Quantitative proteomics analysis of glioblastoma cell lines after lncRNA HULC silencing

Abstract 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...

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Autores principales: Shan Ye, Jing Wu, Yiran Wang, Yuchen Hu, Tiantian Yin, Jie He
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Lenguaje:EN
Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/f6ad6007c76148809832dab960d78bd0
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spelling oai:doaj.org-article:f6ad6007c76148809832dab960d78bd02021-12-02T17:23:03ZQuantitative proteomics analysis of glioblastoma cell lines after lncRNA HULC silencing10.1038/s41598-021-92089-z2045-2322https://doaj.org/article/f6ad6007c76148809832dab960d78bd02021-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-92089-zhttps://doaj.org/toc/2045-2322Abstract 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.Shan YeJing WuYiran WangYuchen HuTiantian YinJie HeNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-13 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Shan Ye
Jing Wu
Yiran Wang
Yuchen Hu
Tiantian Yin
Jie He
Quantitative proteomics analysis of glioblastoma cell lines after lncRNA HULC silencing
description Abstract 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.
format article
author Shan Ye
Jing Wu
Yiran Wang
Yuchen Hu
Tiantian Yin
Jie He
author_facet Shan Ye
Jing Wu
Yiran Wang
Yuchen Hu
Tiantian Yin
Jie He
author_sort Shan Ye
title 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_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_sort quantitative proteomics analysis of glioblastoma cell lines after lncrna hulc silencing
publisher Nature Portfolio
publishDate 2021
url https://doaj.org/article/f6ad6007c76148809832dab960d78bd0
work_keys_str_mv AT shanye quantitativeproteomicsanalysisofglioblastomacelllinesafterlncrnahulcsilencing
AT jingwu quantitativeproteomicsanalysisofglioblastomacelllinesafterlncrnahulcsilencing
AT yiranwang quantitativeproteomicsanalysisofglioblastomacelllinesafterlncrnahulcsilencing
AT yuchenhu quantitativeproteomicsanalysisofglioblastomacelllinesafterlncrnahulcsilencing
AT tiantianyin quantitativeproteomicsanalysisofglioblastomacelllinesafterlncrnahulcsilencing
AT jiehe quantitativeproteomicsanalysisofglioblastomacelllinesafterlncrnahulcsilencing
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