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      RUNX3 regulates hepatocellular carcinoma cell metastasis via targeting miR-186/E-cadherin/EMT pathway

      research-article
      Author(s): 1 , 2 , 3 , 4
      Publication date (Electronic):
      Journal: Oncotarget
      Publisher: Impact Journals LLC
      Keywords: RUNX3, miR-186, E-cadherin, HCC

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          Abstract

          Runt-related transcription factor 3 (RUNX3) has been reported as a tumor suppressor in some kinds of cancers. In the present study, hepatocellular carcinoma (HCC) microarray analysis showed that RUNX3 expression was significantly lower in HCC tissues compared with that in adjacent non-tumor tissues, and was negatively associated with metastasis and TNM stage. RUNX3 was an independently prognostic factor for 5-year overall and disease-free patient survival. Mechanically, RUNX3 repressed metastasis and invasion of HCC, and increased E-cadherin expression. RUNX3 also repressed microRNA-186 to increase E-cadherin expression. We demonstrated that miR-186 mimics attenuated RUNX3-induced increase of E-cadherin and inhibition of metastasis and invasion. In conclusion, RUNX3 suppressed HCC cell migration and invasion by targeting the miR-186/E-cadherin/EMT pathway. RUNX3 may be recommended as an effective prognostic indicator and therapeutic target for patients with HCC.

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          Causal relationship between the loss of RUNX3 expression and gastric cancer.

          Qing-Lin Li, Kosei Ito, Chohei Sakakura … (2002)
          Runx3/Pebp2alphaC null mouse gastric mucosa exhibits hyperplasias due to stimulated proliferation and suppressed apoptosis in epithelial cells, and the cells are resistant to growth-inhibitory and apoptosis-inducing action of TGF-beta, indicating that Runx3 is a major growth regulator of gastric epithelial cells. Between 45% and 60% of human gastric cancer cells do not significantly express RUNX3 due to hemizygous deletion and hypermethylation of the RUNX3 promoter region. Tumorigenicity of human gastric cancer cell lines in nude mice was inversely related to their level of RUNX3 expression, and a mutation (R122C) occurring within the conserved Runt domain abolished the tumor-suppressive effect of RUNX3, suggesting that a lack of RUNX3 function is causally related to the genesis and progression of human gastric cancer.
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            Twist overexpression correlates with hepatocellular carcinoma metastasis through induction of epithelial-mesenchymal transition.

            Hong-Hui Wang, William Kwok, Anthony Yuen … (2006)
            Hepatocellular carcinoma (HCC) is a rapidly growing tumor associated with a high propensity for vascular invasion and metastasis. Epithelial-mesenchymal transition (EMT) is a key event in the tumor invasion process. Recently, Twist has been identified to play an important role in EMT-mediated metastasis through the regulation of E-cadherin expression. However, the actual role of Twist in tumor invasiveness remains unclear. The purpose of this study is to investigate the expression and possible role of Twist in HCC. We evaluated Twist and E-cadherin expression in HCC tissue microarray of paired primary and metastatic HCC by immunohistochemical staining. The role of Twist in EMT-mediated invasiveness was also evaluated in vitro in HCC cell lines. We first showed that overexpression of Twist was correlated with HCC metastasis (P=0.001) and its expression was negatively correlated with E-cadherin expression (P=0.001, r=-0.443) by tissue microarray. A significant increase of Twist at the mRNA level was also found in metastatic HCC cell lines MHCC-97H, MHCC-97L, and H2M when compared with nonmetastatic Huh-7, H2P, and PLC cell lines. The MHCC-97H cell line, which has a higher metastatic ability, was found to have a higher level of Twist than MHCC-97L. Accompanied with increased Twist expression in the metastatic HCC cell lines when compared with the nonmetastatic primary ones, we found decreased E-cadherin mRNA expression in the metastatic HCC cell lines. By ectopic transfection of Twist into PLC cells, Twist was able to suppress E-cadherin expression and induce EMT changes, which was correlated with increased HCC cell invasiveness. This study shows that Twist overexpression was correlated with HCC metastasis through induction of EMT changes and HCC cell invasiveness.
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              PEBP2/PEA2 represents a family of transcription factors homologous to the products of the Drosophila runt gene and the human AML1 gene.

              Y. J. Lu, K Shigesada, H Kagoshima … (1993)
              cDNAs representing the alpha subunit of polyomavirus enhancer binding protein 2 (PEBP2; also called PEA2) were isolated. The products of the cDNAs are highly homologous to that of Drosophila segmentation gene runt (run) for an N-proximal 128-amino acid region showing 66% identity. The run homology region encompasses the domain capable of binding to a specific nucleotide sequence motif and of dimerizing with the companion beta subunit. The human AML1 gene related to t(8;21) acute myeloid leukemia also had a run homology region. Together with the beta subunit, which increases the affinity of the alpha subunit to DNA without binding to DNA by itself, PEBP2 represents a newly discovered family of transcription factor. The major species of PEBP2 alpha mRNA was expressed in T-cell lines but not in B-cell lines tested. Evidence indicated that PEBP2 functions as a transcriptional activator and is involved in regulation of T-cell-specific gene expression.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Oncotarget
                Journal ID (iso-abbrev): Oncotarget
                Journal ID (publisher-id): Oncotarget
                Journal ID (publisher-id): ImpactJ
                Title: Oncotarget
                Publisher: Impact Journals LLC
                ISSN (Electronic): 1949-2553
                Publication date Collection: 22 September 2017
                Publication date (Electronic): 9 June 2017
                Volume: 8
                Issue: 37
                Pages: 61475-61486
                Affiliations
                1 Department of Hepatobiliary Surgery, The Second Affiliated Hospital of Dalian Medical University, Dalian 116027, Liaoning, China
                2 Department of Radiology, The Second Affiliated Hospital of Dalian Medical University, Dalian 116027, Liaoning, China
                3 Department of Interventional Therapy, The Second Affiliated Hospital of Dalian Medical University, Dalian 116027, Liaoning, China
                4 Department of Ophthalmology, The Second Affiliated Hospital of Dalian Medical University, Dalian 116027, Liaoning, China
                Author notes
                Correspondence to: Liang Zhang, zhangliangdlmu@ 123456163.com
                [*]

                These authors have contributed equally to this work as the co-first authors

                Article
                Publisher ID: 18424
                DOI: 10.18632/oncotarget.18424
                PMC ID: 5617438
                PubMed ID: 28977878
                SO-VID: efa0beb0-678e-4aac-8fd9-f3da1ac9df96
                Copyright © Copyright: © 2017 Gou et al.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date received : 4 May 2017
                Date accepted : 23 May 2017
                Categories
                Subject: Research Paper

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: runx3,mir-186,e-cadherin,hcc
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: runx3, mir-186, e-cadherin, hcc

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