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      Non-coding RNA in hepatocellular carcinoma: Mechanisms, biomarkers and therapeutic targets

      Author(s): , , ,
      Publication date Created:
      Publication date (Print):
      Journal: Journal of Hepatology
      Publisher: Elsevier BV

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          Abstract

          The majority of the human genome is not translated into proteins but can be transcribed into RNA. Even though the resulting non-coding RNAs (ncRNAs) do not encode for proteins, they contribute to diseases such as cancer. Here, we review examples of the functions of ncRNAs in liver cancer and their potential use for the detection and treatment of liver cancer.

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          Epithelial-mesenchymal transitions in development and disease.

          Jean Paul Thiery, Hervé Acloque, Ruby Y J Huang … (2009)
          The epithelial to mesenchymal transition (EMT) plays crucial roles in the formation of the body plan and in the differentiation of multiple tissues and organs. EMT also contributes to tissue repair, but it can adversely cause organ fibrosis and promote carcinoma progression through a variety of mechanisms. EMT endows cells with migratory and invasive properties, induces stem cell properties, prevents apoptosis and senescence, and contributes to immunosuppression. Thus, the mesenchymal state is associated with the capacity of cells to migrate to distant organs and maintain stemness, allowing their subsequent differentiation into multiple cell types during development and the initiation of metastasis.
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            Non-coding RNAs: regulators of disease.

            Ryan J. Taft, Ken C. Pang, Timothy Mercer … (2010)
            For 50 years the term 'gene' has been synonymous with regions of the genome encoding mRNAs that are translated into protein. However, recent genome-wide studies have shown that the human genome is pervasively transcribed and produces many thousands of regulatory non-protein-coding RNAs (ncRNAs), including microRNAs, small interfering RNAs, PIWI-interacting RNAs and various classes of long ncRNAs. It is now clear that these RNAs fulfil critical roles as transcriptional and post-transcriptional regulators and as guides of chromatin-modifying complexes. Here we review the biology of ncRNAs, focusing on the fundamental mechanisms by which ncRNAs facilitate normal development and physiology and, when dysfunctional, underpin disease. We also discuss evidence that intergenic regions associated with complex diseases express ncRNAs, as well as the potential use of ncRNAs as diagnostic markers and therapeutic targets. Taken together, these observations emphasize the need to move beyond the confines of protein-coding genes and highlight the fact that continued investigation of ncRNA biogenesis and function will be necessary for a comprehensive understanding of human disease.
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              Whole-genome mutational landscape and characterization of noncoding and structural mutations in liver cancer.

              Akihiro Fujimoto, Mayuko Furuta, Yasushi Totoki … (2016)
              Liver cancer, which is most often associated with virus infection, is prevalent worldwide, and its underlying etiology and genomic structure are heterogeneous. Here we provide a whole-genome landscape of somatic alterations in 300 liver cancers from Japanese individuals. Our comprehensive analysis identified point mutations, structural variations (STVs), and virus integrations, in noncoding and coding regions. We discovered mutational signatures related to liver carcinogenesis and recurrently mutated coding and noncoding regions, such as long intergenic noncoding RNA genes (NEAT1 and MALAT1), promoters, CTCF-binding sites, and regulatory regions. STV analysis found a significant association with replication timing and identified known (CDKN2A, CCND1, APC, and TERT) and new (ASH1L, NCOR1, and MACROD2) cancer-related genes that were recurrently affected by STVs, leading to altered expression. These results emphasize the value of whole-genome sequencing analysis in discovering cancer driver mutations and understanding comprehensive molecular profiles of liver cancer, especially with regard to STVs and noncoding mutations.
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                Author and article information

                Journal
                Title: Journal of Hepatology
                Abbreviated Title: Journal of Hepatology
                Publisher: Elsevier BV
                ISSN (Print): 01688278
                Publication date Created: September 2017
                Publication date (Print): September 2017
                Volume: 67
                Issue: 3
                Pages: 603-618
                Article
                DOI: 10.1016/j.jhep.2017.04.009
                PubMed ID: 28438689
                SO-VID: 5b1dfe3e-3461-40ad-8bb8-91ea813a28c2
                Copyright © © 2017
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