title: Nondenatured soy extracts reduce UVB-induced skin damage via multiple mechanisms.
abstract: UV irradiation results in DNA damage, inflammation and immunosuppression, leading to the development of basal and squamous cell carcinomas. Earlier data show that topical treatment with nondenatured soy extracts reduced the incidence and delayed the development/progression of already-initiated skin tumors in high-risk hairless mice. Here we show that pretreatment with nondenatured soy extracts reduced UVB-induced Thymine-Thymine (TT) dimer formation. In vitro, nondenatured soy extracts enhanced UVB-induced checkpoint kinase-1 (Chk1) activation, suggesting a delay in cell cycle progression that enables longer time for DNA repair. Soy also reduced UVB-induced cyclo-oxygenase-2 (COX-2) expression and prostaglandin E2 secretion, and inhibited p38 MAP kinase activation, suggesting its anti-inflammatory activity. Mice pretreated topically with nondenatured soy extracts had reduced levels of UVB-induced TT dimers and COX-2 expression in their skins compared to UVB alone. The nondenatured soy extracts also inhibited vascular endothelial growth factor-induced endothelial tube formation in Matrigel, suggesting a possible inhibitory effect on angiogenesis and tumor progression. Taken together, nondenatured soy extracts could prevent or reduce UVB-induced skin damage via multiple mechanisms, affecting both the initiation and the progression of skin cancer. These data suggest that topical application of nondenatured soy extracts could potentially reduce the incidence of skin cancer.
authors.affiliation: The Johnson & Johnson Skin Research Center, Consumer Products Worldwide, Johnson & Johnson Consumer Companies, Inc., Skillman, NJ, USA.
authors.forename: Nannan
authors.initials: N
authors.lastname: Chen
authors.forename: Richard
authors.initials: R
authors.lastname: Scarpa
authors.forename: Li
authors.initials: L
authors.lastname: Zhang
authors.forename: Miri
authors.initials: M
authors.lastname: Seiberg
authors.forename: Connie B
authors.initials: CB
authors.lastname: Lin
mesh_terms: D000818:Animals; D002460:Cell Line; D000071877:Checkpoint Kinase 1; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism; D004249:DNA Damage; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000473:pathology; D051379:Mice; D010936:Plant Extracts / Q000737:chemistry* / Q000627:therapeutic use*; D011494:Protein Kinases / Q000378:metabolism; D012867:Skin / Q000378:metabolism / Q000528:radiation effects*; D012871:Skin Diseases / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D013025:Glycine max / Q000737:chemistry*; D014466:Ultraviolet Rays; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D010936:Plant Extracts; D042461:Vascular Endothelial Growth Factor A; D051546:Cyclooxygenase 2; D011494:Protein Kinases; C000605867:CHEK1 protein, human; D000071877:Checkpoint Kinase 1; C000605869:Chek1 protein, mouse