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Clinical Potential of Non-coding RNAs in Cancer

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

Deadline for manuscript submissions: closed (30 June 2020) | Viewed by 15628

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Special Issue Editor

Prof. Dr. Eleonora Leucci

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Guest Editor

Laboratory of RNA Cancer Biology, Department of Oncology, LKI, KU Leuven, 3000 Leuven, Belgium
Interests: Functional characterization of lncRNAs; Cancer and RNA biology

Special Issue Information

Dear Colleagues,

The increasing awareness of inter- and intra-tumour heterogeneity calls for the introduction of new biomarkers for patient stratification and new therapeutic strategies to target the most aggressive tumour subpopulations. Cancer research has thus far been focusing on alterations in protein-coding genes. However, recent genome-wide studies suggest that disease-causing mutations and chromosome rearrangements often span transcribed areas of the genome lacking a known protein-coding gene. Often expressed in a tissue-, disease- and stage-specific manner, non-coding RNAs (ncRNAs) are attractive cancer-selective markers and therapeutic targets.

Non-coding RNA is now accepting submissions for a Special Issue on the promises and pitfalls of implanting research on non-coding RNAs into the clinic.

Dr. Eleonora Leucci
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 submissions that pass pre-check are 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 semimonthly 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 1800 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

Non-coding RNAs in cancer
Non-coding RNAs and mechanism tumourigenesis
Non-coding RNAs as biomarkers
Non-coding RNAs as therapeutic targets
Non-coding RNAs in therapy resistance

Published Papers (3 papers)

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Research

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14 pages, 1237 KiB

Open AccessArticle

How Does a Tumor Get Its Shape? MicroRNAs Act as Morphogens at the Cancer Invasion Front

by Catalin Vasilescu, Mihai Tanase, Dana Giza, Livia Procopiuc, Mihnea P. Dragomir and George A. Calin

Non-Coding RNA 2020, 6(2), 23; https://doi.org/10.3390/ncrna6020023 - 10 Jun 2020

Cited by 3 | Viewed by 3978

Abstract

The generation and organization of the invasion front shape of neoplasms is an intriguing problem. The intimate mechanism is not yet understood, but the prevailing theory is that it represents an example of morphogenesis. Morphogenesis requires the presence of specific molecules, known as morphogens (activators and inhibitors), which can diffuse and elicit dose-dependent responses in their target cells. Due to their ability to modulate most of the coding transcriptome, their well-established role in embryogenesis, and their capacity to rapidly move between neighboring and distant cells, we propose microRNAs as inhibitors that could shape the cancer invasion front. In order to explain the genesis of the tumor border, we use Alan Turing’s reaction diffusion model, refined by Meinhardt and Gierer. This assumes the existence of an activator called a, and an inhibitor called h, which we hypothesize could be a freely moving microRNA. We used the fractal dimension as a measure of tumor border irregularity. We observed that the change in fractal dimension associates with variations in the diffusion coefficient of the activator (D_a) or the inhibitor (D_h). We determined that the fractal dimension remains constant (i.e., the irregularity of the tumor border does not change) across a D_h interval, which becomes narrower as D_a rises. We therefore conclude that a change in fractal dimension occurs when the balance between D_a and D_h is disrupted. Biologically, this could be explained by a faulty distribution of the inhibitor caused by an abnormal density of the intercellular connection network. From a translational perspective, if experimentally confirmed, our observations can be used for a better diagnosis of cancer aggressiveness. Full article

(This article belongs to the Special Issue Clinical Potential of Non-coding RNAs in Cancer)

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13 pages, 2673 KiB

Open AccessArticle

HOX Transcript Antisense RNA HOTAIR Abrogates Vasculogenic Mimicry by Targeting the AngiomiR-204/FAK Axis in Triple Negative Breast Cancer Cells

by Allan Lozano-Romero, Horacio Astudillo-de la Vega, María Cruz del Rocío Terrones-Gurrola, Laurence A. Marchat, Daniel Hernández-Sotelo, Yarely M. Salinas-Vera, Rosalío Ramos-Payan, Macrina B. Silva-Cázares, Stephanie I. Nuñez-Olvera, Olga N. Hernández-de la Cruz and César López-Camarillo

Non-Coding RNA 2020, 6(2), 19; https://doi.org/10.3390/ncrna6020019 - 26 May 2020

Cited by 16 | Viewed by 5049

Abstract

HOX transcript antisense RNA (HOTAIR) is an oncogenic long non-coding RNA frequently overexpressed in cancer. HOTAIR can enhance the malignant behavior of tumors by sponging microRNAs with tumor suppressor functions. Vasculogenic mimicry is a hypoxia-activated process in which tumor cells form three-dimensional (3D) channel-like networks, resembling endothelial blood vessels, to obtain nutrients. However, the role of HOTAIR in vasculogenic mimicry and the underlying mechanisms are unknown in human cancers. In the current study, we investigated the relevance of HOTAIR in hypoxia-induced vasculogenic mimicry in metastatic MDA-MB-231 and invasive Hs-578t triple negative breast cancer cells. Analysis of The Cancer Genome Atlas (TCGA) database using cBioPortal confirmed that HOTAIR was upregulated in clinical breast tumors relative to normal mammary tissues. Our quantitative RT-PCR assays showed a significant increase in HOTAIR levels after 48 h hypoxia relative to normoxia in breast cancer cell lines. Remarkably, knockdown of HOTAIR significantly abolished the hypoxia-induced vasculogenic mimicry which was accompanied by a reduction in the number of 3D channel-like networks and branch points. Likewise, HOTAIR silencing leads to reduced cell migration abilities of cancer cells. Bioinformatic analysis predicted that HOTAIR has a potential binding site for tumor suppressor miR-204. Luciferase reporter assays confirmed that HOTAIR is a competitive endogenous sponge of miR-204. Congruently, forced inhibition of HOTAIR in cells resulted in augmented miR-204 levels in breast cancer cells. Further bioinformatic analysis suggested that miR-204 can bind to the 3′ untranslated region of focal adhesion kinase 1 (FAK) transcript involved in cell migration. Western blot and luciferase reporter assays confirmed that FAK is a novel target of miR-204. Finally, silencing of HOTAIR resulted in low levels of cytoplasmic FAK protein and alterations in the organization of cellular cytoskeleton and focal adhesions. In summary, our results showed, for the first time, that HOTAIR mitigates cell migration and vasculogenic mimicry by targeting the miR-204/FAK axis in triple negative breast cancer cells. Full article

(This article belongs to the Special Issue Clinical Potential of Non-coding RNAs in Cancer)

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Review

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22 pages, 3372 KiB

Open AccessFeature PaperReview

The Growth-Arrest-Specific (GAS)-5 Long Non-Coding RNA: A Fascinating lncRNA Widely Expressed in Cancers

by Anton Scott Goustin, Pattaraporn Thepsuwan, Mary Ann Kosir and Leonard Lipovich

Non-Coding RNA 2019, 5(3), 46; https://doi.org/10.3390/ncrna5030046 - 17 Sep 2019

Cited by 50 | Viewed by 6153

Abstract

Long non-coding RNA (lncRNA) genes encode non-messenger RNAs that lack open reading frames (ORFs) longer than 300 nucleotides, lack evolutionary conservation in their shorter ORFs, and do not belong to any classical non-coding RNA category. LncRNA genes equal, or exceed in number, protein-coding genes in mammalian genomes. Most mammalian genomes harbor ~20,000 protein-coding genes that give rise to conventional messenger RNA (mRNA) transcripts. These coding genes exhibit sweeping evolutionary conservation in their ORFs. LncRNAs function via different mechanisms, including but not limited to: (1) serving as “enhancer” RNAs regulating nearby coding genes in cis; (2) functioning as scaffolds to create ribonucleoprotein (RNP) complexes; (3) serving as sponges for microRNAs; (4) acting as ribo-mimics of consensus transcription factor binding sites in genomic DNA; (5) hybridizing to other nucleic acids (mRNAs and genomic DNA); and, rarely, (6) as templates encoding small open reading frames (smORFs) that may encode short proteins. Any given lncRNA may have more than one of these functions. This review focuses on one fascinating case—the growth-arrest-specific (GAS)-5 gene, encoding a complicated repertoire of alternatively-spliced lncRNA isoforms. GAS5 is also a host gene of numerous small nucleolar (sno) RNAs, which are processed from its introns. Publications about this lncRNA date back over three decades, covering its role in cell proliferation, cell differentiation, and cancer. The GAS5 story has drawn in contributions from prominent molecular geneticists who attempted to define its tumor suppressor function in mechanistic terms. The evidence suggests that rodent Gas5 and human GAS5 functions may be different, despite the conserved multi-exonic architecture featuring intronic snoRNAs, and positional conservation on syntenic chromosomal regions indicating that the rodent Gas5 gene is the true ortholog of the GAS5 gene in man and other apes. There is no single answer to the molecular mechanism of GAS5 action. Our goal here is to summarize competing, not mutually exclusive, mechanistic explanations of GAS5 function that have compelling experimental support. Full article

(This article belongs to the Special Issue Clinical Potential of Non-coding RNAs in Cancer)

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