Introduction

Medulloblastoma is recognized as the most prevalent form of brain tumor among children, accounting for nearly 20% of all brain tumors found in pediatric patients [1]. Medulloblastoma is most commonly diagnosed before age 15 and has two incidence peaks between the ages of 3–4 and 8–9 [2]. The occurrence of this tumor in older patients is rare, comprising less than 1% of all primary CNS tumors in adults [3]. According to the latest classification scheme, medulloblastoma is divided into two distinct categories, i.e., histologically defined and genetically defined. Histologically, medulloblastoma can be categorized into different types, including classic, desmoplastic/nodular (DN), and large cell/anaplastic (LCA). Genetic classification divides it into four molecular subtypes, i.e., wingless (WNT), sonic hedgehog (SHH), group 3, and group 4. Each of these subtypes has distinct clinical and molecular characteristics [4]. The primary therapeutic strategies for medulloblastoma include a combination of surgical resection, radiotherapy, and chemotherapy. However, clinical outcomes have been not desirable, and 5-year survival rates range between 60 and 80% [5, 6]. Hence, an in-depth investigation of the molecular mechanisms involved in the pathogenesis of medulloblastoma is essential to improve patients' prognoses and clinical outcomes.

Non-coding RNAs (ncRNAs) are a class of RNAs that lack the ability to encode functional proteins [7]. Since their discovery, the biological significance of ncRNAs has become increasingly evident, which has led to a shift in the perspective of RNA from being a simple intermediary of protein synthesis to being a functional molecule with essential roles in regulating gene expression and genome organization [8]. In recent years, studies have indicated that these ncRNAs play vital regulatory roles in the initiation and progression of various types of cancer [7]. In line with this, it has been demonstrated that the expression levels of various ncRNAs are notably different between medulloblastoma and normal cerebellar cells [9]. NcRNAs can be classified into various classes based on size and function. The three primary classes of regulatory ncRNAs are microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs). Owing to their intrinsic characteristics, they may exhibit tissue or disease specificity and can be detected in all bodily fluids, which makes them potentially desirable to be used as biomarkers [10]. LncRNAs are a class of RNA molecules that are longer than 200 nucleotides in length [11]. Through multiple mechanisms, they play a crucial role in regulating gene expression at various levels, including epigenetic, transcriptional, and post-transcriptional regulation. This regulatory role holds particular significance in the central nervous system (CNS) [12]. Most lncRNAs are presumed to be transcribed and processed similarly to mRNAs. They are primarily transcribed by RNA polymerase II and often possess 5′-end m7G caps and 3′-end poly(A) tails [13]. Regarding the chromosomal position, lncRNAs are classified into promoter-associated lncRNAs, antisense, intronic, enhancer RNAs, divergent, intergenic, and transcription start site-associated lncRNAs [14]. LncRNAs function as competing endogenous RNAs (ceRNAs) within a regulatory network by serving as a "sponge" for target miRNAs [15]. Circular RNAs (circRNAs) are single-stranded RNA transcripts with a covalently closed circular structure. They are produced through an alternative splicing process and lack the 5′ caps and 3′ poly(A) tails; this structural feature in circRNAs renders them resistant to degradation by ribonucleases [16]. Furthermore, most circRNAs exhibit evolutionary conservation across various species [17]. CircRNAs are generated through the transcription of precursor mRNA (pre-mRNA) by RNA polymerase II. They can function as molecular sponges for miRNAs, thus regulating their biological activities [18]. Recent evidence has indicated that aberrant expression of circRNAs occurs in various types of cancer, including breast cancer [19], pancreatic ductal adenocarcinoma [20], bladder carcinoma [21], glioblastoma [

Method

Sco** review protocol

The guidelines for preferred reporting items for systematic reviews and meta-analyses extension for sco** reviews (PRISMA-ScR) are followed by the present sco** review [39] (Supplementary data). The five steps of the present sco** review include formulating the research question, identifying the relevant publications, selecting studies, charting the data, and summarizing and disclosing the findings.

Research question

Given the significant role of the ceRNA networks in the regulation of gene expression, the present study aimed to comprehensively review the current knowledge on the circRNA and lncRNA-associated ceRNA networks in medulloblastoma development.

Relevant publication identification

The Web of Science, PubMed, Scopus, and Embase were systematically searched to find the relevant studies published before 16 September 2023; the systematic searches did not have any restriction on language, country, or time. LncRNA, circRNA, miRNA, ceRNA, medulloblastoma, and their different versions, along with the Emtree and medical subject headings (MeSh) terms, were used for the systematic search.

Study selection

After retrieving the publications from the above-mentioned databases and removing duplicated records, the papers were reviewed in two phases. In the first phase, the title and abstract of the obtained studies were reviewed. In the second phase, the full texts of the remaining papers were thoroughly reviewed. The criteria for inclusion were the following. First, the included study must be an original paper published in English. Second, the included study must study the interaction between lncRNA with miRNA or circRNA with miRNAs in medulloblastoma. Third, the experimental study must contain at least one of the human medulloblastoma cell lines.

Data charting

The studied ncRNAs and the related axis, medulloblastoma cell line, and the effect of the studied axis on medulloblastoma formation were all extracted from the included studies.

Summarizing and reporting the obtained results

The present sco** review summarizes the results of the studies that were included and also investigates the effect of the identified miRNAs, circRNAs, and lncRNAs on the development of medulloblastoma that were not present in the included studies.

In silico study

To extend the understanding of the impact of ceRNA on cellular singling pathways, miRPathDB v2.0 was used to access the Reactome database. A minimum of two significant miRNAs per pathway and strong experimental evidence were the criteria for the related analysis.

Results

Systematic search results

The systematic search on Web of Science, PubMed, Scopus, and Embase identified 149 papers published before 16 September 2023. After removing duplicated studies, 57 papers were also excluded based on reviewing their title and abstracts. Ultimately, seven papers were excluded from the present sco** review because they did not meet the above-mentioned inclusion criteria in the full-text assessment phase. Figure 1 shows the study's flowchart.

Fig. 1
figure 1

The flowchart of the study

Full size image

The characteristics of the included papers

The included studies were published between 2017 and 2023. Daoy was the most studied medulloblastoma human cell line. According to the ATCC, this cell line was obtained from a 4-year-old white male with desmoplastic cerebellar type. HOTAIR, NEAT1, linc-NeD125, HHIP-AS1, CRNDE, and TP73-AS1 are the identified oncogenic lncRNA in medulloblastoma, and Nkx2-2as is a tumor-suppressive lncRNA in medulloblastoma. Based on the current experimental evidence, circSKA3, which sponges miR-326, miR-520 h, and miR-383-5p, and circRNA_103128, which sponges miR-129-5p, are upregulated oncogenic circRNA in medulloblastoma (Table 1).

Table 1 The characteristics of the included studies
Full size table

The enrichment analysis

Based on the Reactome database, the identified miRNAs regulate various cellular pathways, like cell cycle, apoptosis, MAPK1/ERK2 pathway, etc. For instance, miR-106a-5p, miR-23a-3p, and miR-129-5p are enriched for apoptosis (Fig. 2).

Fig. 2
figure 2

The enrichment analysis of studied microRNAs

Full size image

Discussion

Despite the recent advances in our understanding of medulloblastoma biology, the clinical outcome of affected patients is still unfavorable. A better understanding of ncRNAs and ceRNAs might provide valuable insights regarding treating medulloblastoma [40]. The following discusses the current evidence on the significance of circRNA and lncRNA-associated ceRNA networks in medulloblastoma.

HOTAIR-mediated ceRNA

As a located lncRNA on chromosome 12, homeobox transcript antisense intergenic RNA (HOTAIR) can interact with PRC2, LSD1, and miRNAs, leading to gene expression regulation [41]. Zhang et al. have reported that HOTAIR expression level is substantially upregulated in medulloblastoma tissues and cell lines compared with non-tumoral ones. HOTAIR knockdown improves apoptosis rate, decreases the cell viability, clonogenicity, migration, and invasion, and reduces tumor volume in animal models; this oncogenic effect is medicated via the HOTAIR/miR-1-3p and miR-206/ YY1 axes in medulloblastoma. Also, the ectopic expression of miR-1-3p and miR-206 has been associated with decreased tumor growth in animal models [42]. In line with this, it has been shown that miR-206 is downregulated in medulloblastoma tissues, and its increased expression decreased the cell viability and migration of medulloblastoma cells via the miR-206/LASP1 axis [43].

NEAT1-mediated ceRNA

As a component of nuclear paraspeckles, nuclear-enriched abundant transcript 1 (NEAT1) is located on chromosome 11q13.1; this lncRNA is dysregulated in various cancers, like glioma and medulloblastoma [44, 45]. Ge et al. have shown that NEAT1 knockdown increases the chemosensivity of medulloblastoma cells and potentiates cisplatin-mediated apoptosis activation. This chemoresistance of medulloblastoma cells is mediated via the NEAT1/miR-23a-3p/GLS axis [44]. In line with this, the in-silico results have shown that miR-23a-3p is enriched for apoptosis. Apoptosis is a type of regulated cell death that has two pathways, i.e., intrinsic and extrinsic pathways [46]. In the intrinsic pathway, the insertion of BAX and BAK into the mitochondrial membrane releases cytochrome c, leading to the activation of caspase-9 and executioner caspases. In the extrinsic pathway, the death-inducing signaling complex results in the activation of caspase-8, caspase-10, caspases-3, caspases-6, and caspases-7; these events stimulate apoptosis activation [47, 48]. In addition, the in-silico results have shown that miR-23a-3p is enriched for the MAPK pathway as well. The MAPK/ERK pathway is among the activated oncogenic pathways in medulloblastoma and its blockade is associated with decreased proliferation, stemness, and invasion in medulloblastoma cells [49, 50]. Also, it has been reported that NEAT1 knockdown increases the chemosensitivity of glioblastoma cells to temozolomide [51].

Linc-NeD125-mediated ceRNA

Linc-NeD125 is a long intergenic ncRNA that is located on chromosome 11. Laneve et al. have reported that linc-NeD125 expression level is substantially increased in G4 medulloblastoma, and its knockdown decreases the proliferation of G4 medulloblastoma cells and downregulates the protein expression of CDK6, MYCN, SNCAIP, and KDM6A via the linc-NeD125/miR-19a-3p, miR-19b-3p, miR-106a-5p/CDK6, MYCN, SNCAIP, and KDM6A axes [52]. Consistent with this, the in-silico results have shown that miR-106a-5p is enriched for the G1 phase, cyclin D-associated events at the G1 phase, cyclin E-associated events during G1-S transition, cyclin A-CDK2 associated events at S phase entry as well as apoptosis. The complex of cyclin D with CDK4/CDK6 causes the RB-phosphorization and RB-phosphorization-mediated E2F release, leading to the transition from the G1 phase to the S phase. Cyclin E1 and E2 bind and activate CDK2, leading to RB and p27KIP1 phosphorylation. The cyclin E/CDK2 active complex leads to the S phase initiation and cyclin A/CDK2 is formed near the end of the S phase and leads to cell cycle progression from the S phase to the G2 phase. The cyclin A/CDK1 complex results in M phase entry [

Availability of data and materials

The datasets analyzed during the current study for enrichment analyses are available in the miRPathDB V 2.0 (https://mpd.bioinf.uni-sb.de/overview.html).

Abbreviations

CNS:

Central nervous system

circRNA:

Circular RNA

lncRNA:

Long non-coding RNA

miRNA:

MicroRNA

ceRNA:

Competing endogenous RNA

DN:

Desmoplastic/nodular

LCA:

Large cell/anaplastic

WNT:

Wingless

SHH:

Sonic hedgehog

pri-miRNAs:

Primary miRNA

RISC:

RNA-induced silencing complex

MREs:

MiRNA recognition elements

PRISMA-ScR:

Preferred reporting items for systematic reviews and meta-analyses extension for sco** reviews

HOTAIR:

Homeobox transcript antisense intergenic RNA

HHIP-AS1:

Hedgehog interacting protein-antisense 1

CRNDE:

Colorectal neoplasia differentially expressed

MAPK:

Mitogen-activated protein kinase

ERK:

Extracellular signal-regulated kinase

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Acknowledgements

The authors appreciate all the cancer researchers working in the field of ncRNAs to develop novel treatments for patients.

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This research received no specific grant from any funding agency, commercial or not-for-profit sectors.

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  1. Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran

    Fatemeh Nejadi Orang

  2. Department of Immunology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran

    Mahdi Abdoli Shadbad

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FNO: conceptualization, methodology, software, investigation, writing—original draft, MAS: conceptualization, methodology, writing—review & editing, supervision. All authors read and approved the final manuscript.

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Correspondence to Mahdi Abdoli Shadbad.

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Nejadi Orang, F., Abdoli Shadbad, M. CircRNA and lncRNA-associated competing endogenous RNA networks in medulloblastoma: a sco** review. Cancer Cell Int 24, 248 (2024). https://doi.org/10.1186/s12935-024-03427-w

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