Knockdown of linc01023 restrains glioma proliferation, migration and invasion by regulating IGF-1R/AKT pathway

LncRNAs have been proved to be involved in the promotion of glioma cell malignant development. However, the exact roles and molecular mechanisms of linc01023 in glioma remain blurred. In this study, we confirm linc01023 is up-regulated in glioma tissues and cell lines. In addition, elevated linc0102...

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Detalles Bibliográficos
Autores principales: Yu, Mingjun, Yu, Shijia, Gong, Wei, Chen, Duo, Guan, Junhong, Liu, Yunhui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2019
Materias:
Research Paper
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6590038/
https://www.ncbi.nlm.nih.gov/pubmed/31281473
http://dx.doi.org/10.7150/jca.31004
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author Yu, Mingjun
Yu, Shijia
Gong, Wei
Chen, Duo
Guan, Junhong
Liu, Yunhui
author_facet Yu, Mingjun
Yu, Shijia
Gong, Wei
Chen, Duo
Guan, Junhong
Liu, Yunhui
author_sort Yu, Mingjun
collection PubMed
description LncRNAs have been proved to be involved in the promotion of glioma cell malignant development. However, the exact roles and molecular mechanisms of linc01023 in glioma remain blurred. In this study, we confirm linc01023 is up-regulated in glioma tissues and cell lines. In addition, elevated linc01023 expression indicates shorter survival times in patients with glioma. Moreover, loss-of-function studies reveal that restoration of linc01023 restrains glioma cell proliferation, migration and invasion by regulating IGF1R/AKT pathway in vitro and in vivo. Collectively, the study indicates that linc01023 plays an oncogenic role in glioma through activation of IGF1R/AKT signal pathway, and it could be a candidate therapeutic target.
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spelling pubmed-65900382019-07-06 Knockdown of linc01023 restrains glioma proliferation, migration and invasion by regulating IGF-1R/AKT pathway Yu, Mingjun Yu, Shijia Gong, Wei Chen, Duo Guan, Junhong Liu, Yunhui J Cancer Research Paper LncRNAs have been proved to be involved in the promotion of glioma cell malignant development. However, the exact roles and molecular mechanisms of linc01023 in glioma remain blurred. In this study, we confirm linc01023 is up-regulated in glioma tissues and cell lines. In addition, elevated linc01023 expression indicates shorter survival times in patients with glioma. Moreover, loss-of-function studies reveal that restoration of linc01023 restrains glioma cell proliferation, migration and invasion by regulating IGF1R/AKT pathway in vitro and in vivo. Collectively, the study indicates that linc01023 plays an oncogenic role in glioma through activation of IGF1R/AKT signal pathway, and it could be a candidate therapeutic target. Ivyspring International Publisher 2019-06-02 /pmc/articles/PMC6590038/ /pubmed/31281473 http://dx.doi.org/10.7150/jca.31004 Text en © Ivyspring International Publisher This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license (https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions.
spellingShingle Research Paper
Yu, Mingjun
Yu, Shijia
Gong, Wei
Chen, Duo
Guan, Junhong
Liu, Yunhui
Knockdown of linc01023 restrains glioma proliferation, migration and invasion by regulating IGF-1R/AKT pathway
title Knockdown of linc01023 restrains glioma proliferation, migration and invasion by regulating IGF-1R/AKT pathway
title_full Knockdown of linc01023 restrains glioma proliferation, migration and invasion by regulating IGF-1R/AKT pathway
title_fullStr Knockdown of linc01023 restrains glioma proliferation, migration and invasion by regulating IGF-1R/AKT pathway
title_full_unstemmed Knockdown of linc01023 restrains glioma proliferation, migration and invasion by regulating IGF-1R/AKT pathway
title_short Knockdown of linc01023 restrains glioma proliferation, migration and invasion by regulating IGF-1R/AKT pathway
title_sort knockdown of linc01023 restrains glioma proliferation, migration and invasion by regulating igf-1r/akt pathway
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6590038/
https://www.ncbi.nlm.nih.gov/pubmed/31281473
http://dx.doi.org/10.7150/jca.31004
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