MiR-23a transcriptional activated by Runx2 increases metastatic potential of mouse hepatoma cell via directly targeting Mgat3

Abstract MicroRNAs (miRNAs) and aberrant glycosylation both play important roles in tumor metastasis. In this study, the role of miR-23a in N-glycosylation and the metastasis of mouse hepatocellular carcinoma (HCC) cells was investigated. The miRNA expression array profiles that were confirmed by qP...

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Autores principales: Huang Huang, Yubo Liu, Peishan Yu, Jianhua Qu, Yanjie Guo, Wenli Li, Shujing Wang, Jianing Zhang
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Publicado: Nature Portfolio 2018
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spelling oai:doaj.org-article:6df8d4236ca14a2c8ac9d2b070b099ab2021-12-02T11:41:25ZMiR-23a transcriptional activated by Runx2 increases metastatic potential of mouse hepatoma cell via directly targeting Mgat310.1038/s41598-018-25768-z2045-2322https://doaj.org/article/6df8d4236ca14a2c8ac9d2b070b099ab2018-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-25768-zhttps://doaj.org/toc/2045-2322Abstract MicroRNAs (miRNAs) and aberrant glycosylation both play important roles in tumor metastasis. In this study, the role of miR-23a in N-glycosylation and the metastasis of mouse hepatocellular carcinoma (HCC) cells was investigated. The miRNA expression array profiles that were confirmed by qPCR and Western blot analyses revealed higher miR-23a expression levels in Hca-P cells (with lymphatic metastasis potential) than in Hepa1–6 cells (with no lymphatic metastasis potential), while the expression of mannoside acetylglucosaminyltransferase 3 (Mgat3) was negatively associated with metastasis potential. Mgat3 is a key glycosyltransferase in the synthesis of the bisecting (β1,4GlcNAc branching) N-glycan structure. Bioinformatics analysis indicated that Mgat3 may be a target of miR-23a, and this hypothesis was verified by dual-luciferase reporter gene assays. Furthermore, we found that the transcription factor Runx2 can directly bind to the miR-23a gene promoter and promote its expression, as shown in dual-luciferase reporter gene assays and ChIP assays. Collectively, these results indicate that miR-23a might increase the metastatic potential of mouse HCC by affecting the branch formation of N-glycan chains presented on the cell surface through the targeting of the glycosyltransferase Mgat3. These findings may provide insight into the relationship between abnormal miRNA expression and aberrant glycosylation during tumor lymphatic metastasis.Huang HuangYubo LiuPeishan YuJianhua QuYanjie GuoWenli LiShujing WangJianing ZhangNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-11 (2018)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Huang Huang
Yubo Liu
Peishan Yu
Jianhua Qu
Yanjie Guo
Wenli Li
Shujing Wang
Jianing Zhang
MiR-23a transcriptional activated by Runx2 increases metastatic potential of mouse hepatoma cell via directly targeting Mgat3
description Abstract MicroRNAs (miRNAs) and aberrant glycosylation both play important roles in tumor metastasis. In this study, the role of miR-23a in N-glycosylation and the metastasis of mouse hepatocellular carcinoma (HCC) cells was investigated. The miRNA expression array profiles that were confirmed by qPCR and Western blot analyses revealed higher miR-23a expression levels in Hca-P cells (with lymphatic metastasis potential) than in Hepa1–6 cells (with no lymphatic metastasis potential), while the expression of mannoside acetylglucosaminyltransferase 3 (Mgat3) was negatively associated with metastasis potential. Mgat3 is a key glycosyltransferase in the synthesis of the bisecting (β1,4GlcNAc branching) N-glycan structure. Bioinformatics analysis indicated that Mgat3 may be a target of miR-23a, and this hypothesis was verified by dual-luciferase reporter gene assays. Furthermore, we found that the transcription factor Runx2 can directly bind to the miR-23a gene promoter and promote its expression, as shown in dual-luciferase reporter gene assays and ChIP assays. Collectively, these results indicate that miR-23a might increase the metastatic potential of mouse HCC by affecting the branch formation of N-glycan chains presented on the cell surface through the targeting of the glycosyltransferase Mgat3. These findings may provide insight into the relationship between abnormal miRNA expression and aberrant glycosylation during tumor lymphatic metastasis.
format article
author Huang Huang
Yubo Liu
Peishan Yu
Jianhua Qu
Yanjie Guo
Wenli Li
Shujing Wang
Jianing Zhang
author_facet Huang Huang
Yubo Liu
Peishan Yu
Jianhua Qu
Yanjie Guo
Wenli Li
Shujing Wang
Jianing Zhang
author_sort Huang Huang
title MiR-23a transcriptional activated by Runx2 increases metastatic potential of mouse hepatoma cell via directly targeting Mgat3
title_short MiR-23a transcriptional activated by Runx2 increases metastatic potential of mouse hepatoma cell via directly targeting Mgat3
title_full MiR-23a transcriptional activated by Runx2 increases metastatic potential of mouse hepatoma cell via directly targeting Mgat3
title_fullStr MiR-23a transcriptional activated by Runx2 increases metastatic potential of mouse hepatoma cell via directly targeting Mgat3
title_full_unstemmed MiR-23a transcriptional activated by Runx2 increases metastatic potential of mouse hepatoma cell via directly targeting Mgat3
title_sort mir-23a transcriptional activated by runx2 increases metastatic potential of mouse hepatoma cell via directly targeting mgat3
publisher Nature Portfolio
publishDate 2018
url https://doaj.org/article/6df8d4236ca14a2c8ac9d2b070b099ab
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AT wenlili mir23atranscriptionalactivatedbyrunx2increasesmetastaticpotentialofmousehepatomacellviadirectlytargetingmgat3
AT shujingwang mir23atranscriptionalactivatedbyrunx2increasesmetastaticpotentialofmousehepatomacellviadirectlytargetingmgat3
AT jianingzhang mir23atranscriptionalactivatedbyrunx2increasesmetastaticpotentialofmousehepatomacellviadirectlytargetingmgat3
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