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2018 ; 15
(6
): 8723-8728
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Transforming growth factor-? decreases side population cells in hepatocellular
carcinoma in vitro
#MMPMID29805610
Kim JB
; Lee S
; Kim HR
; Park SY
; Lee M
; Yoon JH
; Kim YJ
Oncol Lett
2018[Jun]; 15
(6
): 8723-8728
PMID29805610
show ga
Hepatocellular carcinoma (HCC) can result from hepatitis B or C infection,
fibrosis or cirrhosis. Transforming growth factor-? (TGF-?) is one of the main
growth factors associated with fibrosis or cirrhosis progression in the liver,
but its role is controversial in hepatocarcinogenesis. In the present study, the
effect of TGF-? on the HCC Huh-7 and Huh-Bat cell lines was evaluated. To study
the effect of TGF-?, Huh-7 and Huh-Bat cells were treated with TGF-? and a TGF-?
receptor inhibitor (SB431542). Cell survival, cell cycle, numbers of side
population (SP) cells and expression of the cancer stem cell marker cluster of
differentiation (CD)133, epithelial-mesenchymal transition markers (E-cadherin,
?-smooth muscle actin and vimentin) and TGF-?-regulated proteins [phospho-c-Jun
N-terminal kinase (p-JNK), p-c-Jun and p-smad2] were investigated. TGF-?
treatment resulted in decreased cell survival with a targeted effect on SP cells.
Expression of CD133 and vimentin was upregulated by treatment with the TGF-?
receptor antagonist SB431542, but not with TGF-?. By contrast, TGF-? induced
accumulation of cells at G0/G1, and upregulated expression of p-JNK, p-c-Jun and
p-smad2. However, these effects were blocked when cells were treated with TGF-?
plus SB431542, indicating the specificity of the TGF-? effect. The present
results indicated that TGF-? has anticancer effects mediated by survival
inhibition of cancer stem cells, which may be developed as a novel therapy for
HCC.