Integrin-linked kinase overexpression and its oncogenic role in promoting tumorigenicity of hepatocellular carcinoma.

<h4>Background</h4>Integrin-linked kinase (ILK) was first discovered as an integrin β1-subunit binding protein. It localizes at the focal adhesions and is involved in cytoskeleton remodeling. ILK overexpression and its dysregulated signaling cascades have been reported in many human canc...

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Autores principales:	Jenny Chan, Frankie Chi Fat Ko, Yin-Shan Yeung, Irene Oi-Lin Ng, Judy Wai Ping Yam
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2011
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/32fb391e30b64fe1a17cb0495dfcdd40
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spelling	oai:doaj.org-article:32fb391e30b64fe1a17cb0495dfcdd402021-11-18T06:59:03ZIntegrin-linked kinase overexpression and its oncogenic role in promoting tumorigenicity of hepatocellular carcinoma.1932-620310.1371/journal.pone.0016984https://doaj.org/article/32fb391e30b64fe1a17cb0495dfcdd402011-02-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21347395/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Integrin-linked kinase (ILK) was first discovered as an integrin β1-subunit binding protein. It localizes at the focal adhesions and is involved in cytoskeleton remodeling. ILK overexpression and its dysregulated signaling cascades have been reported in many human cancers. Aberrant expression of ILK influenced a wide range of signaling pathways and cellular functions. Although ILK has been well characterized in many malignancies, its role in hepatocellular carcinoma (HCC) is still largely unknown.<h4>Methodology/principal findings</h4>Quantitative PCR analysis was used to examine ILK mRNA expression in HCC clinical samples. It was shown that ILK was overexpressed in 36.9% (21/57) of HCC tissues when compared to the corresponding non-tumorous livers. The overall ILK expression level was significantly higher in tumorous tissues (P = 0.004), with a significant stepwise increase in expression level along tumor progression from tumor stage I to IV (P = 0.045). ILK knockdown stable clones were established in two HCC cell lines, BEL7402 and HLE, and were subjected to different functional assays. Knockdown of ILK significantly suppressed HCC cell growth, motility and invasion in vitro and inhibited tumorigenicity in vivo. Western blot analysis revealed a reduced phosphorylated-Akt (pAkt) at Serine-473 expression in ILK knockdown stable clones when compared to control clones.<h4>Conclusion/significance</h4>This study provides evidence about the clinical relevance of ILK in hepatocarcinogenesis. ILK was found to be progressively elevated along HCC progression. Here our findings also provide the first validation about the oncogenic capacity of ILK in vivo by suppressing its expression in HCC cells. The oncogenic role of ILK is implicated to be mediated by Akt pathway.Jenny ChanFrankie Chi Fat KoYin-Shan YeungIrene Oi-Lin NgJudy Wai Ping YamPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 2, p e16984 (2011)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Jenny Chan Frankie Chi Fat Ko Yin-Shan Yeung Irene Oi-Lin Ng Judy Wai Ping Yam Integrin-linked kinase overexpression and its oncogenic role in promoting tumorigenicity of hepatocellular carcinoma.
description	<h4>Background</h4>Integrin-linked kinase (ILK) was first discovered as an integrin β1-subunit binding protein. It localizes at the focal adhesions and is involved in cytoskeleton remodeling. ILK overexpression and its dysregulated signaling cascades have been reported in many human cancers. Aberrant expression of ILK influenced a wide range of signaling pathways and cellular functions. Although ILK has been well characterized in many malignancies, its role in hepatocellular carcinoma (HCC) is still largely unknown.<h4>Methodology/principal findings</h4>Quantitative PCR analysis was used to examine ILK mRNA expression in HCC clinical samples. It was shown that ILK was overexpressed in 36.9% (21/57) of HCC tissues when compared to the corresponding non-tumorous livers. The overall ILK expression level was significantly higher in tumorous tissues (P = 0.004), with a significant stepwise increase in expression level along tumor progression from tumor stage I to IV (P = 0.045). ILK knockdown stable clones were established in two HCC cell lines, BEL7402 and HLE, and were subjected to different functional assays. Knockdown of ILK significantly suppressed HCC cell growth, motility and invasion in vitro and inhibited tumorigenicity in vivo. Western blot analysis revealed a reduced phosphorylated-Akt (pAkt) at Serine-473 expression in ILK knockdown stable clones when compared to control clones.<h4>Conclusion/significance</h4>This study provides evidence about the clinical relevance of ILK in hepatocarcinogenesis. ILK was found to be progressively elevated along HCC progression. Here our findings also provide the first validation about the oncogenic capacity of ILK in vivo by suppressing its expression in HCC cells. The oncogenic role of ILK is implicated to be mediated by Akt pathway.
format	article
author	Jenny Chan Frankie Chi Fat Ko Yin-Shan Yeung Irene Oi-Lin Ng Judy Wai Ping Yam
author_facet	Jenny Chan Frankie Chi Fat Ko Yin-Shan Yeung Irene Oi-Lin Ng Judy Wai Ping Yam
author_sort	Jenny Chan
title	Integrin-linked kinase overexpression and its oncogenic role in promoting tumorigenicity of hepatocellular carcinoma.
title_short	Integrin-linked kinase overexpression and its oncogenic role in promoting tumorigenicity of hepatocellular carcinoma.
title_full	Integrin-linked kinase overexpression and its oncogenic role in promoting tumorigenicity of hepatocellular carcinoma.
title_fullStr	Integrin-linked kinase overexpression and its oncogenic role in promoting tumorigenicity of hepatocellular carcinoma.
title_full_unstemmed	Integrin-linked kinase overexpression and its oncogenic role in promoting tumorigenicity of hepatocellular carcinoma.
title_sort	integrin-linked kinase overexpression and its oncogenic role in promoting tumorigenicity of hepatocellular carcinoma.
publisher	Public Library of Science (PLoS)
publishDate	2011
url	https://doaj.org/article/32fb391e30b64fe1a17cb0495dfcdd40
work_keys_str_mv	AT jennychan integrinlinkedkinaseoverexpressionanditsoncogenicroleinpromotingtumorigenicityofhepatocellularcarcinoma AT frankiechifatko integrinlinkedkinaseoverexpressionanditsoncogenicroleinpromotingtumorigenicityofhepatocellularcarcinoma AT yinshanyeung integrinlinkedkinaseoverexpressionanditsoncogenicroleinpromotingtumorigenicityofhepatocellularcarcinoma AT ireneoilinng integrinlinkedkinaseoverexpressionanditsoncogenicroleinpromotingtumorigenicityofhepatocellularcarcinoma AT judywaipingyam integrinlinkedkinaseoverexpressionanditsoncogenicroleinpromotingtumorigenicityofhepatocellularcarcinoma
_version_	1718424093440606208

Integrin-linked kinase overexpression and its oncogenic role in promoting tumorigenicity of hepatocellular carcinoma.

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