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2016 ; 7
(39
): 63856-63869
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Lipid rafts promote liver cancer cell proliferation and migration by
up-regulation of TLR7 expression
#MMPMID27588480
Liu Y
; Guo X
; Wu L
; Yang M
; Li Z
; Gao Y
; Liu S
; Zhou G
; Zhao J
Oncotarget
2016[Sep]; 7
(39
): 63856-63869
PMID27588480
show ga
Hepatocellular carcinoma (HCC) occurs predominantly in patients with underlying
chronic liver disease and cirrhosis. Toll-like receptors (TLRs) play an important
role in innate immune responses and TLR signaling has been associated with
various chronic liver diseases. Lipid rafts provide the necessary
microenvironment for certain specialized signaling events to take place, such as
the innate immune recognition. The purpose of this study was to determine the
pattern of TLR7 expression in HCC, how to recruit TLR7 into lipid rafts responded
to ligands and whether targeting TLR7 might have beneficial effects. The study
group was comprised of 130 human liver tissues: 23 chronic hepatitis B (CHB), 18
liver cirrhosis (LC), 68 HCC and 21 normal livers. The expression of TLR7 was
evaluated using immunohistochemistry, western blotting, and flow cytometry.
Proliferation and migration of human HepG2 cells were studied following
stimulation of TLR7 using the agonist gardiquimod and inhibition with a specific
antagonist 20S-protopanaxadiol (aPPD). The activation of lipid raft-associated
TLR7 signaling was measured using western blotting, double immunohistochemistry
and immunoprecipitation in liver tissues and HepG2 cells. TLR7 expression was
up-regulated in human HCC tissues and hepatoma cell line. Proliferation and
migration of HepG2 cells in vitro increased significantly in response to
stimulation of TLR7. TLR7 inhibition using aPPD significantly reduced HepG2 cell
migration in vitro. The lipid raft protein caveolin-1 and flotillin-1 were
involved with enhanced TLR7 signaling in HCC. CONCLUSIONS: The data suggest that
inhibiting TLR7 with antagonists, like aPPD, could potentially be used as a novel
therapeutic approach for HCC.
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