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      LINC00152: A pivotal oncogenic long non‐coding RNA in human cancers

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          Abstract

          In recent years, increasing evidence has shown the potential role of long non‐coding RNAs (lncRNAs) in multiple cancers. Deregulation of lnc RNAs was detected being closely associated with many kinds of tumours where they can act as a tumour suppressor or accelerator. LINC00152 was identified as an oncogene involved in many kinds of cancers, such as gastric cancer, hepatocellular carcinoma, colon cancer, gallbladder cancer and renal cell carcinoma. Moreover, inhibition of LINC00152 can suppress proliferation, migration and invasion of the cancer cells. Increasing evidence has showed that LINC00152 may act as a diagnostic and prognostic biomarker for the above‐mentioned cancers. In our review, we summarize the recent research progress of the expression and role of LINC00152 in various kinds of cancers.

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          Most cited references31

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          Non-coding RNA genes and the modern RNA world.

          S. Eddy (2001)
          Non-coding RNA (ncRNA) genes produce functional RNA molecules rather than encoding proteins. However, almost all means of gene identification assume that genes encode proteins, so even in the era of complete genome sequences, ncRNA genes have been effectively invisible. Recently, several different systematic screens have identified a surprisingly large number of new ncRNA genes. Non-coding RNAs seem to be particularly abundant in roles that require highly specific nucleic acid recognition without complex catalysis, such as in directing post-transcriptional regulation of gene expression or in guiding RNA modifications.
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            LncRNA HOXA11-AS Promotes Proliferation and Invasion of Gastric Cancer by Scaffolding the Chromatin Modification Factors PRC2, LSD1, and DNMT1.

            Long noncoding RNAs (lncRNA) have been implicated in human cancer but their mechanisms of action are mainly undocumented. In this study, we investigated lncRNA alterations that contribute to gastric cancer through an analysis of The Cancer Genome Atlas RNA sequencing data and other publicly available microarray data. Here we report the gastric cancer-associated lncRNA HOXA11-AS as a key regulator of gastric cancer development and progression. Patients with high HOXA11-AS expression had a shorter survival and poorer prognosis. In vitro and in vivo assays of HOXA11-AS alterations revealed a complex integrated phenotype affecting cell growth, migration, invasion, and apoptosis. Strikingly, high-throughput sequencing analysis after HOXA11-AS silencing highlighted alterations in cell proliferation and cell-cell adhesion pathways. Mechanistically, EZH2 along with the histone demethylase LSD1 or DNMT1 were recruited by HOXA11-AS, which functioned as a scaffold. HOXA11-AS also functioned as a molecular sponge for miR-1297, antagonizing its ability to repress EZH2 protein translation. In addition, we found that E2F1 was involved in HOXA11-AS activation in gastric cancer cells. Taken together, our findings support a model in which the EZH2/HOXA11-AS/LSD1 complex and HOXA11-AS/miR-1297/EZH2 cross-talk serve as critical effectors in gastric cancer tumorigenesis and progression, suggesting new therapeutic directions in gastric cancer. Cancer Res; 76(21); 6299-310. ©2016 AACR.
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              A peptide mimicking VGLL4 function acts as a YAP antagonist therapy against gastric cancer.

              The Hippo pathway has been implicated in suppressing tissue overgrowth and tumor formation by restricting the oncogenic activity of YAP. However, transcriptional regulators that inhibit YAP activity have not been well studied. Here, we uncover clinical importance for VGLL4 in gastric cancer suppression and find that VGLL4 directly competes with YAP for binding TEADs. Importantly, VGLL4's tandem Tondu domains are not only essential but also sufficient for its inhibitory activity toward YAP. A peptide mimicking this function of VGLL4 potently suppressed tumor growth in vitro and in vivo. These findings suggest that disruption of YAP-TEADs interaction by a VGLL4-mimicking peptide may be a promising therapeutic strategy against YAP-driven human cancers. Copyright © 2014 Elsevier Inc. All rights reserved.
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                Author and article information

                Contributors
                miaolinxh@163.com
                Journal
                Cell Prolif
                Cell Prolif
                10.1111/(ISSN)1365-2184
                CPR
                Cell Proliferation
                John Wiley and Sons Inc. (Hoboken )
                0960-7722
                1365-2184
                02 May 2017
                August 2017
                : 50
                : 4 ( doiID: 10.1111/cpr.2017.50.issue-4 )
                : e12349
                Affiliations
                [ 1 ] Medical Center for Digestive Diseases Second Affiliated Hospital Nanjing Medical University Nanjing Jiangsu Province China
                [ 2 ] Department of Urology Second Affiliated Hospital Nanjing Medical University Nanjing Jiangsu Province China
                [ 3 ] Department of Oncology Second Affiliated Hospital Nanjing Medical University Nanjing Jiangsu Province China
                Author notes
                [*] [* ] Correspondence

                Dr. Lin Miao, Medical Center for Digestive Diseases, The Second Affiliated Hospital of Nanjing Medical University, 121 Jiangjiayuan, Nanjing 210011, Jiangsu Province, China.

                Email: miaolinxh@ 123456163.com

                Author information
                http://orcid.org/0000-0002-1114-0530
                Article
                CPR12349
                10.1111/cpr.12349
                6529135
                28464433
                2feaa81b-2e41-4e56-82f2-3f41465f48ea
                © 2017 The Authors. Cell Proliferation Published by John Wiley & Sons Ltd

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                : 07 January 2017
                : 01 March 2017
                Page count
                Figures: 1, Tables: 2, Pages: 6, Words: 4497
                Funding
                Funded by: Standard Diagnosis and Treatment of Key Disease of Jiangsu Province
                Award ID: BE2015722
                Funded by: Jiangsu Province
                Award ID: WSN‐018
                Funded by: Scientific Research Foundation for Health of Jiangsu Province
                Award ID: H201408
                Categories
                Review Article
                Review Article
                Custom metadata
                2.0
                cpr12349
                August 2017
                Converter:WILEY_ML3GV2_TO_NLMPMC version:5.6.2.1 mode:remove_FC converted:02.05.2019

                Cell biology
                Cell biology

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