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Dysregulated serum response factor triggers formation of hepatocellular carcinoma.

Ohrnberger, Stefan
; 
Thavamani, Abhishek
; 
Braeuning, Albert
; 
Lipka, Daniel B
; 
Kirilov, Milen
; ; 
Authenrieth, Stella E
; 
Römer, Michael
; 
Zell, Andreas
; 
Bonin, Michael
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2015-03
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Abstract
The ubiquitously expressed transcriptional regulator serum response factor (SRF) is controlled by both Ras/MAPK (mitogen-activated protein kinase) and Rho/actin signaling pathways, which are frequently activated in hepatocellular carcinoma (HCC). We generated SRF-VP16(iHep) mice, which conditionally express constitutively active SRF-VP16 in hepatocytes, thereby controlling subsets of both Ras/MAPK- and Rho/actin-stimulated target genes. All SRF-VP16(iHep) mice develop hyperproliferative liver nodules that progresses to lethal HCC. Some murine (m)HCCs acquire Ctnnb1 mutations equivalent to those in human (h)HCC. The resulting transcript signatures mirror those of a distinct subgroup of hHCCs, with shared activation of oncofetal genes including Igf2, correlating with CpG hypomethylation at the imprinted Igf2/H19 locus.
Citation
Dysregulated serum response factor triggers formation of hepatocellular carcinoma. 2015, 61 (3):979-89 Hepatology
Affiliation
Helmholtz Centre for infection research, Inhoffenstr. 7., 38124 Braunschweig, Germany.
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Journal
Hepatology (Baltimore, Md.)
URI
http://hdl.handle.net/10033/346988
DOI
10.1002/hep.27539
PubMed ID
25266280
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Article
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en
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1527-3350
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publications of the research group genomeanalytics (GMAK)