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2017 ; 25
(4
): 417-426
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4-O-Methylhonokiol Protects HaCaT Cells from TGF-?1-Induced Cell Cycle Arrest by
Regulating Canonical and Non-Canonical Pathways of TGF-? Signaling
#MMPMID28190316
Kim SC
; Kang JI
; Hyun JW
; Kang JH
; Koh YS
; Kim YH
; Kim KH
; Ko JH
; Yoo ES
; Kang HK
Biomol Ther (Seoul)
2017[Jul]; 25
(4
): 417-426
PMID28190316
show ga
4-O-methylhonokiol, a neolignan compound from Magnolia Officinalis, has been
reported to have various biological activities including hair growth promoting
effect. However, although transforming growth factor-? (TGF-?) signal pathway has
an essential role in the regression induction of hair growth, the effect of
4-O-methylhonokiol on the TGF-? signal pathway has not yet been elucidated. We
thus examined the effect of 4-O-methylhonokiol on TGF-?-induced canonical and
noncanonical pathways in HaCaT human keratinocytes. When HaCaT cells were
pretreated with 4-O-methylhonokiol, TGF-?1-induced G1/G0 phase arrest and
TGF-?1-induced p21 expression were decreased. Moreover, 4-O-methylhonokiol
inhibited nuclear translocation of Smad2/3, Smad4 and Sp1 in TGF-?1-induced
canonical pathway. We observed that ERK phosphorylation by TGF-?1 was
significantly attenuated by treatment with 4-O-methylhonokiol. 4-O-methylhonokiol
inhibited TGF-?1-induced reactive oxygen species (ROS) production and reduced the
increase of NADPH oxidase 4 (NOX4) mRNA level in TGF-?1-induced noncanonical
pathway. These results indicate that 4-O-methylhonokiol could inhibit
TGF-?1-induced cell cycle arrest through inhibition of canonical and noncanonical
pathways in human keratinocyte HaCaT cell and that 4-O-methylhonokiol might have
protective action on TGF-?1-induced cell cycle arrest.