Sulforaphane suppresses cell growth and collagen expression of keloid fibroblasts

被引:24
|
作者
Kawarazaki, Ayako [1 ,2 ]
Horinaka, Mano [1 ]
Yasuda, Shusuke [1 ]
Numajiri, Toshiaki [2 ]
Nishino, Kenichi [2 ]
Sakai, Toshiyuki [1 ]
机构
[1] Kyoto Prefectural Univ Med, Grad Sch Med Sci, Dept Mol Targeting Canc Prevent, Kyoto, Japan
[2] Kyoto Prefectural Univ Med, Grad Sch Med Sci, Div Plast & Reconstruct Surg, Dept Surg, Kyoto, Japan
关键词
MUSCLE ACTIN EXPRESSION; PROSTATE-CANCER CELLS; NF-KAPPA-B; FACTOR-BETA; CYCLE ARREST; SIGNALING PATHWAY; IN-VIVO; APOPTOSIS; PATHOGENESIS; INHIBITION;
D O I
10.1111/wrr.12512
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Keloids are fibroproliferative diseases characterized by the accumulation of an extracellular matrix including collagen. Various growth factors, or cytokines, and their receptors are overexpressed in keloids, and they are expected to be therapy targets. Sulforaphane, a dietary isothiocyanate, has recently shown anti-tumor, anti-inflammatory, and anti-fibrotic properties. In this study, we found that sulforaphane inhibited cell growth and reduced collagen at the mRNA and protein levels in keloid fibroblasts. Moreover, sulforaphane markedly suppressed the expression of IL-6 and -SMA and inhibited Stat3 and Smad3 signaling pathways in keloid fibroblast KF112 cells. Sulforaphane induced G2/M cell-cycle arrest with the induction of p21 in KF112 cells. In addition, sulforaphane inhibited cell growth and suppressed the expression of collagen in keloid fibroblasts under a coculture with peripheral blood mononuclear cells. Furthermore, sulforaphane suppressed IL-6, Stat3, and Smad3 signaling in the coculture system. This study suggests that sulforaphane may be a novel keloid treatment.
引用
收藏
页码:224 / 233
页数:10
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