A Loss of Smad2 dependent TGF-beta signaling correlates with poor differentiation in gastric cancer

Hao-Cheng Weng(University Medical Centre Mannheim), Yalan Wu(Zhejiang University), Q Li(University Medical Centre Mannheim), Jun Yu(Zhejiang University), Yang Mu(Zhejiang University), Y Liu(Heidelberg University), Chunhua Xu(Zhejiang University), Zheyu Shen(Zhejiang University), Y Li(Zhejiang University), Matthias Ebert(Heidelberg University), S Dooley(Heidelberg University)
Zeitschrift für Gastroenterologie
August 1, 2011
10.1055/s-0031-1285287
Cited by 0

Abstract

Background: TGF-beta plays dual roles in progression of human cancer. In precancerous stages, TGF-beta acts as tumor suppressor by providing cytostatic downstream signaling, whereas in late cancer stages, it induces processes that support tumor progression, including stroma fibroblast activation, epithelial mesenchymal transition and metastasis. Due to the high complexity of the TGF-beta signaling pathway, molecular details of this dramatic functional switch are only poorly understood. Recently, a shift from Smad2/3 C-terminal to linker site phosphorylation was hypothesized as key event for the cancer facilitating outcome of TGF-beta in colorectal and hepatocellular carcinoma. In the present study, we investigated this assumption in gastric adenocarcinoma.

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