Dysregulated serum response factor triggers formation of hepatocellular carcinoma.
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Authors
Ohrnberger, StefanThavamani, Abhishek
Braeuning, Albert
Lipka, Daniel B
Kirilov, Milen
Geffers, Robert

Authenrieth, Stella E
Römer, Michael
Zell, Andreas
Bonin, Michael
Schwarz, Michael
Schütz, Günther
Schirmacher, Peter
Plass, Christoph
Longerich, Thomas
Nordheim, Alfred
Issue Date
2015-03
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Show full item recordAbstract
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 HepatologyAffiliation
Helmholtz Centre for infection research, Inhoffenstr. 7., 38124 Braunschweig, Germany.Journal
Hepatology (Baltimore, Md.)PubMed ID
25266280Type
ArticleLanguage
enISSN
1527-3350ae974a485f413a2113503eed53cd6c53
10.1002/hep.27539
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