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Chidambaranathan-Reghupaty et al. Hepatoma Research 2018;4:32    Hepatoma Research
               DOI: 10.20517/2394-5079.2018.34


               Review                                                                        Open Access


               The multifaceted oncogene SND1 in cancer: focus
               on hepatocellular carcinoma


                                                 1
                                                                 1
               Saranya Chidambaranathan-Reghupaty , Rachel Mendoza , Paul B. Fisher 1,2,3 , Devanand Sarkar 1,2,3
               1 Department of Human and Molecular Genetics, Virginia Commonwealth University, Richmond, VA 23298, USA.
               2 Massey Cancer Center, Virginia Commonwealth University, Richmond, VA 23298, USA.
               3 VCU Institute of Molecular Medicine, Virginia Commonwealth University, Richmond, VA 23298, USA.

               Correspondence to: Dr. Devanand Sarkar, 1220 E Broad St, PO Box 980035, Richmond, VA 23298, USA.
               E-mail: devanand.sarkar@vcuhealth.org

               How to cite this article: Chidambaranathan-Reghupaty S, Mendoza R, Fisher PB, Sarkar D. The multifaceted oncogene SND1 in cancer:
               focus on hepatocellular carcinoma. Hepatoma Res 2018;4:32. http://dx.doi.org/10.20517/2394-5079.2018.34

               Received: 2 Apr 2018    First Decision: 11 Jun 2018    Revised: 19 Jun 2018    Accepted: 19 Jun 2018    Published: 10 Jul 2018
               Science Editor: Guang-Wen Cao    Copy Editor: Jun-Yao Li    Production Editor: Huan-Liang Wu



               Abstract
               Staphylococcal nuclease and tudor domain containing 1 (SND1) is a protein that regulates a complex array of
               functions. It controls gene expression through transcriptional activation, mRNA degradation, mRNA stabilization,
               ubiquitination and alternative splicing. More than two decades of research has accumulated evidence of the role of
               SND1 as an oncogene in various cancers. It is a promoter of cancer hallmarks like proliferation, invasion, migration,
               angiogenesis and metastasis. In addition to these functions, it has a role in lipid metabolism, inflammation and
               stress response. The participation of SND1 in such varied functions makes it distinct from most oncogenes that
               are relatively more focused in their role. This becomes important in the case of hepatocellular carcinoma (HCC)
               since in addition to typical cancer drivers, factors like lipid metabolism deregulation and chronic inflammation can
               predispose hepatocytes to HCC. The objective of this review is to provide a summary of the current knowledge
               available on SND1, specifically in relation to HCC and to shed light on its prospect as a therapeutic target.

               Keywords: Staphylococcal nuclease and tudor domain containing 1, hepatocellular carcinoma, inflammation





               INTRODUCTION
               Hepatocellular carcinoma (HCC) is the primary liver malignancy arising from hepatocytes. It is the fifth
               common cancer in men and the ninth common cancer in women. It is the second leading cause of cancer-
               related deaths worldwide. A high mortality to incidence ratio of 0.95 reflects its poor prognosis and makes
               it an important public health burden (Globocan 2012). The main causes of HCC are viral infections like
               hepatitis B and hepatitis C, chronic alcoholism, obesity, liver cirrhosis and non-alcoholic steatohepatitis


                           © The Author(s) 2018. Open Access This article is licensed under a Creative Commons Attribution 4.0
                           International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use,
                sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long
                as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license,
                and indicate if changes were made.


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