Wilms’ tumor 1 gene modulates Fas-related death signals and anti-apoptotic functions in hepatocellular carcinoma View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2012-11-10

AUTHORS

Kazuhiro Uesugi, Yoichi Hiasa, Yoshio Tokumoto, Toshie Mashiba, Yohei Koizumi, Masashi Hirooka, Masanori Abe, Bunzo Matsuura, Morikazu Onji

ABSTRACT

BackgroundThe Wilms’ tumor 1 (WT1) gene is known to be overexpressed in hepatocellular carcinoma (HCC) and to upregulate tumor growth and oncogenic potential, although the detailed mechanisms remain to be elucidated.MethodsWe identified host genes involved in WT1 gene modulation of human liver cancer cell lines in vitro, and further characterized genes related to apoptosis. Moreover, we evaluated the alteration of genes by WT1 in 40 HCC and 58 non-HCC human liver samples collected at resection.ResultsAnalysis of the effect of small interfering RNAs-mediated knock-down of WT1 on apoptosis using an annexin V labeling assay, and on modulation of the activity of caspases-3, -8 and -9, indicated that WT1 has an anti-apoptotic role. We identified three apoptosis-related genes that were modulated by WT1; the cellular FLICE-inhibitory proteins (cFLIP) gene was upregulated, and Fas-associated death domain (FADD) and nuclear factor kappa B (NF-κB) were downregulated. Interestingly, knock-down of FADD or NF-κB resulted in the upregulation of WT1, and the expression of cFLIP changed in parallel with WT1 expression. We further evaluated WT1-mediated alteration of genes in HCC and non-HCC human liver samples. Both HCC and non-HCC tissues that expressed relatively high levels of WT1 showed cFLIP overexpression.ConclusionsWT1 modulates cFLIP, FADD and NF-κB, and has an anti-apoptotic role in HCC. This mechanism of action of WT1 could be related to the tumor growth and oncogenic potential of HCC. More... »

PAGES

1069-1080

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00535-012-0708-7

DOI

http://dx.doi.org/10.1007/s00535-012-0708-7

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1028109066

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/23142971


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