scholarly journals Role of Hepatocyte‐Derived Osteopontin in Liver Carcinogenesis

2021 ◽  
Author(s):  
Romain Desert ◽  
Xiaodong Ge ◽  
Zhuolun Song ◽  
Hui Han ◽  
Daniel Lantvit ◽  
...  
Keyword(s):  
2010 ◽  
Vol 88 (2) ◽  
pp. 234-237 ◽  
Author(s):  
M.L. Martinez-Chantar ◽  
S.C. Lu ◽  
J.M. Mato ◽  
Z. Luka ◽  
C. Wagner ◽  
...  

2016 ◽  
Vol 37 (6) ◽  
pp. 541-546 ◽  
Author(s):  
Michael Karin ◽  
Debanjan Dhar
Keyword(s):  

1988 ◽  
Vol 42 (5) ◽  
pp. 803-806 ◽  
Author(s):  
F. S. Liotti ◽  
A. R. Menghini ◽  
P. Guerrieri ◽  
G. Mariucci ◽  
P. Locci ◽  
...  

2012 ◽  
Vol 48 ◽  
pp. S165
Author(s):  
A. Bopp ◽  
F. Wartlick ◽  
M. Schwarz ◽  
G. Fritz
Keyword(s):  

2020 ◽  
Vol 126 ◽  
pp. 110064 ◽  
Author(s):  
Nariman K. Badr El-Din ◽  
Doaa A. Ali ◽  
Reem Othman ◽  
Samuel W. French ◽  
Mamdooh Ghoneum

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-9 ◽  
Author(s):  
Howard P. Glauert ◽  
Karen Calfee-Mason ◽  
Yixin Li ◽  
Vani Nilakantan ◽  
Michelle L. Twaroski ◽  
...  

In this review, the role of NF-κB in the induction of hepatocarcinogenesis by peroxisome proliferators is examined. The administration of peroxisome proliferators for more than a three-day period leads to the activation of NF-κB in the livers of rats and mice. On the other hand, peroxisome proliferator activated receptor-α(PPARα) activation in non-hepatic tissues can lead to the inhibition of NF-κB activation. Several lines of evidence support the hypothesis that the activation of NF-κB by peroxisome proliferators in the liver is mediated by oxidative stress. The role of NF-κB in peroxisome proliferator-induced hepatocarcinogenesis has been examined using NF-κB knockout models. Specifically, the induction of cell proliferation and the promotion of liver carcinogenesis are inhibited in mice lacking the p50 subunit of NF-κB. Overall, the activation of NF-κB appears to be important in the carcinogenic activity of peroxisome proliferators.


2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Bo Shen ◽  
Aimin Li ◽  
Yu-Jui Yvonne Wan ◽  
Guijia Shen ◽  
Jinshui Zhu ◽  
...  

Objective. The present study examined the role of PPARβ/δ in hepatocellular carcinoma (HCC). Methods. The effect of PPARβ/δ on HCC development was analyzed using PPARβ/δ-overexpressed liver cancer cells and PPARβ/δ-knockout mouse models. Results. PPARβ/δ(-/-) mice were susceptible to diethylnitrosamine- (DEN-) induced HCC (87.5% vs. 37.5%, p<0.05). In addition, PPARβ/δ-overexpressed HepG2 cells had reduced proliferation, migration, and invasion capabilities accompanied by increased apoptosis and cell cycle arrest at the G0/G1 phase. Moreover, differential gene expression profiling uncovered that the levels of serine/threonine-protein kinase (SGK-1) mRNA and its encoded protein were reduced in PPARβ/δ-overexpressed HepG2 cells. Consistently, elevated SGK-1 levels were found in PPARβ/δ(-/-) mouse livers as well as PPARβ/δ-knockdown human SMMC-7721 HCC cells. Chromatin immunoprecipitation (ChIP) assays followed by real-time quantitative polymerase chain reaction (qPCR) assays further revealed the binding of PPARβ/δ to the SGK-1 regulatory region in HepG2 cells. Conclusions. Due to the known tumor-promoting effect of SGK1, the present data suggest that PPARβ/δ-deactivated SGK1 is a novel pathway for inhibiting liver carcinogenesis.


Author(s):  
Yoichi Konishi ◽  
Seiichi Takahashi ◽  
Takeo Ohnishi ◽  
Ayumi Denda ◽  
Shuji Mikami ◽  
...  

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