Delphinidin inhibits epidermal growth factor‐induced epithelial‐to‐mesenchymal transition in hepatocellular carcinoma cells

2018 ◽  
Vol 120 (6) ◽  
pp. 9887-9899 ◽  
Author(s):  
Won‐Chul Lim ◽  
Hyunhee Kim ◽  
Hyeonseok Ko
Keyword(s):  
Hepatocellular Carcinoma ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Epithelial To Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Hepatocellular Carcinoma Cells ◽  
Mesenchymal Transition ◽  
Epidermal Growth

Epidermal growth factor induces tumour marker AKR1B10 expression through activator protein-1 signalling in hepatocellular carcinoma cells

2012 ◽  
Vol 442 (2) ◽  
pp. 273-282 ◽  
Author(s):  
Ziwen Liu ◽  
Ruilan Yan ◽  
Ahmed Al-Salman ◽  
Yi Shen ◽  
Yiwen Bu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Hepg2 Cells ◽  
Promoter Activity ◽  
Tumour Marker ◽  
Carcinoma Cells ◽  
Activator Protein 1 ◽  
Hepatocellular Carcinoma Cells ◽  
Epidermal Growth

AKR1B10 (aldo-keto reductase 1B10) is overexpressed in liver and lung cancer, and plays a critical role in tumour development and progression through promoting lipogenesis and eliminating cytotoxic carbonyls. AKR1B10 is a secretory protein and potential tumour marker; however, little is known about the regulatory mechanism of AKR1B10 expression. The present study showed that AKR1B10 is induced by mitogen EGF (epidermal growth factor) and insulin through the AP-1 (activator protein-1) signalling pathway. In human HCC (hepatocellular carcinoma) cells (HepG2 and Hep3B), EGF (50 ng/ml) and insulin (10 nM) stimulated endogenous AKR1B10 expression and promoter activity. In the AKR1B10 promoter, a putative AP-1 element was found at bp −222 to −212. Deletion or mutation of this AP-1 element abrogated the basal promoter activity and response to EGF and AP-1 proteins. This AP-1 element bound to nuclear proteins extracted from HepG2 cells, and this binding was stimulated by EGF and insulin in a dose-dependent manner. Chromatin immunoprecipitation showed that the AP-1 proteins c-Fos and c-Jun were the predominant factors bound to the AP-1 consensus sequence, followed by JunD and then JunB. The same order was followed in the stimulation of endogenous AKR1B10 expression by AP-1 proteins. Furthermore, c-Fos shRNA (short hairpin RNA) and AP-1 inhibitors/antagonists (U0126 and Tanshinone IIA) inhibited endogenous AKR1B10 expression and promoter activity in HepG2 cells cultured in vitro or inoculated subcutaneously in nude mice. U0126 also inhibited AKR1B10 expression induced by EGF. Taken together, these results suggest that AKR1B10 is up-regulated by EGF and insulin through AP-1 mitogenic signalling and may be implicated in hepatocarcinogenesis.

Epidermal growth factor receptor and HER-3 restrict cell response to sorafenib in hepatocellular carcinoma cells

2012 ◽  
Vol 57 (1) ◽  
pp. 108-115 ◽  
Author(s):  
Marie-José Blivet-Van Eggelpoël ◽  
Hamza Chettouh ◽  
Laetitia Fartoux ◽  
Lynda Aoudjehane ◽  
Véronique Barbu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cell Response ◽  
Growth Factor Receptor ◽  
Carcinoma Cells ◽  
Hepatocellular Carcinoma Cells ◽  
Epidermal Growth
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