%0 Journal Article
%A Feng, Teng
%A Dzieran, Johanna
%A Gu, Xing
%A Marhenke, Silke
%A Vogel, Arndt
%A Machida, Keigo
%A Weiss, Thomas S
%A Ruemmele, Petra
%A Kollmar, Otto
%A Hoffmann, Patrick
%A Grässer, Friedrich
%A Allgayer, Heike
%A Fabian, Jasmin
%A Weng, Hong Lei
%A Teufel, Andreas
%A Maass, Thorsten
%A Meyer, Christoph
%A Lehmann, Ulrich
%A Zhu, Cheng
%A Mertens, Peter R
%A Gao, Chun Fang
%A Dooley, Steven
%A Meindl-Beinker, Nadja M
%T Smad7 regulates compensatory hepatocyte proliferation in damaged mouse liver and positively relates to better clinical outcome in human hepatocellular carcinoma.
%J Clinical science
%V 128
%N 11
%@ 1470-8736
%C London
%I Portland
%M DKFZ-2017-02532
%P 761 - 774
%D 2015
%X Transforming growth factor β (TGF-β) is cytostatic towards damage-induced compensatory hepatocyte proliferation. This function is frequently lost during hepatocarcinogenesis, thereby switching the TGF-β role from tumour suppressor to tumour promoter. In the present study, we investigate Smad7 overexpression as a pathophysiological mechanism for cytostatic TGF-β inhibition in liver damage and hepatocellular carcinoma (HCC). Transgenic hepatocyte-specific Smad7 overexpression in damaged liver of fumarylacetoacetate hydrolase (FAH)-deficient mice increased compensatory proliferation of hepatocytes. Similarly, modulation of Smad7 expression changed the sensitivity of Huh7, FLC-4, HLE and HLF HCC cell lines for cytostatic TGF-β effects. In our cohort of 140 HCC patients, Smad7 transcripts were elevated in 41.4
%K Smad7 Protein (NLM Chemicals)
%K Transforming Growth Factor beta (NLM Chemicals)
%K Y-Box-Binding Protein 1 (NLM Chemicals)
%K YBX1 protein, human (NLM Chemicals)
%F PUB:(DE-HGF)16
%9 Journal Article
%$ pmid:25602745
%R 10.1042/CS20140606
%U https://inrepo02.dkfz.de/record/126504