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      Diagnostic and prognostic potential of tissue and circulating long non-coding RNAs in colorectal tumors

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          Abstract

          Long non-coding RNAs (lncRNAs) are members of the non-protein coding RNA family longer than 200 nucleotides. They participate in the regulation of gene and protein expression influencing apoptosis, cell proliferation and immune responses, thereby playing a critical role in the development and progression of various cancers, including colorectal cancer (CRC). As CRC is one of the most frequently diagnosed malignancies worldwide with high mortality, its screening and early detection are crucial, so the identification of disease-specific biomarkers is necessary. LncRNAs are promising candidates as they are involved in carcinogenesis, and certain lncRNAs ( e.g., CCAT1, CRNDE, CRCAL1-4) show altered expression in adenomas, making them potential early diagnostic markers. In addition to being useful as tissue-specific markers, analysis of circulating lncRNAs ( e.g., CCAT1, CCAT2, BLACAT1, CRNDE, NEAT1, UCA1) in peripheral blood offers the possibility to establish minimally invasive, liquid biopsy-based diagnostic tests. This review article aims to describe the origin, structure, and functions of lncRNAs and to discuss their contribution to CRC development. Moreover, our purpose is to summarise lncRNAs showing altered expression levels during tumor formation in both colon tissue and plasma/serum samples and to demonstrate their clinical implications as diagnostic or prognostic biomarkers for CRC.

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          Most cited references 250

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          RNA-Seq: a revolutionary tool for transcriptomics.

          RNA-Seq is a recently developed approach to transcriptome profiling that uses deep-sequencing technologies. Studies using this method have already altered our view of the extent and complexity of eukaryotic transcriptomes. RNA-Seq also provides a far more precise measurement of levels of transcripts and their isoforms than other methods. This article describes the RNA-Seq approach, the challenges associated with its application, and the advances made so far in characterizing several eukaryote transcriptomes.
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            A programmable dual-RNA-guided DNA endonuclease in adaptive bacterial immunity.

            Clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated (Cas) systems provide bacteria and archaea with adaptive immunity against viruses and plasmids by using CRISPR RNAs (crRNAs) to guide the silencing of invading nucleic acids. We show here that in a subset of these systems, the mature crRNA that is base-paired to trans-activating crRNA (tracrRNA) forms a two-RNA structure that directs the CRISPR-associated protein Cas9 to introduce double-stranded (ds) breaks in target DNA. At sites complementary to the crRNA-guide sequence, the Cas9 HNH nuclease domain cleaves the complementary strand, whereas the Cas9 RuvC-like domain cleaves the noncomplementary strand. The dual-tracrRNA:crRNA, when engineered as a single RNA chimera, also directs sequence-specific Cas9 dsDNA cleavage. Our study reveals a family of endonucleases that use dual-RNAs for site-specific DNA cleavage and highlights the potential to exploit the system for RNA-programmable genome editing.
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              Long noncoding RNA HOTAIR reprograms chromatin state to promote cancer metastasis

              Large intervening noncoding RNAs (lincRNAs) are pervasively transcribed in the genome1, 2, 3 yet their potential involvement in human disease is not well understood4,5. Recent studies of dosage compensation, imprinting, and homeotic gene expression suggest that individual lincRNAs can function as the interface between DNA and specific chromatin remodeling activities6,7,8. Here we show that lincRNAs in the HOX loci become systematically dysregulated during breast cancer progression. The lincRNA termed HOTAIR is increased in expression in primary breast tumors and metastases, and HOTAIR expression level in primary tumors is a powerful predictor of eventual metastasis and death. Enforced expression of HOTAIR in epithelial cancer cells induced genome-wide re-targeting of Polycomb Repressive Complex 2 (PRC2) to an occupancy pattern more resembling embryonic fibroblasts, leading to altered histone H3 lysine 27 methylation, gene expression, and increased cancer invasiveness and metastasis in a manner dependent on PRC2. Conversely, loss of HOTAIR can inhibit cancer invasiveness, particularly in cells that possess excessive PRC2 activity. These findings suggest that lincRNAs play active roles in modulating the cancer epigenome and may be important targets for cancer diagnosis and therapy.
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                Author and article information

                Contributors
                Journal
                World J Gastroenterol
                World J. Gastroenterol
                WJG
                World Journal of Gastroenterology
                Baishideng Publishing Group Inc
                1007-9327
                2219-2840
                14 September 2019
                14 September 2019
                : 25
                : 34
                : 5026-5048
                Affiliations
                Molecular Medicine Research Group, Hungarian Academy of Sciences, Budapest H-1088, Hungary. udvardyne_galamb.orsolya@ 123456semmelweis-univ.hu
                2 nd Department of Internal Medicine, Semmelweis University, Budapest H-1088, Hungary
                Molecular Medicine Research Group, Hungarian Academy of Sciences, Budapest H-1088, Hungary
                2 nd Department of Internal Medicine, Semmelweis University, Budapest H-1088, Hungary
                2 nd Department of Internal Medicine, Semmelweis University, Budapest H-1088, Hungary
                Molecular Medicine Research Group, Hungarian Academy of Sciences, Budapest H-1088, Hungary
                Molecular Medicine Research Group, Hungarian Academy of Sciences, Budapest H-1088, Hungary
                2 nd Department of Internal Medicine, Semmelweis University, Budapest H-1088, Hungary
                Molecular Medicine Research Group, Hungarian Academy of Sciences, Budapest H-1088, Hungary
                Author notes

                Author contributions: All authors contributed to this paper with conception and design of the study, literature review and analysis, drafting and critical revision and editing, and final approval of the final version.

                Supported by the National Research, Development and Innovation Office, No. NVKP_16-1-2016-0004.

                Corresponding author: Orsolya Galamb, MSc, PhD, Research Fellow, Senior Scientist, 2 nd Department of Internal Medicine, Semmelweis University, Szentkirályi Str 46, Budapest H-1088, Hungary. udvardyne_galamb.orsolya@ 123456semmelweis-univ.hu

                Telephone: +36-1-2660926 Fax: +36-1-2660816

                Article
                jWJG.v25.i34.pg5026
                10.3748/wjg.v25.i34.5026
                6747286
                ©The Author(s) 2019. Published by Baishideng Publishing Group Inc. All rights reserved.

                This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.

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