Cyto‑biological effects of microRNA‑424‑5p on human colorectal cancer cells

MicroRNA (miR)-424-5p is overexpressed in colorectal cancer (CRC); however, its role, clinical significance and underlying molecular mechanism have remained to be fully elucidated. The aim of the present study was to investigate the roles of miR-424-5p in CRC and the underlying mechanisms. It was de...

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Veröffentlicht in:Oncology letters 2020-10, Vol.20 (4), p.1-1
Hauptverfasser: Yan, Weitao, Jiang, Xia, Wang, Guiqi, Li, Wei, Zhai, Congjie, Chen, Shihao, Shang, Fangjian, Zhao, Zengren, Yu, Weifang
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container_end_page 1
container_issue 4
container_start_page 1
container_title Oncology letters
container_volume 20
creator Yan, Weitao
Jiang, Xia
Wang, Guiqi
Li, Wei
Zhai, Congjie
Chen, Shihao
Shang, Fangjian
Zhao, Zengren
Yu, Weifang
description MicroRNA (miR)-424-5p is overexpressed in colorectal cancer (CRC); however, its role, clinical significance and underlying molecular mechanism have remained to be fully elucidated. The aim of the present study was to investigate the roles of miR-424-5p in CRC and the underlying mechanisms. It was demonstrated that miR-424-5p is overexpressed in CRC, based on bioinformatics analysis using The Cancer Genome Atlas TCGA and analysis of tissue samples from patients with CRC from The First Hospital of Hebei Medical University, and the expression of miR-424-5p was associated with the depth of invasion and Dukes' staging. In CRC cells, the oncogenic roles of miR-424-5p were also verified by Cell Counting Kit-8, wound healing and Transwell assays. To identify target genes, all transcripts were compared between miR-424-5p mimic-transfected SW480 cells and mimic control cells by transcriptome sequencing. Subsequently, the differentially expressed genes (DEGs) were subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. The DEGs were revealed to be significantly enriched inthe GO terms 'serine hydrolase activity,' 'serine-type peptidase activity' and 'serine-type endopeptidase activity'. KEGG signaling pathway analysis indicated that the DEGs were significantly enriched in 'endocytosis', 'regulation of actin cytoskeleton', 'Wnt signaling pathway' and 'ubiquitin-mediated proteolysis signaling pathway'. These results suggested that miR-424-5p is a potential target in the treatment of CRC.
doi_str_mv 10.3892/ol.2020.11982
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The aim of the present study was to investigate the roles of miR-424-5p in CRC and the underlying mechanisms. It was demonstrated that miR-424-5p is overexpressed in CRC, based on bioinformatics analysis using The Cancer Genome Atlas TCGA and analysis of tissue samples from patients with CRC from The First Hospital of Hebei Medical University, and the expression of miR-424-5p was associated with the depth of invasion and Dukes' staging. In CRC cells, the oncogenic roles of miR-424-5p were also verified by Cell Counting Kit-8, wound healing and Transwell assays. To identify target genes, all transcripts were compared between miR-424-5p mimic-transfected SW480 cells and mimic control cells by transcriptome sequencing. Subsequently, the differentially expressed genes (DEGs) were subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. The DEGs were revealed to be significantly enriched inthe GO terms 'serine hydrolase activity,' 'serine-type peptidase activity' and 'serine-type endopeptidase activity'. KEGG signaling pathway analysis indicated that the DEGs were significantly enriched in 'endocytosis', 'regulation of actin cytoskeleton', 'Wnt signaling pathway' and 'ubiquitin-mediated proteolysis signaling pathway'. 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source Spandidos Publications Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central
subjects Analysis
Cancer genetics
Cell adhesion & migration
Cell culture
Cell growth
Colorectal cancer
Experiments
Genetic aspects
Genomes
Genomics
Medical schools
Methylene blue
MicroRNA
MicroRNAs
Oncology
Scientific equipment industry
Wound healing
title Cyto‑biological effects of microRNA‑424‑5p on human colorectal cancer cells
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