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Cells
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Non-coding RNA in Cancer
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Non-coding RNA in Cancer

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Nuclei: Function, Transport and Receptors".

Deadline for manuscript submissions: closed (31 July 2020) | Viewed by 19144

Special Issue Editors

Prof. Dr. Soichiro Yamamura

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Guest Editor
Department of Urology, University of California, San Francisco, CA 94121, USA
Interests: non-coding RNA; cancer; gene expression; cell signaling
Special Issues, Collections and Topics in MDPI journals
Dr. Marisa Shiina

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Assistant Editor
Department of Urology, University of California, San Francisco, CA 94121, USA
Interests: cancer cell biology; non-coding RNA; drug resistance; cancer stem cells; cell signaling

Special Issue Information

Dear Colleagues,

Next-generation RNA sequencing of whole genomes and transcriptomes has revealed that non-coding RNAs (ncRNAs) constitute most of the transcriptome.

Two classes of ncRNAs, microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), have been extensively studied and shown to regulate gene expression and thus control cellular processes such as cell proliferation, motility, and apoptosis. Aberrant expression of miRNAs and lncRNAs has been found in cancer cells and shown to play pivotal roles in cancer. miRNAs bind mainly to the 3’UTR region of target mRNA and suppress target gene expression at the post-transcriptional level, while lncRNAs regulate gene expression by diverse mechanisms such as chromatin, protein, and mRNA interactions.

Accumulating evidence indicates that miRNAs and lncRNAs interact and regulate each other through biding sites. This cross-regulation has also been shown to regulate gene expression and tumorigenesis. In competitive endogenous RNA (ceRNA) mechanisms, lncRNAs sponge miRNAs, suppressing their regulatory effects on mRNAs.

Other ncRNA species such as small nucleolar RNAs (snoRNAs), PIWI-interacting RNAs (piRNAs), and vault RNAs (vtRNAs), have also been implicated in regulating gene expression. piRNAs which derive from snoRNAs function in similar ways to miRNAs. vtRNAs have been shown to induce drug resistance in cancer cells and recently shown to suppress autophagy.

This Special Issue aims to cover recent advances in any ncRNA cancer studies, such as functions, mechanism of action, mode of interaction, and clinical studies. We invite contributions in the form of original research articles and reviews.

Prof. Soichiro Yamamura
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. Cells 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 2700 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 RNA
  • cancer
  • interaction
  • ceRNA
  • tumorigenesis
  • tumor suppression

Published Papers (5 papers)

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Research

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19 pages, 1845 KiB  
Article
hsa-miR-20b-5p and hsa-miR-363-3p Affect Expression of PTEN and BIM Tumor Suppressor Genes and Modulate Survival of T-ALL Cells In Vitro
by Monika Drobna, Bronisława Szarzyńska, Roman Jaksik, Łukasz Sędek, Anna Kuchmiy, Tom Taghon, Pieter Van Vlierberghe, Tomasz Szczepański, Michał Witt and Małgorzata Dawidowska
Cells 2020, 9(5), 1137; https://0-doi-org.brum.beds.ac.uk/10.3390/cells9051137 - 05 May 2020
Cited by 25 | Viewed by 3993
Abstract
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy arising from T lymphocyte precursors. We have previously shown by miRNA-seq, that miRNAs from the mir-106a-363 cluster are overexpressed in pediatric T-ALL. In silico analysis indicated their potential involvement in the regulation of apoptosis. [...] Read more.
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy arising from T lymphocyte precursors. We have previously shown by miRNA-seq, that miRNAs from the mir-106a-363 cluster are overexpressed in pediatric T-ALL. In silico analysis indicated their potential involvement in the regulation of apoptosis. Here, we aimed to test the hypothesis on the pro-tumorigenic roles of these miRNAs in T-ALL cells in vitro. We demonstrate, for the first time, that hsa-miR-20b-5p and hsa-miR-363-3p from the mir-106a-363 cluster, when upregulated in T-ALL cells in vitro, protect leukemic cells from apoptosis, enhance proliferation, and contribute to growth advantage. We show, using dual luciferase reporter assays, Ago2-RNA immunoprecipitation, RT-qPCR, and Western blots, that the oncogenic effects of these upregulated miRNAs might, at least in part, be mediated by the downregulation of two important tumor suppressor genes, PTEN and BIM, targeted by both miRNAs. Additionally, we demonstrate the cooperative effects of these two miRNAs by simultaneous inhibition of both miRNAs as compared to the inhibition of single miRNAs. We postulate that hsa-miR-20b-5p and hsa-miR-363-3p from the mir-106a-363 cluster might serve as oncomiRs in T-ALL, by contributing to post-transcriptional repression of key tumor suppressors, PTEN and BIM. Full article
(This article belongs to the Special Issue Non-coding RNA in Cancer)
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23 pages, 4766 KiB  
Article
Targeting the Epigenetic Non-Coding RNA MALAT1/Wnt Signaling Axis as a Therapeutic Approach to Suppress Stemness and Metastasis in Hepatocellular Carcinoma
by Hang-Lung Chang, Oluwaseun Adebayo Bamodu, Jiann-Ruey Ong, Wei-Hwa Lee, Chi-Tai Yeh and Jo-Ting Tsai
Cells 2020, 9(4), 1020; https://0-doi-org.brum.beds.ac.uk/10.3390/cells9041020 - 20 Apr 2020
Cited by 25 | Viewed by 3778
Abstract
Background: With recorded under-performance of current standard therapeutic strategies as highlighted by high rates of post-treatment (resection or local ablation) recurrence, resistance to chemotherapy, poor overall survival, and an increasing global incidence, hepatocellular carcinoma (HCC) constitutes a medical challenge. Accumulating evidence implicates the [...] Read more.
Background: With recorded under-performance of current standard therapeutic strategies as highlighted by high rates of post-treatment (resection or local ablation) recurrence, resistance to chemotherapy, poor overall survival, and an increasing global incidence, hepatocellular carcinoma (HCC) constitutes a medical challenge. Accumulating evidence implicates the presence of HCC stem cells (HCC-SCs) in HCC development, drug-resistance, recurrence, and progression. Therefore, treatment strategies targeting both HCC-SCs and non-CSCs are essential. Methods: Recently, there has been an increasing suggestion of MALAT1 oncogenic activity in HCC; however, its role in HCC stemness remains unexplored. Herein, we investigated the probable role of MALAT1 in the SCs-like phenotype of HCC and explored likely molecular mechanisms by which MALAT1 modulates HCC-SCs-like and metastatic phenotypes. Results: We showed that relative to normal, cirrhotic, or dysplastic liver conditions, MALAT1 was aberrantly expressed in HCC, similar to its overexpression in Huh7, Mahlavu, and SK-Hep1 HCC cells lines, compared to the normal liver cell line THLE-2. We also demonstrated a positive correlation between MALAT1 expression and poor cell differentiation status in HCC using RNAscope. Interestingly, we demonstrated that shRNA-mediated silencing of MALAT1 concomitantly downregulated the expression levels of β-catenin, Stat3, c-Myc, CK19, vimentin, and Twist1 proteins, inhibited HCC oncogenicity, and significantly suppressed the HCC-SCs-related dye-effluxing potential of HCC cells and reduced their ALDH-1 activity, partially due to inhibited MALAT1-β-catenin interaction. Additionally, using TOP/FOP (TCL/LEF-Firefly luciferase) Flash, RT-PCR, and western blot assays, we showed that silencing MALAT1 downregulates β-catenin expression, dysregulates the canonical Wnt signaling pathway, and consequently attenuates HCC tumorsphere formation efficiency, with concurrent reduction in CD133+ and CD90+ HCC cell population, and inhibits tumor growth in SK-Hep1-bearing mice. Conclusions: Taken together, our data indicate that MALAT1/Wnt is a targetable molecular candidate, and the therapeutic targeting of MALAT1/Wnt may constitute a novel promising anticancer strategy for HCC treatment. Full article
(This article belongs to the Special Issue Non-coding RNA in Cancer)
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20 pages, 4088 KiB  
Article
MicroRNA-361-Mediated Inhibition of HSP90 Expression and EMT in Cervical Cancer Is Counteracted by Oncogenic lncRNA NEAT1
by Daozhi Xu, Peixin Dong, Ying Xiong, Junming Yue, Yosuke Konno, Kei Ihira, Noriko Kobayashi, Yukiharu Todo and Hidemichi Watari
Cells 2020, 9(3), 632; https://0-doi-org.brum.beds.ac.uk/10.3390/cells9030632 - 05 Mar 2020
Cited by 41 | Viewed by 3521
Abstract
Epithelial-mesenchymal transition (EMT) is a key process contributing to cervical cancer (CC) metastasis, and microRNAs (miRNAs) modulate the expression of genes implicated in EMT. However, the accurate role of miR-361 in CC-associated EMT and the mechanisms underlying its function in CC remains largely [...] Read more.
Epithelial-mesenchymal transition (EMT) is a key process contributing to cervical cancer (CC) metastasis, and microRNAs (miRNAs) modulate the expression of genes implicated in EMT. However, the accurate role of miR-361 in CC-associated EMT and the mechanisms underlying its function in CC remains largely unknown. The functional roles of miR-361 in CC cells were explored by a series of cell functional assays. Luciferase reporter assays were used to demonstrate the potential interaction between miR-361, HSP90, and long non-coding RNA (lncRNA) NEAT1. We detected a reduction of miR-361 expression in CC tissues compared with normal tissues, and miR-361 overexpression inhibited invasion and EMT phenotypes of CC cells by directly targeting a key EMT activator HSP90. Additionally, we detected significantly higher levels of HSP90 in CC tissues compared with normal tissues, and high expression of HSP90 predicted a poorer prognosis. We further identified NEAT1 as a significantly upregulated lncRNA in CC tissues and high expression of NEAT1 was associated with worse survival in CC patients. NEAT1 directly repressed miR-361 expression and played an oncogenic role in CC cell invasion and sphere formation. Conclusions: These results demonstrated that miR-361 directly targets HSP90 to inhibit the invasion and EMT features, and NEAT1 functions as an oncogenic lncRNA that suppresses miR-361 expression and induces EMT and sphere formation in CC cells, thus providing critical insights into the molecular pathways operating in this malignancy. Full article
(This article belongs to the Special Issue Non-coding RNA in Cancer)
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21 pages, 2124 KiB  
Article
Molecular and Functional Characterization of the Somatic PIWIL1/piRNA Pathway in Colorectal Cancer Cells
by Assunta Sellitto, Konstantinos Geles, Ylenia D’Agostino, Marisa Conte, Elena Alexandrova, Domenico Rocco, Giovanni Nassa, Giorgio Giurato, Roberta Tarallo, Alessandro Weisz and Francesca Rizzo
Cells 2019, 8(11), 1390; https://0-doi-org.brum.beds.ac.uk/10.3390/cells8111390 - 05 Nov 2019
Cited by 15 | Viewed by 4242
Abstract
PIWI-like (PIWIL) proteins and small non-coding piRNAs, involved in genome regulation in germline cells, are found aberrantly expressed in human tumors. Gene expression data from The Cancer Genome Atlas (TCGA), the Genotype-Tissue Expression (GTEx) project, and the European Genome-Phenome Archive (EGA) indicate that [...] Read more.
PIWI-like (PIWIL) proteins and small non-coding piRNAs, involved in genome regulation in germline cells, are found aberrantly expressed in human tumors. Gene expression data from The Cancer Genome Atlas (TCGA), the Genotype-Tissue Expression (GTEx) project, and the European Genome-Phenome Archive (EGA) indicate that the PIWIL1 gene is ectopically activated in a significant fraction of colorectal cancers (CRCs), where this is accompanied by promoter demethylation, together with germline factors required for piRNA production. Starting from this observation, the PIWIL/piRNA pathway was studied in detail in COLO 205 CRC cells, which express significant levels of this protein, to investigate role and significance of ectopic PIWIL1 expression in human tumors. RNA sequencing and cell and computational biology led to the demonstration that PIWIL1 localizes in a nuage-like structure located in the perinuclear region of the cell and that a significant fraction of the piRNAs expressed in these cells are methylated, and, therefore, present in an active form. This was further supported by RNA immunoprecipitation, which revealed how several piRNAs can be found loaded into PIWIL1 to form complexes also comprising their target mRNAs. The mature transcripts associated with the PIWIL–piRNA complex encode key regulatory proteins involved in the molecular mechanisms sustaining colorectal carcinogenesis, suggesting that the PIWI/piRNA pathway may actively contribute to the establishment and/or maintenance of clinico-pathological features of CRCs. Full article
(This article belongs to the Special Issue Non-coding RNA in Cancer)
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Review

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25 pages, 1118 KiB  
Review
miR-615 Fine-Tunes Growth and Development and Has a Role in Cancer and in Neural Repair
by Marisol Godínez-Rubí and Daniel Ortuño-Sahagún
Cells 2020, 9(7), 1566; https://0-doi-org.brum.beds.ac.uk/10.3390/cells9071566 - 27 Jun 2020
Cited by 18 | Viewed by 3026
Abstract
MicroRNAs (miRNAs) are small noncoding RNAs that function as epigenetic modulators regulating almost any gene expression. Similarly, other noncoding RNAs, as well as epigenetic modifications, can regulate miRNAs. This reciprocal interaction forms a miRNA-epigenetic feedback loop, the deregulation of which affects physiological processes [...] Read more.
MicroRNAs (miRNAs) are small noncoding RNAs that function as epigenetic modulators regulating almost any gene expression. Similarly, other noncoding RNAs, as well as epigenetic modifications, can regulate miRNAs. This reciprocal interaction forms a miRNA-epigenetic feedback loop, the deregulation of which affects physiological processes and contributes to a great diversity of diseases. In the present review, we focus on miR-615, a miRNA highly conserved across eutherian mammals. It is involved not only during embryogenesis in the regulation of growth and development, for instance during osteogenesis and angiogenesis, but also in the regulation of cell growth and the proliferation and migration of cells, acting as a tumor suppressor or tumor promoter. It therefore serves as a biomarker for several types of cancer, and recently has also been found to be involved in reparative processes and neural repair. In addition, we present the pleiad of functions in which miR-615 is involved, as well as their multiple target genes and the multiple regulatory molecules involved in its own expression. We do this by introducing in a comprehensible way the reported knowledge of their actions and interactions and proposing an integral view of its regulatory mechanisms. Full article
(This article belongs to the Special Issue Non-coding RNA in Cancer)
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