Exploring stemness gene expression and vasculogenic mimicry capacity in well- and poorly-differentiated hepatocellular carcinoma cell lines

Vasculogenic mimicry (VM) is the phenomenon where cancer cells mimic endothelial cells by forming blood vessels. A stem cell-like phenotype has been proposed to be involved in this tumor plasticity. VM seems to correlate with metastasis rate, but there have been no reports on the effects of pro-meta...

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Main Authors: Kriengsak Lirdprapamongkol, Khajeelak Chiablaem, Monnipha Sila-Asna, Rudee Surarit, Ahnond Bunyaratvej, Jisnuson Svasti
Other Authors: Chulabhorn Research Institute
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Published: 2018
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Online Access:https://repository.li.mahidol.ac.th/handle/123456789/13701
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spelling th-mahidol.137012018-06-11T11:36:13Z Exploring stemness gene expression and vasculogenic mimicry capacity in well- and poorly-differentiated hepatocellular carcinoma cell lines Kriengsak Lirdprapamongkol Khajeelak Chiablaem Monnipha Sila-Asna Rudee Surarit Ahnond Bunyaratvej Jisnuson Svasti Chulabhorn Research Institute Mahidol University Biochemistry, Genetics and Molecular Biology Vasculogenic mimicry (VM) is the phenomenon where cancer cells mimic endothelial cells by forming blood vessels. A stem cell-like phenotype has been proposed to be involved in this tumor plasticity. VM seems to correlate with metastasis rate, but there have been no reports on the effects of pro-metastatic and pro-angiogenic factors or hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF) on VM formation of hepatocellular carcinoma (HCC) cells. Here, we determine VM capacity and expression of stemness genes (Oct4, Sox2, Nanog and CD133) in well- and poorly-differentiated HCC cell lines. The poorly-differentiated cell line SK-Hep-1 with mesenchymal features (high invasiveness and expressing Vimentin, with no E-cadherin) could form VM in vitro, while the well-differentiated cell line HepG2 did not form VM. There was no correlation between expression of stemness genes and intrinsic VM capacity. However, HGF but not VEGF, could induce VM formation in HepG2, concomitant with epithelial-mesenchymal transition (EMT), de-differentiation and increased expression of stemness genes. Our results show that the role of stemness genes in VM capacity of HCC cells is likely to depend on differentiation status. © 2012 Elsevier Inc. 2018-06-11T04:36:13Z 2018-06-11T04:36:13Z 2012-06-08 Article Biochemical and Biophysical Research Communications. Vol.422, No.3 (2012), 429-435 10.1016/j.bbrc.2012.05.009 10902104 0006291X 2-s2.0-84861944077 https://repository.li.mahidol.ac.th/handle/123456789/13701 Mahidol University SCOPUS https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84861944077&origin=inward
institution Mahidol University
building Mahidol University Library
continent Asia
country Thailand
Thailand
content_provider Mahidol University Library
collection Mahidol University Institutional Repository
topic Biochemistry, Genetics and Molecular Biology
spellingShingle Biochemistry, Genetics and Molecular Biology
Kriengsak Lirdprapamongkol
Khajeelak Chiablaem
Monnipha Sila-Asna
Rudee Surarit
Ahnond Bunyaratvej
Jisnuson Svasti
Exploring stemness gene expression and vasculogenic mimicry capacity in well- and poorly-differentiated hepatocellular carcinoma cell lines
description Vasculogenic mimicry (VM) is the phenomenon where cancer cells mimic endothelial cells by forming blood vessels. A stem cell-like phenotype has been proposed to be involved in this tumor plasticity. VM seems to correlate with metastasis rate, but there have been no reports on the effects of pro-metastatic and pro-angiogenic factors or hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF) on VM formation of hepatocellular carcinoma (HCC) cells. Here, we determine VM capacity and expression of stemness genes (Oct4, Sox2, Nanog and CD133) in well- and poorly-differentiated HCC cell lines. The poorly-differentiated cell line SK-Hep-1 with mesenchymal features (high invasiveness and expressing Vimentin, with no E-cadherin) could form VM in vitro, while the well-differentiated cell line HepG2 did not form VM. There was no correlation between expression of stemness genes and intrinsic VM capacity. However, HGF but not VEGF, could induce VM formation in HepG2, concomitant with epithelial-mesenchymal transition (EMT), de-differentiation and increased expression of stemness genes. Our results show that the role of stemness genes in VM capacity of HCC cells is likely to depend on differentiation status. © 2012 Elsevier Inc.
author2 Chulabhorn Research Institute
author_facet Chulabhorn Research Institute
Kriengsak Lirdprapamongkol
Khajeelak Chiablaem
Monnipha Sila-Asna
Rudee Surarit
Ahnond Bunyaratvej
Jisnuson Svasti
format Article
author Kriengsak Lirdprapamongkol
Khajeelak Chiablaem
Monnipha Sila-Asna
Rudee Surarit
Ahnond Bunyaratvej
Jisnuson Svasti
author_sort Kriengsak Lirdprapamongkol
title Exploring stemness gene expression and vasculogenic mimicry capacity in well- and poorly-differentiated hepatocellular carcinoma cell lines
title_short Exploring stemness gene expression and vasculogenic mimicry capacity in well- and poorly-differentiated hepatocellular carcinoma cell lines
title_full Exploring stemness gene expression and vasculogenic mimicry capacity in well- and poorly-differentiated hepatocellular carcinoma cell lines
title_fullStr Exploring stemness gene expression and vasculogenic mimicry capacity in well- and poorly-differentiated hepatocellular carcinoma cell lines
title_full_unstemmed Exploring stemness gene expression and vasculogenic mimicry capacity in well- and poorly-differentiated hepatocellular carcinoma cell lines
title_sort exploring stemness gene expression and vasculogenic mimicry capacity in well- and poorly-differentiated hepatocellular carcinoma cell lines
publishDate 2018
url https://repository.li.mahidol.ac.th/handle/123456789/13701
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