Special Issue "Non-Coding RNA and Brain Tumors"

A special issue of Non-Coding RNA (ISSN 2311-553X).

Deadline for manuscript submissions: closed (1 December 2018).

Special Issue Editor

Dr. Agnieszka M Bronisz
E-Mail Website
Guest Editor
Department of Neurosurgery, Harvey Cushing Neuro-oncology Laboratories, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, USA
Interests: ncRNAs; exosomes and extracellular vesicles; tumor heterogenity; stem cells

Special Issue Information

Dear Colleagues,

Brain tumors, as other cancers, are complex genetic diseases involving expressional abnormalities of both protein-coding and non-coding genes. Together, they form complex RNA networks within the molecular microcosm, which are not fully recognized yet.

Considering that protein-coding genes constitute only small fraction of human genome, researchers increasingly switched their focus toward non-protein-coding transcriptome that may provide vast panoply of targets for anti-cancer therapy.

In fact, non-coding RNA (ncRNA) is much more than the mundane messenger between DNA and the protein—it springs up into multiple species (including long non-coding RNAs (lncRNAs), microRNAs or circular RNAs (circRNAs)). Differences between cells during normal development and pathogenesis are in many cases due to differences in when, where and how genes are turned on or off.

It is believed that ncRNAs play enormous role in these processes by facilitating or impeding transcription, translation and activity of protein-coding genes and their products. Additional layers of complexity are the microenvironmental rearrangements contributing to intra-tumoral heterogeneity inducing abnormalities/alteration of gene expression via cellular and acellular (exosomal) ncRNA.

In this Special Issue of Non-coding RNA we invite many experts in the field of brain tumor to present their point of view on various aspects of ncRNA function, regulation and therapeutic advances. 

Dr. Agnieszka M Bronisz
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Non-Coding RNA is an international peer-reviewed open access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • ncRNA
  • primary and metastatic brain tumor
  • tumor microenvironment
  • tumor heterogeneity exosomes
  • therapeutic targeting and delivery
  • immunotherapy
  • stem cells
  • epigenetics

Published Papers (4 papers)

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Review

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Open AccessReview
The Transcribed-Ultra Conserved Regions: Novel Non-Coding RNA Players in Neuroblastoma Progression
Non-Coding RNA 2019, 5(2), 39; https://doi.org/10.3390/ncrna5020039 - 04 Jun 2019
Abstract
The Transcribed-Ultra Conserved Regions (T-UCRs) are a class of novel non-coding RNAs that arise from the dark matter of the genome. T-UCRs are highly conserved between mouse, rat, and human genomes, which might indicate a definitive role for these elements in health and [...] Read more.
The Transcribed-Ultra Conserved Regions (T-UCRs) are a class of novel non-coding RNAs that arise from the dark matter of the genome. T-UCRs are highly conserved between mouse, rat, and human genomes, which might indicate a definitive role for these elements in health and disease. The growing body of evidence suggests that T-UCRs contribute to oncogenic pathways. Neuroblastoma is a type of childhood cancer that is challenging to treat. The role of non-coding RNAs in the pathogenesis of neuroblastoma, in particular for cancer development, progression, and therapy resistance, has been documented. Exosmic non-coding RNAs are also involved in shaping the biology of the tumor microenvironment in neuroblastoma. In recent years, the involvement of T-UCRs in a wide variety of pathways in neuroblastoma has been discovered. Here, we present an overview of the involvement of T-UCRs in various cellular pathways, such as DNA damage response, proliferation, chemotherapy response, MYCN (v-myc myelocytomatosis viral related oncogene, neuroblastoma derived (avian)) amplification, gene copy number, and immune response, as well as correlate it to patient survival in neuroblastoma. Full article
(This article belongs to the Special Issue Non-Coding RNA and Brain Tumors)
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Open AccessReview
MicroRNA in Brain pathology: Neurodegeneration the Other Side of the Brain Cancer
Non-Coding RNA 2019, 5(1), 20; https://doi.org/10.3390/ncrna5010020 - 23 Feb 2019
Cited by 2
Abstract
The mammalian brain is made up of billions of neurons and supporting cells (glial cells), intricately connected. Molecular perturbations often lead to neurodegeneration by progressive loss of structure and malfunction of neurons, including their death. On the other side, a combination of genetic [...] Read more.
The mammalian brain is made up of billions of neurons and supporting cells (glial cells), intricately connected. Molecular perturbations often lead to neurodegeneration by progressive loss of structure and malfunction of neurons, including their death. On the other side, a combination of genetic and cellular factors in glial cells, and less frequently in neurons, drive oncogenic transformation. In both situations, microenvironmental niches influence the progression of diseases and therapeutic responses. Dynamic changes that occur in cellular transcriptomes during the progression of developmental lineages and pathogenesis are controlled through a variety of regulatory networks. These include epigenetic modifications, signaling pathways, and transcriptional and post-transcriptional mechanisms. One prominent component of the latter is small non-coding RNAs, including microRNAs, that control the vast majority of these networks including genes regulating neural stemness, differentiation, apoptosis, projection fates, migration and many others. These cellular processes are also profoundly dependent on the microenvironment, stemness niche, hypoxic microenvironment, and interactions with associated cells including endothelial and immune cells. Significantly, the brain of all other mammalian organs expresses the highest number of microRNAs, with an additional gain in expression in the early stage of neurodegeneration and loss in expression in oncogenesis. However, a mechanistic explanation of the concept of an apparent inverse correlation between the odds of cancer and neurodegenerative diseases is only weakly developed. In this review, we thus will discuss widespread de-regulation of microRNAome observed in these two major groups of brain pathologies. The deciphering of these intricacies is of importance, as therapeutic restoration of pre-pathological microRNA landscape in neurodegeneration must not lead to oncogenesis and vice versa. We thus focus on microRNAs engaged in cellular processes that are inversely regulated in these diseases. We also aim to define the difference in microRNA networks between pro-survival and pro-apoptotic signaling in the brain. Full article
(This article belongs to the Special Issue Non-Coding RNA and Brain Tumors)
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Open AccessReview
Extracellular Vesicles as Conduits of Non-Coding RNA Emission and Intercellular Transfer in Brain Tumors
Non-Coding RNA 2019, 5(1), 1; https://doi.org/10.3390/ncrna5010001 - 25 Dec 2018
Cited by 2
Abstract
Non-coding RNA (ncRNA) species have emerged in as molecular fingerprints and regulators of brain tumor pathogenesis and progression. While changes in ncRNA levels have been traditionally regarded as cell intrinsic there is mounting evidence for their extracellular and paracrine function. One of the [...] Read more.
Non-coding RNA (ncRNA) species have emerged in as molecular fingerprints and regulators of brain tumor pathogenesis and progression. While changes in ncRNA levels have been traditionally regarded as cell intrinsic there is mounting evidence for their extracellular and paracrine function. One of the key mechanisms that enables ncRNA to exit from cells is their selective packaging into extracellular vesicles (EVs), and trafficking in the extracellular space and biofluids. Vesicular export processes reduce intracellular levels of specific ncRNA in EV donor cells while creating a pool of EV-associated ncRNA in the extracellular space and biofluids that enables their uptake by other recipient cells; both aspects have functional consequences. Cancer cells produce several EV subtypes (exosomes, ectosomes), which differ in their ncRNA composition, properties and function. Several RNA biotypes have been identified in the cargo of brain tumor EVs, of which microRNAs are the most studied, but other species (snRNA, YRNA, tRNA, and lncRNA) are often more abundant. Of particular interest is the link between transforming oncogenes and the biogenesis, cargo, uptake and function of tumor-derived EV, including EV content of oncogenic RNA. The ncRNA repertoire of EVs isolated from cerebrospinal fluid and serum is being developed as a liquid biopsy platform in brain tumors. Full article
(This article belongs to the Special Issue Non-Coding RNA and Brain Tumors)
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Other

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Open AccessBrief Report
MicroRNA-451 Inhibits Migration of Glioblastoma while Making It More Susceptible to Conventional Therapy
Non-Coding RNA 2019, 5(1), 25; https://doi.org/10.3390/ncrna5010025 - 15 Mar 2019
Cited by 2
Abstract
Malignant glioblastoma (GBM, glioma) is the most common and aggressive primary adult brain tumor. The prognosis of GBM patients remains poor, despite surgery, radiation and chemotherapy. The major obstacles for successful remedy are invasiveness and therapy resistance of GBM cells. Invasive glioma cells [...] Read more.
Malignant glioblastoma (GBM, glioma) is the most common and aggressive primary adult brain tumor. The prognosis of GBM patients remains poor, despite surgery, radiation and chemotherapy. The major obstacles for successful remedy are invasiveness and therapy resistance of GBM cells. Invasive glioma cells leave primary tumor core and infiltrate surrounding normal brain leading to inevitable recurrence, even after surgical resection, radiation and chemotherapy. Therapy resistance allowing for selection of more aggressive and resistant sub-populations including GBM stem-like cells (GSCs) upon treatment is another serious impediment to successful treatment. Through their regulation of multiple genes, microRNAs can orchestrate complex programs of gene expression and act as master regulators of cellular processes. MicroRNA-based therapeutics could thus impact broad cellular programs, leading to inhibition of invasion and sensitization to radio/chemotherapy. Our data show that miR-451 attenuates glioma cell migration in vitro and invasion in vivo. In addition, we have found that miR-451 sensitizes glioma cells to conventional chemo- and radio-therapy. Our data also show that miR-451 is regulated in vivo by AMPK pathway and that AMPK/miR-451 loop has the ability to switch between proliferative and migratory pattern of glioma cells behavior. We therefore postulate that AMPK/miR-451 negative reciprocal feedback loop allows GBM cells/GSCs to adapt to tumor “ecosystem” by metabolic and behavioral flexibility, and that disruption of such a loop reduces invasiveness and diminishes therapy resistance. Full article
(This article belongs to the Special Issue Non-Coding RNA and Brain Tumors)
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