Licochalcone B (Lico B), which is normally isolated from the roots of Glycyrrhiza inflata (Chinese Licorice), generally classified into organic compounds including retrochalcones. Potential pharmacological properties of Lico B include anti-inflammatory, anti-bacterial, anti-oxidant, and anti-cancer activities. However, its biological effects on melanoma and squamous cell carcinoma (SCC) are unknown. Based on these known facts, this study investigated the role of Lico B in apoptosis, through the extrinsic and intrinsic pathways and additional regulation of specificity protein 1 in human skin cancer cell lines. Annexin V/7-aminoactinomycin D staining, western blot analysis, mitochondrial membrane potential assay, and an anchorage-independent cell transformation assay demonstrated that Lico B treatment of human melanoma and SCC cells significantly inhibited cell proliferation and induced apoptotic cell death. More specifically, Lico B induced apoptosis through the regulation of specificity protein 1 and apoptosis-related proteins including CCAAT/enhancer-binding protein homologous protein, death receptors, and poly (ADP-ribose) polymerase. These results indicate that Lico B has apoptotic effect on A375 and A431 skin cancer cells, suggesting the potential value of Lico B for the treatment of human melanoma and SCC. Copyright © 2017 John Wiley & Sons, Ltd.

Unlike the indispensable function of the steroid hormone brassinosteroid (BR) in regulating growth and development of plants, the metabolism of secondary metabolites regulated by BR is not well known. Here we show that BR reduces carotenoid accumulation in Arabidopsis seedlings. BR-deficient or BR-insensitive mutants accumulated a higher level of carotenoids than the wild-type plant whereas BR treatment reduced carotenoid contents. We demonstrated that BR transcriptionally suppresses 4-hydroxyphenylpyruvate dioxygenase (HPPD) gene involved in carotenogenesis via plastoquinone production. We found that the expression of HPPD displays an oscillation pattern that is expressed more strongly in dark than in the light conditions. Moreover, BR appeared to inhibit more strongly HPPD expression in darkness than in light, leading to suppression of a diurnal oscillation of HPPD expression. BR-responsive transcription factor BZR1 directly bound to HPPD promoter and the HPPD suppression by BR was increased by the bzr1-1D gain-of-function mutation. Interestingly, dark-induced HPPD expression did not cause carotenoid accumulation due to downregulation of other carotenoid biosynthetic genes in the dark. Our results suggest that BR regulates different physiological responses in dark and light through inhibition of HPPD expression.