A Novel Inflammatory lncRNAs Prognostic Signature for Predicting the Prognosis of Low-Grade Glioma Patients.

glioma immunity inflammation lncRNA prognosis

Journal

Frontiers in genetics
ISSN: 1664-8021
Titre abrégé: Front Genet
Pays: Switzerland
ID NLM: 101560621

Informations de publication

Date de publication:
2021
Historique:
received: 05 05 2021
accepted: 05 07 2021
entrez: 19 8 2021
pubmed: 20 8 2021
medline: 20 8 2021
Statut: epublish

Résumé

As immunotherapy has received attention as new treatments for brain cancer, the role of inflammation in the process of glioma is of particular importance. Increasing studies have further shown that long non-coding RNAs (lncRNAs) are important factors that promote the development of glioma. However, the relationship between inflammation-related lncRNAs and the prognosis of glioma patients remains unclear. The purpose of this study is to construct and validate an inflammation-related lncRNA prognostic signature to predict the prognosis of low-grade glioma patients. By downloading and analyzing the gene expression data and clinical information of the Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas (CGGA) patients with low-grade gliomas, we could screen for inflammatory gene-related lncRNAs. Furthermore, through Cox and the Least Absolute Shrinkage and Selection Operator regression analyses, we established a risk model and divided patients into high- and low-risk groups based on the median value of the risk score to analyze the prognosis. In addition, we analyzed the tumor mutation burden (TMB) between the two groups based on somatic mutation data, and explored the difference in copy number variations (CNVs) based on the GISTIC algorithm. Finally, we used the MCPCounter algorithm to study the relationship between the risk model and immune cell infiltration, and used gene set enrichment analysis (GSEA), Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses to explore the enrichment pathways and biological processes of differentially expressed genes between the high- and low-risk groups. A novel prognostic signature was constructed including 11 inflammatory lncRNAs. This risk model could be an independent prognostic predictor. The patients in the high-risk group had a poor prognosis. There were significant differences in TMB and CNVs for patients in the high- and low-risk groups. In the high-risk group, the immune system was activated more significantly, and the expression of immune checkpoint-related genes was also higher. The GSEA, GO, and KEGG analyses showed that highly expressed genes in the high-risk group were enriched in immune-related processes, while lowly expressed genes were enriched in neuromodulation processes. The risk model of 11 inflammation-related lncRNAs can serve as a promising prognostic biomarker for low-grade gliomas patients.

Sections du résumé

BACKGROUND BACKGROUND
As immunotherapy has received attention as new treatments for brain cancer, the role of inflammation in the process of glioma is of particular importance. Increasing studies have further shown that long non-coding RNAs (lncRNAs) are important factors that promote the development of glioma. However, the relationship between inflammation-related lncRNAs and the prognosis of glioma patients remains unclear. The purpose of this study is to construct and validate an inflammation-related lncRNA prognostic signature to predict the prognosis of low-grade glioma patients.
METHODS METHODS
By downloading and analyzing the gene expression data and clinical information of the Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas (CGGA) patients with low-grade gliomas, we could screen for inflammatory gene-related lncRNAs. Furthermore, through Cox and the Least Absolute Shrinkage and Selection Operator regression analyses, we established a risk model and divided patients into high- and low-risk groups based on the median value of the risk score to analyze the prognosis. In addition, we analyzed the tumor mutation burden (TMB) between the two groups based on somatic mutation data, and explored the difference in copy number variations (CNVs) based on the GISTIC algorithm. Finally, we used the MCPCounter algorithm to study the relationship between the risk model and immune cell infiltration, and used gene set enrichment analysis (GSEA), Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses to explore the enrichment pathways and biological processes of differentially expressed genes between the high- and low-risk groups.
RESULTS RESULTS
A novel prognostic signature was constructed including 11 inflammatory lncRNAs. This risk model could be an independent prognostic predictor. The patients in the high-risk group had a poor prognosis. There were significant differences in TMB and CNVs for patients in the high- and low-risk groups. In the high-risk group, the immune system was activated more significantly, and the expression of immune checkpoint-related genes was also higher. The GSEA, GO, and KEGG analyses showed that highly expressed genes in the high-risk group were enriched in immune-related processes, while lowly expressed genes were enriched in neuromodulation processes.
CONCLUSION CONCLUSIONS
The risk model of 11 inflammation-related lncRNAs can serve as a promising prognostic biomarker for low-grade gliomas patients.

Identifiants

pubmed: 34408772
doi: 10.3389/fgene.2021.697819
pmc: PMC8365518
doi:

Types de publication

Journal Article

Langues

eng

Pagination

697819

Informations de copyright

Copyright © 2021 Xiang, Chen, Lv and Peng.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Références

Int J Biochem Cell Biol. 2017 Aug;89:171-181
pubmed: 28549626
Nucleic Acids Res. 2017 Jul 3;45(W1):W98-W102
pubmed: 28407145
Adv Exp Med Biol. 2014;816:75-105
pubmed: 24818720
Int J Mol Sci. 2017 Jun 20;18(6):
pubmed: 28632155
Cancer Med. 2019 Dec;8(17):7454-7468
pubmed: 31599129
Cell Death Dis. 2020 Aug 11;11(8):685
pubmed: 32826862
Mol Cancer. 2018 Feb 19;17(1):61
pubmed: 29458374
Aging (Albany NY). 2020 Aug 29;12(15):15624-15637
pubmed: 32805727
Int J Radiat Oncol Biol Phys. 2016 Nov 15;96(4):877-887
pubmed: 27788958
Anesth Analg. 2018 May;126(5):1763-1768
pubmed: 29481436
Biomolecules. 2017 Mar 27;7(2):
pubmed: 28346397
Acta Neuropathol. 2016 Jun;131(6):803-20
pubmed: 27157931
Neurol Clin. 2016 Nov;34(4):981-998
pubmed: 27720005
Cancer Sci. 2020 Aug;111(8):2696-2707
pubmed: 32519436
Biomed Pharmacother. 2018 Aug;104:110-118
pubmed: 29772430
J Cell Mol Med. 2020 Oct;24(20):11755-11767
pubmed: 32918360
Front Oncol. 2021 Feb 05;10:597877
pubmed: 33614485
Genome Biol. 2011;12(4):R41
pubmed: 21527027
Clin Transl Oncol. 2017 Aug;19(8):931-944
pubmed: 28255650
Int J Mol Sci. 2020 May 24;21(10):
pubmed: 32456359
Genome Res. 2018 Nov;28(11):1747-1756
pubmed: 30341162
Front Oncol. 2020 Sep 02;10:1508
pubmed: 32983994
Lancet Neurol. 2003 Jul;2(7):395-403
pubmed: 12849117
Nat Methods. 2015 May;12(5):453-7
pubmed: 25822800
CA Cancer J Clin. 2020 Jan;70(1):7-30
pubmed: 31912902
J Neurooncol. 2016 Nov;130(2):269-282
pubmed: 27174197
Exp Mol Pathol. 2020 Oct;116:104490
pubmed: 32663487
Onco Targets Ther. 2018 Apr 19;11:2259-2267
pubmed: 29719408
Cancer Manag Res. 2020 Oct 13;12:10035-10046
pubmed: 33116860
Apoptosis. 2018 Dec;23(11-12):651-666
pubmed: 30232656
Genome Biol. 2016 Oct 20;17(1):218
pubmed: 27765066
J Med Syst. 2018 Jun 28;42(8):139
pubmed: 29956014
Cancers (Basel). 2021 Feb 11;13(4):
pubmed: 33670198
J Genet Genomics. 2017 Nov 20;44(11):519-530
pubmed: 29169920
Front Genet. 2019 Nov 13;10:1140
pubmed: 31798634
Aging (Albany NY). 2019 Dec 17;11(24):12246-12269
pubmed: 31844032
Neuro Oncol. 2015 Mar;17(3):332-42
pubmed: 25087230
J Cell Mol Med. 2019 Sep;23(9):6271-6282
pubmed: 31264769
Immunity. 2019 Jul 16;51(1):27-41
pubmed: 31315034
Am J Physiol Cell Physiol. 2018 Jul 1;315(1):C52-C61
pubmed: 29631367
Semin Cancer Biol. 2018 Oct;52(Pt 2):53-65
pubmed: 29196189
J Neuroimmunol. 2016 Aug 15;297:132-40
pubmed: 27397086

Auteurs

Zijin Xiang (Z)

Department of Pharmacy, The Third Xiangya Hospital, Central South University, Changsha, China.

Xueru Chen (X)

Department of Pharmacy, The Third Xiangya Hospital, Central South University, Changsha, China.

Qiaoli Lv (Q)

Jiangxi Key Laboratory of Translational Cancer Research, Jiangxi Cancer Hospital of Nanchang University, Nanchang, China.

Xiangdong Peng (X)

Department of Pharmacy, The Third Xiangya Hospital, Central South University, Changsha, China.

Classifications MeSH