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      Long non-coding RNA ABHD11-AS1 promotes colorectal cancer development through regulation of miR-133a/SOX4 axis

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          Abstract

          Recently, lncRNA has been verified to regulate the development and progression of tumor. LncRNA ABHD11-AS1 has been proven to serve as an oncogene in several cancers. However, the role of ABHD11-AS1 in colorectal cancer remains totally unknown. In the present study, qRT-PCR assay revealed that ABHD11-AS1 expression was markedly higher in colorectal cancer tissues and cell lines. In addition, patients who displayed overexpression of ABHD11-AS1 showed a significantly poorer progression free survival (PFS) and overall survival (OS) by Kaplan–Meier analysis. Loss-of-function experiments suggested that silencing of ABHD11-AS1 expression could significantly reduce the proliferation, colony formation, migration and invasion of colorectal cancer cells, and increase cell apoptosis. Moreover, bioinformatics analysis, biotin pull-down assay, luciferase reporter assay, and RIP assay disclosed that ABHD11-AS1 straightly interacted with miR-133a. We also found that SOX4 was a downstream target of miR-133a and ABHD11-AS1 subsequently exerted its biological effects via modulating the expression of SOX4 in colorectal cancer cells. Collectively, these findings manifested that the ABHD11-AS1/miR-133a/SOX4 axis may be a cogitable and promising therapeutic target for colorectal cancer.

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          The bright side of dark matter: lncRNAs in cancer.

          Joseph Evans, Felix Y Feng, Arul M Chinnaiyan (2016)
          The traditional view of genome organization has been upended in the last decade with the discovery of vast amounts of non-protein-coding transcription. After initial concerns that this "dark matter" of the genome was transcriptional noise, it is apparent that a subset of these noncoding RNAs are functional. Long noncoding RNA (lncRNA) genes resemble protein-coding genes in several key aspects, and they have myriad molecular functions across many cellular pathways and processes, including oncogenic signaling. The number of lncRNA genes has recently been greatly expanded by our group to triple the number of protein-coding genes; therefore, lncRNAs are likely to play a role in many biological processes. Based on their large number and expression specificity in a variety of cancers, lncRNAs are likely to serve as the basis for many clinical applications in oncology.
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            Sox17 and Sox4 differentially regulate beta-catenin/T-cell factor activity and proliferation of colon carcinoma cells.

            Aaron Zorn, Debora Sinner, Robert Opoka … (2007)
            The canonical Wnt pathway is necessary for gut epithelial cell proliferation, and aberrant activation of this pathway causes intestinal neoplasia. We report a novel mechanism by which the Sox family of transcription factors regulate the canonical Wnt signaling pathway. We found that some Sox proteins antagonize while others enhance beta-catenin/T-cell factor (TCF) activity. Sox17, which is expressed in the normal gut epithelium but exhibits reduced expression in intestinal neoplasia, is antagonistic to Wnt signaling. When overexpressed in SW480 colon carcinoma cells, Sox17 represses beta-catenin/TCF activity in a dose-dependent manner and inhibits proliferation. Sox17 and Sox4 are expressed in mutually exclusive domains in normal and neoplastic gut tissues, and gain- and loss-of-function studies demonstrate that Sox4 enhances beta-catenin/TCF activity and the proliferation of SW480 cells. In addition to binding beta-catenin, both Sox17 and Sox4 physically interact with TCF/lymphoid enhancer factor (LEF) family members via their respective high-mobility-group box domains. Results from gain- and loss-of-function experiments suggest that the interaction of Sox proteins with beta-catenin and TCF/LEF proteins regulates the stability of beta-catenin and TCF/LEF. In particular, Sox17 promotes the degradation of both beta-catenin and TCF proteins via a noncanonical, glycogen synthase kinase 3beta-independent mechanism that can be blocked by proteasome inhibitors. In contrast, Sox4 may function to stabilize beta-catenin protein. These findings indicate that Sox proteins can act as both antagonists and agonists of beta-catenin/TCF activity, and this mechanism may regulate Wnt signaling responses in many developmental and disease contexts.
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              LncRNA HOTAIR is a Prognostic Biomarker for the Proliferation and Chemoresistance of Colorectal Cancer via MiR-203a-3p-Mediated Wnt/ß-Catenin Signaling Pathway.

              Zhigang Xiao, Zhan Qu, Zhikang Chen … (2018)
              HOX transcript antisense RNA (HOTAIR) plays a vital role in carcinogenesis. However, its functional and regulatory roles remain unclear. In this study, we aimed to investigate its biological function and clinical significance in human colorectal cancer (CRC).
              Article 0 comments Cited 67 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Biosci Rep
                Journal ID (iso-abbrev): Biosci. Rep
                Journal ID (hwp): ppbioscirep
                Journal ID (publisher-id): BSR
                Title: Bioscience Reports
                Publisher: Portland Press Ltd.
                ISSN (Print): 0144-8463
                ISSN (Electronic): 1573-4935
                Publication date (Electronic preprint): 14 November 2018
                Publication date (Electronic): 14 December 2018
                Publication date Collection: 21 December 2018
                Volume: 38
                Issue: 6
                Electronic Location Identifier: BSR20181386
                Affiliations
                [1 ]Radiology Department, First Affiliated Hospital of Xi’an Jiaotong University, Xi’an city, Shaanxi Province, P.R. China
                [2 ]Department of MRI, Shaanxi Provincial People’s Hospital, Xi’an city, Shaanxi Province, P.R. China
                Author notes
                Correspondence: Xiaoyi Duan ( duanxiaoyiphd@ 1234562980.com )
                [*]

                These authors contributed equally to this work.

                Author information
                http://orcid.org/0000-0002-6579-6906
                Article
                DOI: 10.1042/BSR20181386
                PMC ID: 6294614
                PubMed ID: 30429229
                SO-VID: 61b4dd85-f050-43c1-b3f1-7360e30e0d24
                Copyright © © 2018 The Author(s).
                License:

                This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY).

                History
                Date received : 12 August 2018
                Date revision received : 23 October 2018
                Date accepted : 29 October 2018
                Page count
                Pages: 10
                Categories
                Subject: Research Articles
                Subject: Research Article
                Subject: 25
                Subject: 21
                Subject: 39
                Subject: 10

                ScienceOpen disciplines: Life sciences
                Keywords: colorectal cancer,large intervening non-coding rna,microrna,tumorigenesis
                Data availability:
                ScienceOpen disciplines: Life sciences
                Keywords: colorectal cancer, large intervening non-coding rna, microrna, tumorigenesis

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