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Quantitative proteomics analysis of glioblastoma cell lines after lncRNA HULC silencing

Glioblastoma multiforme (GBM) is a life-threatening brain tumor. This study aimed to identify potential targets of the long noncoding RNA (lncRNA) HULC that promoted the progression of GBM. Two U87 cell lines were constructed: HULC-siRNA and negative control (NC). Quantitative real-time PCR (qRT-PCR...

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Autores principales: Ye, Shan, Wu, Jing, Wang, Yiran, Hu, Yuchen, Yin, Tiantian, He, Jie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8206103/
https://www.ncbi.nlm.nih.gov/pubmed/34131250
http://dx.doi.org/10.1038/s41598-021-92089-z
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author Ye, Shan
Wu, Jing
Wang, Yiran
Hu, Yuchen
Yin, Tiantian
He, Jie
author_facet Ye, Shan
Wu, Jing
Wang, Yiran
Hu, Yuchen
Yin, Tiantian
He, Jie
author_sort Ye, Shan
collection PubMed
description Glioblastoma multiforme (GBM) is a life-threatening brain tumor. This study aimed to identify potential targets of the long noncoding RNA (lncRNA) HULC that promoted the progression of GBM. Two U87 cell lines were constructed: HULC-siRNA and negative control (NC). Quantitative real-time PCR (qRT-PCR) was performed to validate the transfection efficiency of HULC silencing vector. Mass spectrometry (MS) was used to generate proteomic profiles for the two cell lines. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed to distinguish HULC-related genes and pathway mapping. Colony formation, Transwell, and wound-healing assays were used to investigate the functional effects of HULC knockdown on GBM. We identified 112 up-regulated proteins and 24 down-regulated proteins from a total of 4360 quantified proteins. GO enrichment illustrated that these proteins were mainly involved in organelle structure, catalysis, cell movement, and material metabolism. KEGG pathway analysis indicated that some of these proteins were significantly enriched in tight junction, metabolic pathways, and arachidonic acid metabolism. In vitro experiments demonstrated that HULC knockdown inhibited GBM cell proliferation, invasion, and migration. Our KEGG analyses revealed that PLA2G4A was a shared protein in several enriched pathways. HULC silencing significantly down-regulated the expression of PLA2G4A. Knockdown of HULC changed the proteomic characteristics of GBM and altered the behaviors of GBM cells. Specifically, we identified PLA2G4A as an HULC target in GBM. This study provides a new perspective on the mechanisms and potential drug targets of GBM treatment.
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spelling pubmed-82061032021-06-16 Quantitative proteomics analysis of glioblastoma cell lines after lncRNA HULC silencing Ye, Shan Wu, Jing Wang, Yiran Hu, Yuchen Yin, Tiantian He, Jie Sci Rep Article Glioblastoma multiforme (GBM) is a life-threatening brain tumor. This study aimed to identify potential targets of the long noncoding RNA (lncRNA) HULC that promoted the progression of GBM. Two U87 cell lines were constructed: HULC-siRNA and negative control (NC). Quantitative real-time PCR (qRT-PCR) was performed to validate the transfection efficiency of HULC silencing vector. Mass spectrometry (MS) was used to generate proteomic profiles for the two cell lines. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed to distinguish HULC-related genes and pathway mapping. Colony formation, Transwell, and wound-healing assays were used to investigate the functional effects of HULC knockdown on GBM. We identified 112 up-regulated proteins and 24 down-regulated proteins from a total of 4360 quantified proteins. GO enrichment illustrated that these proteins were mainly involved in organelle structure, catalysis, cell movement, and material metabolism. KEGG pathway analysis indicated that some of these proteins were significantly enriched in tight junction, metabolic pathways, and arachidonic acid metabolism. In vitro experiments demonstrated that HULC knockdown inhibited GBM cell proliferation, invasion, and migration. Our KEGG analyses revealed that PLA2G4A was a shared protein in several enriched pathways. HULC silencing significantly down-regulated the expression of PLA2G4A. Knockdown of HULC changed the proteomic characteristics of GBM and altered the behaviors of GBM cells. Specifically, we identified PLA2G4A as an HULC target in GBM. This study provides a new perspective on the mechanisms and potential drug targets of GBM treatment. Nature Publishing Group UK 2021-06-15 /pmc/articles/PMC8206103/ /pubmed/34131250 http://dx.doi.org/10.1038/s41598-021-92089-z Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Ye, Shan
Wu, Jing
Wang, Yiran
Hu, Yuchen
Yin, Tiantian
He, Jie
Quantitative proteomics analysis of glioblastoma cell lines after lncRNA HULC silencing
title Quantitative proteomics analysis of glioblastoma cell lines after lncRNA HULC silencing
title_full Quantitative proteomics analysis of glioblastoma cell lines after lncRNA HULC silencing
title_fullStr Quantitative proteomics analysis of glioblastoma cell lines after lncRNA HULC silencing
title_full_unstemmed Quantitative proteomics analysis of glioblastoma cell lines after lncRNA HULC silencing
title_short Quantitative proteomics analysis of glioblastoma cell lines after lncRNA HULC silencing
title_sort quantitative proteomics analysis of glioblastoma cell lines after lncrna hulc silencing
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8206103/
https://www.ncbi.nlm.nih.gov/pubmed/34131250
http://dx.doi.org/10.1038/s41598-021-92089-z
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