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10.4062/biomolther.2016.003

http://scihub22266oqcxt.onion/10.4062/biomolther.2016.003
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C5499621!5499621!28190316
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suck abstract from ncbi


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pmid28190316      Biomol+Ther+(Seoul) 2017 ; 25 (4): 417-26
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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): 417-26 PMID28190316show 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.
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