title: Sulforaphane suppresses cell growth and collagen expression of keloid fibroblasts.
abstract: 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 α-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.
authors.affiliation: Department of Molecular-Targeting Cancer Prevention.|Department of Surgery, Division of Plastic and Reconstructive Surgery, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
authors.forename: Ayako
authors.initials: A
authors.lastname: Kawarazaki
authors.affiliation: Department of Molecular-Targeting Cancer Prevention.
authors.forename: Mano
authors.initials: M
authors.lastname: Horinaka
authors.affiliation: Department of Molecular-Targeting Cancer Prevention.
authors.forename: Shusuke
authors.initials: S
authors.lastname: Yasuda
authors.affiliation: Department of Surgery, Division of Plastic and Reconstructive Surgery, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Numajiri
authors.affiliation: Department of Surgery, Division of Plastic and Reconstructive Surgery, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
authors.forename: Kenichi
authors.initials: K
authors.lastname: Nishino
authors.affiliation: Department of Molecular-Targeting Cancer Prevention.
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Sakai
mesh_terms: D015153:Blotting, Western; D049109:Cell Proliferation / Q000187:drug effects*; D002478:Cells, Cultured; D003094:Collagen / Q000378:metabolism*; D005109:Extracellular Matrix / Q000187:drug effects / Q000502:physiology; D005347:Fibroblasts / Q000187:drug effects* / Q000502:physiology; D005786:Gene Expression Regulation; D006801:Humans; D015850:Interleukin-6; D017879:Isothiocyanates / Q000494:pharmacology*; D007627:Keloid / Q000188:drug therapy* / Q000473:pathology*; D060888:Real-Time Polymerase Chain Reaction; D050796:STAT3 Transcription Factor; D015398:Signal Transduction / Q000187:drug effects; D051900:Smad3 Protein; D013454:Sulfoxides
chemical_list: C508600:IL6 protein, human; D015850:Interleukin-6; D017879:Isothiocyanates; C497790:SMAD3 protein, human; D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human; D051900:Smad3 Protein; D013454:Sulfoxides; C037152:isothiocyanic acid; D003094:Collagen; C016766:sulforaphane