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2014 ; 7
(7
): 675-85
Nephropedia Template TP
gab.com Text
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English Wikipedia
Alcohol consumption promotes diethylnitrosamine-induced hepatocarcinogenesis in
male mice through activation of the Wnt/?-catenin signaling pathway
#MMPMID24778325
Mercer KE
; Hennings L
; Sharma N
; Lai K
; Cleves MA
; Wynne RA
; Badger TM
; Ronis MJ
Cancer Prev Res (Phila)
2014[Jul]; 7
(7
): 675-85
PMID24778325
show ga
Although alcohol effects within the liver have been extensively studied, the
complex mechanisms by which alcohol causes liver cancer are not well understood.
It has been suggested that ethanol (EtOH) metabolism promotes tumor growth by
increasing hepatocyte proliferation. In this study, we developed a mouse model of
tumor promotion by chronic EtOH consumption in which EtOH feeding began 46 days
after injection of the chemical carcinogen diethylnitrosamine (DEN) and continued
for 16 weeks. With a final EtOH concentration of 28% of total calories, we
observed a significant increase in the total number of preneoplastic foci and
liver tumors per mouse in the EtOH+DEN group compared with corresponding pair-fed
(PF)+DEN and chow+DEN control groups. We also observed a 4-fold increase in
hepatocyte proliferation (P < 0.05) and increased cytoplasmic staining of
active-?-catenin in nontumor liver sections from EtOH+DEN mice compared with
PF+DEN controls. In a rat model of alcohol-induced liver disease, we found
increased hepatocyte proliferation (P < 0.05); depletion of retinol and retinoic
acid stores (P < 0.05); increased expression of cytosolic and nuclear expression
of ?-catenin (P < 0.05) and phosphorylated-glycogen synthase kinase 3? (p-GSK3?),
P < 0.05; significant upregulation in Wnt7a mRNA expression; and increased
expression of several ?-catenin targets, including, glutamine synthetase (GS),
cyclin D1, Wnt1 inducible signaling pathways protein (WISP1), and matrix
metalloproteinase-7(MMP7), P < 0.05. These data suggest that chronic EtOH
consumption activates the Wnt/?-catenin signaling pathways to increase hepatocyte
proliferation, thus promoting tumorigenesis following an initiating insult to the
liver.
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