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Non-coding RNAs in Glioblastoma Multiforme

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (28 February 2023) | Viewed by 6480

Special Issue Editor

Department of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy
Interests: non-coding RNAs; microRNAs; circular RNAs; regulation of gene expression; glioblastoma multiforme
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Glioblastoma multiforme (GBM) is the most frequently diagnosed and aggressive brain and central nervous system (CNS) tumor. Deep study of the molecular mechanisms characterizing this tumor has led to its subtypization and to the identification of intracellular and extracellular molecular signatures that may help physicians to perform precise diagnosis, prognosis, and therapeutic interventions. Recent technological advancements in RNA sequencing have shown that the human genome is pervasively transcribed and that most of the transcriptome is made up of non-coding RNAs (ncRNAs) with a gene regulatory function (e.g., microRNAs, long non-coding RNAs, circular RNAs, etc.). NcRNAs are known to be involved in a plethora of physiological and pathological processes, including cancerogenesis. Some of them have been described as components of complex competitive endogenous RNA (ceRNA) networks and have been suggested either as drugs or therapeutic targets. The aim of this Special Issue is to summarize and expand the knowledge on the link between ncRNAs and GBM. Review, original, and perspective articles on the involvement of ncRNAs in the pathogenesis of GBM as well as on the potential use of ncRNAs for early and non-invasive diagnosis of GBM are of interest.

Dr. Davide Barbagallo
Guest Editor

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Keywords

  • non-coding RNAs
  • microRNAs
  • long non-coding RNAs
  • circular RNAs
  • biomarkers
  • micro- and nanovesicles

Published Papers (3 papers)

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Research

20 pages, 78711 KiB  
Article
LINC01393, a Novel Long Non-Coding RNA, Promotes the Cell Proliferation, Migration and Invasion through MiR-128-3p/NUSAP1 Axis in Glioblastoma
by Deheng Li, Junda Hu, Sen Li, Changshuai Zhou, Mingtao Feng, Liangdong Li, Yang Gao, Xin Chen, Xiaojun Wu, Yiqun Cao, Bin Hao and Lei Chen
Int. J. Mol. Sci. 2023, 24(6), 5878; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24065878 - 20 Mar 2023
Cited by 2 | Viewed by 1471
Abstract
Nucleolar and spindle-associated protein 1 (NUSAP1) is a potential molecular marker and intervention target for glioblastoma (GBM). In this study, we aim to investigate upstream regulatory lncRNAs and miRNAs of NUSAP1 through both experimental and bioinformatic methods. We screened upstream lncRNAs and miRNAs [...] Read more.
Nucleolar and spindle-associated protein 1 (NUSAP1) is a potential molecular marker and intervention target for glioblastoma (GBM). In this study, we aim to investigate upstream regulatory lncRNAs and miRNAs of NUSAP1 through both experimental and bioinformatic methods. We screened upstream lncRNAs and miRNAs of NUSAP1 through multiple databases based on ceRNA theory. Then, in vitro and in vivo experiments were performed to elucidate the relevant biological significance and regulatory mechanism among them. Finally, the potential downstream mechanism was discussed. LINC01393 and miR-128-3p were screened as upstream regulatory molecules of NUSAP1 by TCGA and ENCORI databases. The negative correlations among them were confirmed in clinical specimens. Biochemical studies revealed that overexpression or knockdown of LINC01393 respectively enhanced or inhibited malignant phenotype of GBM cells. MiR-128-3p inhibitor reversed LINC01393 knockdown-mediated impacts on GBM cells. Then, dual-luciferase reporter assay and RNA immunoprecipitation assay were conducted to validate LINC01393/miR-128-3p/NUSAP1 interactions. In vivo, LINC01393-knockdown decreased tumor growth and improved mice survival, while restoration of NUSAP1 partially reversed these effects. Additionally, enrichment analysis and western blot revealed that the roles of LINC01393 and NUSAP1 in GBM progression were associated with NF-κB activation. Our findings showed that LINC01393 sponged miR-128-3p to upregulate NUSAP1, thereby promoting GBM development and progression via activating NF-κB pathway. This work deepens understanding of GBM mechanisms and provides potential novel therapeutic targets for GBM. Full article
(This article belongs to the Special Issue Non-coding RNAs in Glioblastoma Multiforme)
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17 pages, 1480 KiB  
Article
circSMARCA5 Is an Upstream Regulator of the Expression of miR-126-3p, miR-515-5p, and Their mRNA Targets, Insulin-like Growth Factor Binding Protein 2 (IGFBP2) and NRAS Proto-Oncogene, GTPase (NRAS) in Glioblastoma
by Aurora Eliana Merulla, Michele Stella, Cristina Barbagallo, Rosalia Battaglia, Angela Caponnetto, Giuseppe Broggi, Roberto Altieri, Francesco Certo, Rosario Caltabiano, Marco Ragusa, Giuseppe Maria Vincenzo Barbagallo, Cinzia Di Pietro, Michele Purrello and Davide Barbagallo
Int. J. Mol. Sci. 2022, 23(22), 13676; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232213676 - 08 Nov 2022
Cited by 6 | Viewed by 2150
Abstract
The involvement of non-coding RNAs (ncRNAs) in glioblastoma multiforme (GBM) pathogenesis and progression has been ascertained but their cross-talk within GBM cells remains elusive. We previously demonstrated the role of circSMARCA5 as a tumor suppressor (TS) in GBM. In this paper, we explore [...] Read more.
The involvement of non-coding RNAs (ncRNAs) in glioblastoma multiforme (GBM) pathogenesis and progression has been ascertained but their cross-talk within GBM cells remains elusive. We previously demonstrated the role of circSMARCA5 as a tumor suppressor (TS) in GBM. In this paper, we explore the involvement of circSMARCA5 in the control of microRNA (miRNA) expression in GBM. By using TaqMan® low-density arrays, the expression of 748 miRNAs was assayed in U87MG overexpressing circSMARCA5. Differentially expressed (DE) miRNAs were validated through single TaqMan® assays in: (i) U87MG overexpressing circSMARCA5; (ii) four additional GBM cell lines (A172; CAS-1; SNB-19; U251MG); (iii) thirty-eight GBM biopsies; (iv) twenty biopsies of unaffected brain parenchyma (UC). Validated targets of DE miRNAs were selected from the databases TarBase and miRTarbase, and the literature; their expression was inferred from the GBM TCGA dataset. Expression was assayed in U87MG overexpressing circSMARCA5, GBM cell lines, and biopsies through real-time PCR. TS miRNAs 126-3p and 515-5p were upregulated following circSMARCA5 overexpression in U87MG and their expression was positively correlated with that of circSMARCA5 (r-values = 0.49 and 0.50, p-values = 9 × 10−5 and 7 × 10−5, respectively) in GBM biopsies. Among targets, IGFBP2 (target of miR-126-3p) and NRAS (target of miR-515-5p) mRNAs were positively correlated (r-value = 0.46, p-value = 0.00027), while their expression was negatively correlated with that of circSMARCA5 (r-values = −0.58 and −0.30, p-values = 0 and 0.019, respectively), miR-126-3p (r-value = −0.36, p-value = 0.0066), and miR-515-5p (r-value = −0.34, p-value = 0.010), respectively. Our data identified a new GBM subnetwork controlled by circSMARCA5, which regulates downstream miRNAs 126-3p and 515-5p, and their mRNA targets IGFBP2 and NRAS. Full article
(This article belongs to the Special Issue Non-coding RNAs in Glioblastoma Multiforme)
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18 pages, 9244 KiB  
Article
The Long Non-Coding RNA HOXA-AS2 Promotes Proliferation of Glioma Stem Cells and Modulates Their Inflammation Pathway Mainly through Post-Transcriptional Regulation
by Elisa Le Boiteux, Pierre-Olivier Guichet, Konstantin Masliantsev, Bertille Montibus, Catherine Vaurs-Barriere, Céline Gonthier-Gueret, Emmanuel Chautard, Pierre Verrelle, Lucie Karayan-Tapon, Anne Fogli, Franck Court and Philippe Arnaud
Int. J. Mol. Sci. 2022, 23(9), 4743; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23094743 - 25 Apr 2022
Cited by 6 | Viewed by 2139
Abstract
Glioblastomas represent approximatively half of all gliomas and are the most deadly and aggressive form. Their therapeutic resistance and tumor relapse rely on a subpopulation of cells that are called Glioma Stem Cells (GSCs). Here, we investigated the role of the long non-coding [...] Read more.
Glioblastomas represent approximatively half of all gliomas and are the most deadly and aggressive form. Their therapeutic resistance and tumor relapse rely on a subpopulation of cells that are called Glioma Stem Cells (GSCs). Here, we investigated the role of the long non-coding RNA HOXA-AS2 in GSC biology using descriptive and functional analyses of glioma samples classified according to their isocitrate dehydrogenase (IDH) gene mutation status, and of GSC lines. We found that HOXA-AS2 is overexpressed only in aggressive (IDHwt) glioma and GSC lines. ShRNA-based depletion of HOXA-AS2 in GSCs decreased cell proliferation and altered the expression of several hundreds of genes. Integrative analysis revealed that these expression changes were not associated with changes in DNA methylation or chromatin signatures at the promoter of the majority of genes deregulated following HOXA-AS2 silencing in GSCs, suggesting a post-transcriptional regulation. In addition, transcription factor binding motif enrichment and correlation analyses indicated that HOXA-AS2 affects, directly or indirectly, the expression of key transcription factors implicated in GCS biology, including E2F8, E2F1, STAT1, and ATF3, thus contributing to GCS aggressiveness by promoting their proliferation and modulating the inflammation pathway. Full article
(This article belongs to the Special Issue Non-coding RNAs in Glioblastoma Multiforme)
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