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      Correction to: Forkhead box (FOX) G1 promotes hepatocellular carcinoma epithelial-Mesenchymal transition by activating Wnt signal through forming T-cell factor-4/Betacatenin/FOXG1 complex

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          Abstract

          Correction to: J Exp Clin Cancer Res 38, 475 (2019) https://doi.org/10.1186/s13046-019-1433-3 Following publication of the original article [1], the authors identified some minor errors in image-typesetting in Fig. 2; specifically in Fig. 2e. The corrected figure is given below. The correction does not have any effect on the results or conclusions of the paper. Fig. 2 Overexpression of FOXG1 promotes cell mobility and invasion by inducing epithelial-mesenchymal transition (EMT). a Western blotting analysis and b Immunofluorescence analysis of expression of epithelial cell markers (E-cadherin and α-catenin) and mesenchymal cell markers (vimentin and fibronectin) in indicated cells transfected with FOXG1 expression vector or control vector. Nuclei counterstained with DAPI. GAPDH was used as a loading control. c Representative migrating images of the indicated Huh7 and PLC/PRF5y cells on uncoated Transwell devices in five random fields. d Quantification of the invading cells of the indicated Huh7 and PLC/PRF5y cells on Matrigel-coated Transwell devices in five random fields. Values represent mean ± SD. *P < 0.05. e Representative micrographs of wound healing assay of the indicated Huh7 and PLC/ PRF5y cells. Wound closures were photographed at 0, 24, and 36 h after wounding. All experiments were repeated at least three times with similar results

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          Forkhead box (FOX) G1 promotes hepatocellular carcinoma epithelial-Mesenchymal transition by activating Wnt signal through forming T-cell factor-4/Beta-catenin/FOXG1 complex

          Background Forkhead box G1 (FOXG1) is a member of the Fox transcription factor family involved in regulation of many cancers. However, the role of FOXG1 in hepatocellular carcinogenesisis largely unclear. The present study aimed at examining the biological function and underlying mechanism of FOXG1 on hepatocellular carcinoma (HCC) tumor metastasis as well as its clinical significance. Methods Levels of FOXG1 were determined by immunohistochemical and real-time PCR analysis in HCC cell lines and human HCC samples. The effect of FOXG1 on cancer cell invasion and metastasis was investigated in vitro and in vivo in either FOXG1-silenced or overexpressing human HCC cell lines. Immunoprecipitation and chromatin immunoprecipitation assays were performed to investigate the interaction of FOXG1, β-catenin, TCF4 and the effect on Wnt target-gene promoters. Results In human HCC, the level of FOXG1 progressively increased from surrounding non tumorous livers to HCC, reaching the highest levels in metastatic HCC. Furthermore, expression levels of FOXG1 directly correlated with cancer cell epithelial-mesenchymal transition (EMT) phenotype. In FOXG1-overexpressing cells, FOXG1 promotes the stabilization and nuclear accumulation of β-catenin by directly binding to β-catenin and it associates with the lymphoid enhancer factor/T cell factor proteins (LEF/TCFs) on Wnt responsive enhancers (WREs) in chromatin. Conclusions The results show that FOXG1 plays a key role in mediating cancer cell metastasis through the Wnt/β-catenin pathway in HCC cells and predicts HCC prognosis after surgery. Targeting FOXG1 may provide a new approach for therapeutic treatment in the future.
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            Author and article information

            Contributors
            pzp33@hotmail.com
            happyxiechan@hotmail.com
            Journal
            J Exp Clin Cancer Res
            J Exp Clin Cancer Res
            Journal of Experimental & Clinical Cancer Research : CR
            BioMed Central (London )
            0392-9078
            1756-9966
            17 March 2021
            17 March 2021
            2021
            : 40
            : 104
            Affiliations
            [1 ]GRID grid.412558.f, ISNI 0000 0004 1762 1794, Department of Infectious Diseases, , the Third Affiliated Hospital of Sun Yat-sen University, ; 600# Tianhe Road, Guangzhou, 510630 Guangdong Province China
            [2 ]GRID grid.12981.33, ISNI 0000 0001 2360 039X, Key Laboratory of Tropical Disease Control, Ministry of Education, , Sun Yat-sen University, ; Guangzhou, 510630 Guangdong Province China
            [3 ]GRID grid.484195.5, Guangdong Provincial Key Laboratory of Liver Disease, ; Guangzhou, China
            Author information
            http://orcid.org/0000-0002-0225-5483
            Article
            1900
            10.1186/s13046-021-01900-2
            7972186
            33731126
            8ff05728-8257-4cc9-bb03-401cb6d10650
            © The Author(s) 2021

            Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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            Oncology & Radiotherapy
            Oncology & Radiotherapy

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