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miRNA-642a-5p 通过靶向Ⅰ型胶原α1 抑制结肠癌细胞迁移和侵袭

MicroRNA‑642a‑5p inhibits colon cancer cell migration and invasion by targeting collagen type I α1.

机构信息

Department of Surgery, The Second Affiliated Hospital of Jiaxing University, Jiaxing, Zhejiang 314000, P.R. China.

出版信息

Oncol Rep. 2021 Mar;45(3):933-944. doi: 10.3892/or.2020.7905. Epub 2020 Dec 18.

DOI:10.3892/or.2020.7905
PMID:33650641
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7859924/
Abstract

The aim of the present study was to explore the mechanism by which microRNA (miR)‑642a‑5p regulates the migration and invasion of colon cancer cells via collagen type I α1 (COL1A1). The characteristics of miR‑642a‑5p and COL1A1 were analysed through bioinformatics. Cancer and normal tissues were collected from patients with colon cancer. miR‑642a‑5p‑ and COL1A1‑overexpressing cell lines were constructed by transfection. A dual‑luciferase reporter assay was used to verify the targeting of COL1A1 by miR‑642a‑5p. Cell Counting Kit‑8, wound healing and Transwell assays were used to detect cell viability, migration and invasion, respectively. Protein and mRNA expression levels were examined by western blotting and reverse transcription‑quantitative PCR, respectively. The results revealed that miR‑642a‑5p expression was significantly upregulated and COL1A1 expression was downregulated in patients with colon cancer. Low levels of miR‑642a‑5p and high levels of COL1A1 were associated with a poor prognosis in patients with colon cancer. miR‑642a‑5p directly targeted the 3'‑untranslated region of COL1A1 and inhibited COL1A1 expression. Overexpression of miR‑642a‑5p inhibited cell viability, migration, invasion and epithelial mesenchymal transition. Overexpression of COL1A1 promoted cell viability, migration, invasion and EMT, and partially reversed the inhibitory effects of miR‑642a‑5p on colon cancer cells. In conclusion, miR‑642a‑5p inhibited colon cancer cell migration, invasion and EMT by regulating COL1A1.

摘要

本研究旨在探讨 microRNA(miR)-642a-5p 通过胶原蛋白 I 型α1(COL1A1)调控结肠癌细胞迁移和侵袭的机制。通过生物信息学分析 miR-642a-5p 和 COL1A1 的特征。收集结肠癌患者的癌组织和正常组织。通过转染构建 miR-642a-5p 和 COL1A1 过表达细胞系。双荧光素酶报告实验验证 COL1A1 是 miR-642a-5p 的靶基因。细胞计数试剂盒-8 实验、划痕愈合实验和 Transwell 实验分别用于检测细胞活力、迁移和侵袭。Western blot 和逆转录-定量 PCR 分别用于检测蛋白和 mRNA 表达水平。结果显示,结肠癌患者 miR-642a-5p 表达显著上调,COL1A1 表达下调。低水平的 miR-642a-5p 和高水平的 COL1A1 与结肠癌患者的不良预后相关。miR-642a-5p 可直接靶向 COL1A1 的 3'非翻译区并抑制 COL1A1 表达。miR-642a-5p 过表达抑制细胞活力、迁移、侵袭和上皮间质转化。COL1A1 过表达促进细胞活力、迁移、侵袭和 EMT,并部分逆转 miR-642a-5p 对结肠癌细胞的抑制作用。综上所述,miR-642a-5p 通过调节 COL1A1 抑制结肠癌细胞迁移、侵袭和 EMT。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3252/7859924/34241150666a/OR-45-03-0933-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3252/7859924/f057551921f1/OR-45-03-0933-g00.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3252/7859924/b090c2df9304/OR-45-03-0933-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3252/7859924/fbd05f8798df/OR-45-03-0933-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3252/7859924/34241150666a/OR-45-03-0933-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3252/7859924/f057551921f1/OR-45-03-0933-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3252/7859924/82b89f8feb63/OR-45-03-0933-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3252/7859924/234e6157d8f6/OR-45-03-0933-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3252/7859924/54b1cba348d3/OR-45-03-0933-g03.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3252/7859924/fbd05f8798df/OR-45-03-0933-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3252/7859924/34241150666a/OR-45-03-0933-g06.jpg

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