TY  - JOUR
AU  - Feng, Teng
AU  - Dzieran, Johanna
AU  - Gu, Xing
AU  - Marhenke, Silke
AU  - Vogel, Arndt
AU  - Machida, Keigo
AU  - Weiss, Thomas S
AU  - Ruemmele, Petra
AU  - Kollmar, Otto
AU  - Hoffmann, Patrick
AU  - Grässer, Friedrich
AU  - Allgayer, Heike
AU  - Fabian, Jasmin
AU  - Weng, Hong Lei
AU  - Teufel, Andreas
AU  - Maass, Thorsten
AU  - Meyer, Christoph
AU  - Lehmann, Ulrich
AU  - Zhu, Cheng
AU  - Mertens, Peter R
AU  - Gao, Chun Fang
AU  - Dooley, Steven
AU  - Meindl-Beinker, Nadja M
TI  - Smad7 regulates compensatory hepatocyte proliferation in damaged mouse liver and positively relates to better clinical outcome in human hepatocellular carcinoma.
JO  - Clinical science
VL  - 128
IS  - 11
SN  - 1470-8736
CY  - London
PB  - Portland
M1  - DKFZ-2017-02532
SP  - 761 - 774
PY  - 2015
AB  - 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
KW  - Smad7 Protein (NLM Chemicals)
KW  - Transforming Growth Factor beta (NLM Chemicals)
KW  - Y-Box-Binding Protein 1 (NLM Chemicals)
KW  - YBX1 protein, human (NLM Chemicals)
LB  - PUB:(DE-HGF)16
C6  - pmid:25602745
DO  - DOI:10.1042/CS20140606
UR  - https://inrepo02.dkfz.de/record/126504
ER  -