Dysregulated serum response factor triggers formation of hepatocellular carcinoma.
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Lipka, Daniel B
Authenrieth, Stella E
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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.
CitationDysregulated serum response factor triggers formation of hepatocellular carcinoma. 2015, 61 (3):979-89 Hepatology
AffiliationHelmholtz Centre for infection research, Inhoffenstr. 7., 38124 Braunschweig, Germany.
JournalHepatology (Baltimore, Md.)
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