2.50
Hdl Handle:
http://hdl.handle.net/10033/346988
Title:
Dysregulated serum response factor triggers formation of hepatocellular carcinoma.
Authors:
Ohrnberger, Stefan; Thavamani, Abhishek; Braeuning, Albert; Lipka, Daniel B; Kirilov, Milen; Geffers, Robert ( 0000-0003-4409-016X ) ; Authenrieth, Stella E; Römer, Michael; Zell, Andreas; Bonin, Michael; Schwarz, Michael; Schütz, Günther; Schirmacher, Peter; Plass, Christoph; Longerich, Thomas; Nordheim, Alfred
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.
Affiliation:
Helmholtz Centre for infection research, Inhoffenstr. 7., 38124 Braunschweig, Germany.
Citation:
Dysregulated serum response factor triggers formation of hepatocellular carcinoma. 2015, 61 (3):979-89 Hepatology
Journal:
Hepatology (Baltimore, Md.)
Issue Date:
Mar-2015
URI:
http://hdl.handle.net/10033/346988
DOI:
10.1002/hep.27539
PubMed ID:
25266280
Type:
Article
Language:
en
ISSN:
1527-3350
Appears in Collections:
publications of the research group genomeanalytics (GMAK)

Full metadata record

DC FieldValue Language
dc.contributor.authorOhrnberger, Stefanen
dc.contributor.authorThavamani, Abhisheken
dc.contributor.authorBraeuning, Alberten
dc.contributor.authorLipka, Daniel Ben
dc.contributor.authorKirilov, Milenen
dc.contributor.authorGeffers, Roberten
dc.contributor.authorAuthenrieth, Stella Een
dc.contributor.authorRömer, Michaelen
dc.contributor.authorZell, Andreasen
dc.contributor.authorBonin, Michaelen
dc.contributor.authorSchwarz, Michaelen
dc.contributor.authorSchütz, Güntheren
dc.contributor.authorSchirmacher, Peteren
dc.contributor.authorPlass, Christophen
dc.contributor.authorLongerich, Thomasen
dc.contributor.authorNordheim, Alfreden
dc.date.accessioned2015-03-23T13:31:18Zen
dc.date.available2015-03-23T13:31:18Zen
dc.date.issued2015-03en
dc.identifier.citationDysregulated serum response factor triggers formation of hepatocellular carcinoma. 2015, 61 (3):979-89 Hepatologyen
dc.identifier.issn1527-3350en
dc.identifier.pmid25266280en
dc.identifier.doi10.1002/hep.27539en
dc.identifier.urihttp://hdl.handle.net/10033/346988en
dc.description.abstractThe 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.en
dc.language.isoenen
dc.titleDysregulated serum response factor triggers formation of hepatocellular carcinoma.en
dc.typeArticleen
dc.contributor.departmentHelmholtz Centre for infection research, Inhoffenstr. 7., 38124 Braunschweig, Germany.en
dc.identifier.journalHepatology (Baltimore, Md.)en

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