miR-338-3p inhibits cell growth, invasion, and EMT process in neuroblastoma through targeting MMP-2

This study aimed to explore the regulatory mechanisms of miR-338-3p and matrix metalloproteinase-2 (MMP-2) in neuroblastoma. Putative target interaction regions of miR-338-3p on MMP-2 were predicted by miRcode and miRbase bioinformatics tools. Relative expression of miRNA-338-3p and MMP-2 in neurobl...

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Autores principales: Yuan Haibin, Liu Fengli, Ma Tongsheng, Zeng Zhandong, Zhang Ning
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Lenguaje:EN
Publicado: De Gruyter 2021
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spelling oai:doaj.org-article:848019f1ebf9427aa04f630ae5081d952021-12-05T14:10:40ZmiR-338-3p inhibits cell growth, invasion, and EMT process in neuroblastoma through targeting MMP-22391-541210.1515/biol-2021-0013https://doaj.org/article/848019f1ebf9427aa04f630ae5081d952021-03-01T00:00:00Zhttps://doi.org/10.1515/biol-2021-0013https://doaj.org/toc/2391-5412This study aimed to explore the regulatory mechanisms of miR-338-3p and matrix metalloproteinase-2 (MMP-2) in neuroblastoma. Putative target interaction regions of miR-338-3p on MMP-2 were predicted by miRcode and miRbase bioinformatics tools. Relative expression of miRNA-338-3p and MMP-2 in neuroblastoma tissues and GI-LI-N and SK-N-SH cells was determined by reverse transcription polymerase chain reaction experiment. Furthermore, the cell proliferation was determined by Cell Counting Kit-8 assay, the cell apoptosis rate was analyzed by flow cytometry assay, and the cell invasion was evaluated by transwell assay. miR-338-3p expression was downregulated, whereas MMP-2 expression was upregulated in metastasis tissue site compared to that in primary tissue site in total. Furthermore, miR-338-3p overexpression suppressed proliferation, invasion, and epithelial–mesenchymal transition (EMT) of neuroblastoma cells but promoted apoptosis, and the knockdown of MMP-2 triggered similar effects. Furthermore, MMP-2 was directly targeted by miR-338-3p, and overexpression of MMP-2 rescued the inhibitory effects of miR-338-3p on human neuroblastoma cell progression. Collectively, these data demonstrated that miR-338-3p could suppress cell growth, invasion, and EMT pathway and induce apoptosis in neuroblastoma cells by targeting MMP-2. MiR-338-3p sponged MMP-2 to regulate the PI3K/AKT pathway in human neuroblastoma cells.Yuan HaibinLiu FengliMa TongshengZeng ZhandongZhang NingDe Gruyterarticleneuroblastomamir-338-3pmmp-2emt pathwaypi3k/akt signalingBiology (General)QH301-705.5ENOpen Life Sciences, Vol 16, Iss 1, Pp 198-209 (2021)
institution DOAJ
collection DOAJ
language EN
topic neuroblastoma
mir-338-3p
mmp-2
emt pathway
pi3k/akt signaling
Biology (General)
QH301-705.5
spellingShingle neuroblastoma
mir-338-3p
mmp-2
emt pathway
pi3k/akt signaling
Biology (General)
QH301-705.5
Yuan Haibin
Liu Fengli
Ma Tongsheng
Zeng Zhandong
Zhang Ning
miR-338-3p inhibits cell growth, invasion, and EMT process in neuroblastoma through targeting MMP-2
description This study aimed to explore the regulatory mechanisms of miR-338-3p and matrix metalloproteinase-2 (MMP-2) in neuroblastoma. Putative target interaction regions of miR-338-3p on MMP-2 were predicted by miRcode and miRbase bioinformatics tools. Relative expression of miRNA-338-3p and MMP-2 in neuroblastoma tissues and GI-LI-N and SK-N-SH cells was determined by reverse transcription polymerase chain reaction experiment. Furthermore, the cell proliferation was determined by Cell Counting Kit-8 assay, the cell apoptosis rate was analyzed by flow cytometry assay, and the cell invasion was evaluated by transwell assay. miR-338-3p expression was downregulated, whereas MMP-2 expression was upregulated in metastasis tissue site compared to that in primary tissue site in total. Furthermore, miR-338-3p overexpression suppressed proliferation, invasion, and epithelial–mesenchymal transition (EMT) of neuroblastoma cells but promoted apoptosis, and the knockdown of MMP-2 triggered similar effects. Furthermore, MMP-2 was directly targeted by miR-338-3p, and overexpression of MMP-2 rescued the inhibitory effects of miR-338-3p on human neuroblastoma cell progression. Collectively, these data demonstrated that miR-338-3p could suppress cell growth, invasion, and EMT pathway and induce apoptosis in neuroblastoma cells by targeting MMP-2. MiR-338-3p sponged MMP-2 to regulate the PI3K/AKT pathway in human neuroblastoma cells.
format article
author Yuan Haibin
Liu Fengli
Ma Tongsheng
Zeng Zhandong
Zhang Ning
author_facet Yuan Haibin
Liu Fengli
Ma Tongsheng
Zeng Zhandong
Zhang Ning
author_sort Yuan Haibin
title miR-338-3p inhibits cell growth, invasion, and EMT process in neuroblastoma through targeting MMP-2
title_short miR-338-3p inhibits cell growth, invasion, and EMT process in neuroblastoma through targeting MMP-2
title_full miR-338-3p inhibits cell growth, invasion, and EMT process in neuroblastoma through targeting MMP-2
title_fullStr miR-338-3p inhibits cell growth, invasion, and EMT process in neuroblastoma through targeting MMP-2
title_full_unstemmed miR-338-3p inhibits cell growth, invasion, and EMT process in neuroblastoma through targeting MMP-2
title_sort mir-338-3p inhibits cell growth, invasion, and emt process in neuroblastoma through targeting mmp-2
publisher De Gruyter
publishDate 2021
url https://doaj.org/article/848019f1ebf9427aa04f630ae5081d95
work_keys_str_mv AT yuanhaibin mir3383pinhibitscellgrowthinvasionandemtprocessinneuroblastomathroughtargetingmmp2
AT liufengli mir3383pinhibitscellgrowthinvasionandemtprocessinneuroblastomathroughtargetingmmp2
AT matongsheng mir3383pinhibitscellgrowthinvasionandemtprocessinneuroblastomathroughtargetingmmp2
AT zengzhandong mir3383pinhibitscellgrowthinvasionandemtprocessinneuroblastomathroughtargetingmmp2
AT zhangning mir3383pinhibitscellgrowthinvasionandemtprocessinneuroblastomathroughtargetingmmp2
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