,通过 Western blot 鉴定 LAMC2 的蛋白表达水平。为了确定 miR-5580-3p 和 LAMC2 在 OC 中的作用,使用 OC SCC-4 和 Cal-27 细胞系进行了一系列实验,包括细胞计数试剂盒-8、5-溴-2'-脱氧尿苷细胞增殖和划痕愈合迁移实验。此外,还采用荧光素酶报告基因实验来检测 miR-5580-3p 和 LAMC2 mRNA 之间的相互作用。结果表明,miR-5580-3p 的表达下调,而 LAMC2 的表达上调在 OC 组织和细胞系中。除了观察到 miR-5580-3p 促进 OC 的恶性表型外,还发现 miR-5580-3p 通过抑制 LAMC2 来抑制 OC 细胞活力、增殖和迁移。因此,本研究表明 miR-5580-3p 和 LAMC2 可能是未来 OC 诊断和治疗的潜在生物标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3eb/8072311/e394fe5ed70b/mmr-23-06-12092-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3eb/8072311/ae8e63707cd1/mmr-23-06-12092-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3eb/8072311/ce63a86b5f62/mmr-23-06-12092-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3eb/8072311/8a006122806d/mmr-23-06-12092-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3eb/8072311/f629dc31e396/mmr-23-06-12092-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3eb/8072311/e394fe5ed70b/mmr-23-06-12092-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3eb/8072311/ae8e63707cd1/mmr-23-06-12092-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3eb/8072311/ce63a86b5f62/mmr-23-06-12092-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3eb/8072311/8a006122806d/mmr-23-06-12092-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3eb/8072311/f629dc31e396/mmr-23-06-12092-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3eb/8072311/e394fe5ed70b/mmr-23-06-12092-g04.jpg

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