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      MicroRNA-539 inhibits the proliferation and migration of gastric cancer cells by targeting SRY-box 5 gene

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      Author(s): ,
      Publication date (Electronic):
      Journal: Molecular Medicine Reports
      Publisher: D.A. Spandidos
      Keywords: gastric cancer, microRNA-539, SRY-box 5, proliferation, migration

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          Abstract

          The aim of the present study was to investigate the effect of microRNA (miR)-539 on the proliferation and migration of gastric cancer cells, and explore the underlying mechanism. Gastric cancer cell lines with high or low miR-539 and SRY-box 5 (SOX5) expression levels were constructed by transfection. The proliferation of gastric cancer cells was then detected by Cell Counting Kit-8 assay and cell migration was tested by transwell assay. The results revealed low expression of miR-539 and high expression of SOX5 in gastric cancer tissues and cells as compared with the levels in normal tissues and cells, suggesting that there was a negative correlation between miR-539 and SOX5. Dual-luciferase reporter experiments demonstrated that miR-539 directly targeted SOX5. The proliferation and migration of gastric cancer cells were negatively regulated by the overexpression of miR-539, while positively regulated by the overexpression of SOX5. Notably, SOX5 overexpression attenuated the inhibitory effect of miR-539 on gastric cancer cells. The results suggested that SOX5 is a target gene of miR-539, and that miR-539 inhibits the proliferation and migration of gastric cancer cells by targeting SOX5.

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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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            Sox5 induces epithelial to mesenchymal transition by transactivation of Twist1.

            Xin-Hong Pei, Xin-Quan Lv, HUI-XIANG LI (2014)
            The epithelial to mesenchymal transition (EMT), a highly conserved cellular program, plays an important role in normal embryogenesis and cancer metastasis. Twist1, a master regulator of embryonic morphogenesis, is overexpressed in breast cancer and contributes to metastasis by promoting EMT. In exploring the mechanism underlying the increased Twist1 in breast cancer cells, we found that the transcription factor SRY (sex-determining region Y)-box 5(Sox5) is up-regulation in breast cancer cells and depletion of Sox5 inhibits breast cancer cell proliferation, migration, and invasion. Furthermore, depletion of Sox5 in breast cancer cells caused a dramatic decrease in Twist1 and chromosome immunoprecipitation assay showed that Sox5 can bind directly to the Twist1 promoter, suggesting that Sox5 transactivates Twist1 expression. We further demonstrated that knockdown of Sox5 up-regulated epithelial phenotype cell biomarker (E-cadherin) and down-regulated mesenchymal phenotype cell biomarkers (N-cadherin, Vimentin, and Fibronectin 1), resulting in suppression of EMT. Our study suggests that Sox5 transactivates Twist1 expression and plays an important role in the regulation of breast cancer progression.
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              Status of Epstein-Barr Virus Coinfection with Helicobacter pylori in Gastric Cancer

              Shyam Singh, Hem Jha (2017)
              Epstein-Barr virus is a ubiquitous human herpesvirus whose primary infection causes mononucleosis, Burkett's lymphoma, nasopharyngeal carcinoma, autoimmune diseases, and gastric cancer (GC). The persistent infection causes malignancies in lymph and epithelial cells. Helicobacter pylori causes gastritis in human with chronic inflammation. This chronic inflammation is thought to be the cause of genomic instability. About 45%-word population have a probability of having both pathogens, namely, H. pylori and EBV. Approximately 180 per hundred thousand population is developing GC along with many gastric abnormalities. This makes GC the third leading cause of cancer-related death worldwide. Although lots of research are carried out individually for EBV and H. pylori, still there are very few reports available on coinfection of both pathogens. Recent studies suggested that EBV and H. pylori coinfection increases the occurrence of GC as well as the early age of GC detection comparing to individual infection. The aim of this review is to present status on coinfection of both pathogens and their association with GC.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Mol Med Rep
                Journal ID (iso-abbrev): Mol Med Rep
                Title: Molecular Medicine Reports
                Publisher: D.A. Spandidos
                ISSN (Print): 1791-2997
                ISSN (Electronic): 1791-3004
                Publication date (Print): September 2019
                Publication date (Electronic): 11 July 2019
                Publication date PMC-release: 11 July 2019
                Volume: 20
                Issue: 3
                Pages: 2533-2540
                Affiliations
                Department of Medicine, Changde Vocational Technical College, Changde, Hunan 415000, P.R. China
                Author notes
                Correspondence to: Dr Yanping Zhang, Department of Medicine, Changde Vocational Technical College, 4253 Renmin Road, Wulin, Changde, Hunan 415000, P.R. China, E-mail: zhangyanping_0919@ 123456163.com
                Article
                Publisher ID: mmr-20-03-2533
                DOI: 10.3892/mmr.2019.10486
                PMC ID: 6691193
                PubMed ID: 31322222
                SO-VID: e0367625-e7c9-41c3-b3cf-39b90d91093c
                Copyright © Copyright: © Ding et al.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs 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
                Date received : 07 February 2018
                Date accepted : 08 October 2018
                Categories
                Subject: Articles

                Keywords: gastric cancer,microrna-539,sry-box 5,proliferation,migration
                Data availability:
                Keywords: gastric cancer, microrna-539, sry-box 5, proliferation, migration

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