Journal
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
Volume 35, Issue 4, Pages 1623-1632Publisher
KARGER
DOI: 10.1159/000373976
Keywords
HCC; TGF-beta; Treg cells
Categories
Funding
- National Natural Foundation of China [81172020, 81372262, 81472284]
- Shanghai 'Phosphor' Science Foundation of China [12QA1404800]
- Shanghai Program for Excellent Talents in Health System [XYQ2011033]
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Background/Aims: TGF-beta plays a key role in the progression of various tumors. The main objective of our study was to investigate whether TGF-beta is a ble to regulate N-nitrosodiethylamine (DEN)-induced hepatocellular carcinoma (HCC) progression in a mouse model by inducing Treg cell polarization. Methods: HCC progression, TGF-p and Foxp3 expression levels, serum TGF-beta, IL10 and GP73 levels as well as percentage of Treg cells were analyzed in healthy, HCC and HCC+SM-16 mouse groups. The effect of TGF-beta on Treg cell polarization in vitro was measured by flow cytometric analysis. The expression of TGF-beta and IL10 was identified by IHC in HCC patients and the correlation between TGF-beta and IL10 was also assessed. Results: TGF-beta expression is up-regulated in a DEN-induced HCC mouse model. TGF-beta can promote the differentiation of Foxp3(+)CD4(+) T cells (Treg cells) in vitro. However, blocking the TGF-beta pathway with a specific TGF-beta receptor inhibitor, SM-16, reduced HCC progression and the percentage of Treg cells in liver tissue. The correlation between TGF-beta and Treg cells was also confirmed in HCC patients and the expression of both TGF-beta and IL-10 was shown to be associated with HCC progression. Conclusion: TGF-beta is necessary for HCC progression, acting by inducing Treg cell polarization. Copyright (C) 2015 S. Karger AG, Basel
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