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Forkhead Box S1 Inhibits the Progression of Hepatocellular Carcinoma
INTRODUCTION: Forkhead box (FOX) superfamily members were recently shown to play important roles in tumor development and progression. Forkhead box S1 (FOXS1), a member of the FOX family, has been reported to be closely associated with malignant neoplasms. However, its expression and effect on hepat...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7680191/ https://www.ncbi.nlm.nih.gov/pubmed/33235470 http://dx.doi.org/10.2147/OTT.S272596 |
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author | Lei, Dengliang Hu, Gangli Chen, Yue Hao, Tuantuan Gao, Yu Luo, Fang |
author_facet | Lei, Dengliang Hu, Gangli Chen, Yue Hao, Tuantuan Gao, Yu Luo, Fang |
author_sort | Lei, Dengliang |
collection | PubMed |
description | INTRODUCTION: Forkhead box (FOX) superfamily members were recently shown to play important roles in tumor development and progression. Forkhead box S1 (FOXS1), a member of the FOX family, has been reported to be closely associated with malignant neoplasms. However, its expression and effect on hepatocellular carcinoma remain unclear. The aim of this study was to determine the expression and role of FOXS1 in hepatocellular carcinoma (HCC). METHODS: Real-time PCR, Western blot and immunohistochemistry assays were carried out to determine FOXS1 expression in HCC tissues and cells. The biological roles of FOXS1 in HCC were investigated using CCK-8, colony formation, transwell and wound healing. Additionally, the effect of FOXS1 on epithelial–mesenchymal transition (EMT) was investigated by Western blotting. Xenograft model was carried out to evaluate the effect of FOXS1 in vivo. RESULTS: In our study, we confirmed lower FOXS1 expression in HCC samples than in normal liver tissues by performing Western blotting, immunohistochemistry and real-time PCR assays. In addition, FOXS1 expression is strongly associated with the prognosis of patients with HCC. Overexpression of FOXS1 suppressed cell proliferation, colony formation, the epithelial–mesenchymal transition (EMT) and the hedgehog (Hh) signaling pathway in vitro and in vivo. SAG, an activator of Hh signaling, partially reversed the effect of FOXS1 overexpression on HCC cells. CONCLUSION: FOXS1 might suppress HCC cell proliferation, colony formation, and EMT by inhibiting the Hh signaling pathway, indicating that FOXS1 may be a promising biological target in HCC. |
format | Online Article Text |
id | pubmed-7680191 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-76801912020-11-23 Forkhead Box S1 Inhibits the Progression of Hepatocellular Carcinoma Lei, Dengliang Hu, Gangli Chen, Yue Hao, Tuantuan Gao, Yu Luo, Fang Onco Targets Ther Original Research INTRODUCTION: Forkhead box (FOX) superfamily members were recently shown to play important roles in tumor development and progression. Forkhead box S1 (FOXS1), a member of the FOX family, has been reported to be closely associated with malignant neoplasms. However, its expression and effect on hepatocellular carcinoma remain unclear. The aim of this study was to determine the expression and role of FOXS1 in hepatocellular carcinoma (HCC). METHODS: Real-time PCR, Western blot and immunohistochemistry assays were carried out to determine FOXS1 expression in HCC tissues and cells. The biological roles of FOXS1 in HCC were investigated using CCK-8, colony formation, transwell and wound healing. Additionally, the effect of FOXS1 on epithelial–mesenchymal transition (EMT) was investigated by Western blotting. Xenograft model was carried out to evaluate the effect of FOXS1 in vivo. RESULTS: In our study, we confirmed lower FOXS1 expression in HCC samples than in normal liver tissues by performing Western blotting, immunohistochemistry and real-time PCR assays. In addition, FOXS1 expression is strongly associated with the prognosis of patients with HCC. Overexpression of FOXS1 suppressed cell proliferation, colony formation, the epithelial–mesenchymal transition (EMT) and the hedgehog (Hh) signaling pathway in vitro and in vivo. SAG, an activator of Hh signaling, partially reversed the effect of FOXS1 overexpression on HCC cells. CONCLUSION: FOXS1 might suppress HCC cell proliferation, colony formation, and EMT by inhibiting the Hh signaling pathway, indicating that FOXS1 may be a promising biological target in HCC. Dove 2020-11-17 /pmc/articles/PMC7680191/ /pubmed/33235470 http://dx.doi.org/10.2147/OTT.S272596 Text en © 2020 Lei et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Lei, Dengliang Hu, Gangli Chen, Yue Hao, Tuantuan Gao, Yu Luo, Fang Forkhead Box S1 Inhibits the Progression of Hepatocellular Carcinoma |
title | Forkhead Box S1 Inhibits the Progression of Hepatocellular Carcinoma |
title_full | Forkhead Box S1 Inhibits the Progression of Hepatocellular Carcinoma |
title_fullStr | Forkhead Box S1 Inhibits the Progression of Hepatocellular Carcinoma |
title_full_unstemmed | Forkhead Box S1 Inhibits the Progression of Hepatocellular Carcinoma |
title_short | Forkhead Box S1 Inhibits the Progression of Hepatocellular Carcinoma |
title_sort | forkhead box s1 inhibits the progression of hepatocellular carcinoma |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7680191/ https://www.ncbi.nlm.nih.gov/pubmed/33235470 http://dx.doi.org/10.2147/OTT.S272596 |
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