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LncRNA RHPN1-AS1 Targeting miR-625/REG3A Promotes Cell Proliferation And Invasion Of Glioma Cells

INTRODUCTION: Glioma arises from the proliferation of neuroglial cells differentiated from the ectoderm. Evidence has confirmed that differentially expressed long non-coding RNAs (lncRNAs) may be involved in the development and progression of various tumors. The present study aimed to explore the bi...

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Autores principales: Cui, Peng, Su, Jichun, Li, Qingmin, Xu, Guangming, Zhu, Ningxi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6769163/
https://www.ncbi.nlm.nih.gov/pubmed/31576148
http://dx.doi.org/10.2147/OTT.S209563
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author Cui, Peng
Su, Jichun
Li, Qingmin
Xu, Guangming
Zhu, Ningxi
author_facet Cui, Peng
Su, Jichun
Li, Qingmin
Xu, Guangming
Zhu, Ningxi
author_sort Cui, Peng
collection PubMed
description INTRODUCTION: Glioma arises from the proliferation of neuroglial cells differentiated from the ectoderm. Evidence has confirmed that differentially expressed long non-coding RNAs (lncRNAs) may be involved in the development and progression of various tumors. The present study aimed to explore the biological function of lncRNA RHPN1-AS1 in glioma. MATERIALS AND METHODS: The expressions of RHPN1-AS1 in glioma tissues and cells were examined using RT-PCR. Colony formation assay, MTT assay, wound healing assay and transwell assay were performed to detect cell cloning efficiency, proliferation, migration and invasion of glioma cells, respectively. Western blot was applied to assess the expression levels of migration-related and invasion-related proteins. Online bioinformatic tools and luciferase reporter assay were, respectively, employed to predict and verify the downstream target microRNA/gene of RHPN1-AS1. RESULTS: RHPN1-AS1 was up-regulated in glioma tissues and cells. The cell proliferation, migration and invasion of glioma were inhibited when the expression of RHPN1-AS1 was down-regulated in glioma cells. The expressions of migration-related and invasion-related proteins were also suppressed in siRHPN1-AS1 groups. Furthermore, we predicted and verified that RHPN1-AS1 was directly targeted to miR-625-5p/REG3A. Our study demonstrated that the knockdown of RHPN1-AS1 inhibited the proliferation, migration and invasion activity of glioma cells via regulating miR-625-5p/REG3A expression. CONCLUSION: The results revealed that the lncRNA RHPN1-AS1 may be a molecular target in glioma therapy.
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spelling pubmed-67691632019-10-01 LncRNA RHPN1-AS1 Targeting miR-625/REG3A Promotes Cell Proliferation And Invasion Of Glioma Cells Cui, Peng Su, Jichun Li, Qingmin Xu, Guangming Zhu, Ningxi Onco Targets Ther Original Research INTRODUCTION: Glioma arises from the proliferation of neuroglial cells differentiated from the ectoderm. Evidence has confirmed that differentially expressed long non-coding RNAs (lncRNAs) may be involved in the development and progression of various tumors. The present study aimed to explore the biological function of lncRNA RHPN1-AS1 in glioma. MATERIALS AND METHODS: The expressions of RHPN1-AS1 in glioma tissues and cells were examined using RT-PCR. Colony formation assay, MTT assay, wound healing assay and transwell assay were performed to detect cell cloning efficiency, proliferation, migration and invasion of glioma cells, respectively. Western blot was applied to assess the expression levels of migration-related and invasion-related proteins. Online bioinformatic tools and luciferase reporter assay were, respectively, employed to predict and verify the downstream target microRNA/gene of RHPN1-AS1. RESULTS: RHPN1-AS1 was up-regulated in glioma tissues and cells. The cell proliferation, migration and invasion of glioma were inhibited when the expression of RHPN1-AS1 was down-regulated in glioma cells. The expressions of migration-related and invasion-related proteins were also suppressed in siRHPN1-AS1 groups. Furthermore, we predicted and verified that RHPN1-AS1 was directly targeted to miR-625-5p/REG3A. Our study demonstrated that the knockdown of RHPN1-AS1 inhibited the proliferation, migration and invasion activity of glioma cells via regulating miR-625-5p/REG3A expression. CONCLUSION: The results revealed that the lncRNA RHPN1-AS1 may be a molecular target in glioma therapy. Dove 2019-09-26 /pmc/articles/PMC6769163/ /pubmed/31576148 http://dx.doi.org/10.2147/OTT.S209563 Text en © 2019 Cui et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Original Research
Cui, Peng
Su, Jichun
Li, Qingmin
Xu, Guangming
Zhu, Ningxi
LncRNA RHPN1-AS1 Targeting miR-625/REG3A Promotes Cell Proliferation And Invasion Of Glioma Cells
title LncRNA RHPN1-AS1 Targeting miR-625/REG3A Promotes Cell Proliferation And Invasion Of Glioma Cells
title_full LncRNA RHPN1-AS1 Targeting miR-625/REG3A Promotes Cell Proliferation And Invasion Of Glioma Cells
title_fullStr LncRNA RHPN1-AS1 Targeting miR-625/REG3A Promotes Cell Proliferation And Invasion Of Glioma Cells
title_full_unstemmed LncRNA RHPN1-AS1 Targeting miR-625/REG3A Promotes Cell Proliferation And Invasion Of Glioma Cells
title_short LncRNA RHPN1-AS1 Targeting miR-625/REG3A Promotes Cell Proliferation And Invasion Of Glioma Cells
title_sort lncrna rhpn1-as1 targeting mir-625/reg3a promotes cell proliferation and invasion of glioma cells
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6769163/
https://www.ncbi.nlm.nih.gov/pubmed/31576148
http://dx.doi.org/10.2147/OTT.S209563
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