title: Suppression of α-MSH and IBMX-induced melanogenesis by cordycepin via             inhibition of CREB and MITF, and activation of PI3K/Akt and ERK-dependent mechanisms.
abstract: Cordycepin has been a traditional medicine in China and Korea for centuries.             This study explored the inhibitory effect of cordycepin on melanogenesis and the             relative molecular mechanisms. Cordycepin inhibited melanin synthesis-related             enzymes, such as tyrosinase, tyrosinase-related protein-1 (TRP1) and tyrosinase-related             protein-2 (TRP2). α-MSH and IBMX were reported as melanin synthesis enhancers.             Both of them could increase intracellular melanin synthesis by activation of the             microphthalmia-associated transcription factor (MITF) signaling pathway. In the             MITF pathway, the phosphorylation of cAMP related binding protein (CREB) activated             the transcription of MITF, resulting in increasing melanin synthesis. Cordycepin             also decreased the phosphorylation of CREB induced by α-MSH and IBMX in B16F10             melanoma cells. Accordingly, cordycepin inhibited melanogenesis signaling pathways             by activating ERK and AKT signaling pathways to regulate the suppression of MITF             and its downstream pathways including tyrosinase, TRP1 and TRP2. These results             indicate the role of cordycepin as a potent depigmenting agent for cosmetics.
authors.affiliation: Department of Microbiology, Pusan National University, Busan,                     Republic of Korea.
authors.forename: Mei Ling
authors.initials: ML
authors.lastname: Jin
authors.forename: Sun Young
authors.initials: SY
authors.lastname: Park
authors.forename: Young Hun
authors.initials: YH
authors.lastname: Kim
authors.forename: Geuntae
authors.initials: G
authors.lastname: Park
authors.forename: Hong-Joo
authors.initials: HJ
authors.lastname: Son
authors.forename: Sang-Joon
authors.initials: SJ
authors.lastname: Lee
mesh_terms: D015056:1-Methyl-3-isobutylxanthine / Q000037:antagonists & inhibitors / Q000494:pharmacology; D000818:Animals; D045744:Cell Line, Tumor; D002867:Chromones / Q000494:pharmacology; D017362:Cyclic AMP Response Element-Binding Protein / Q000037:antagonists & inhibitors* / Q000378:metabolism; D003839:Deoxyadenosines / Q000494:pharmacology*; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D005419:Flavonoids / Q000494:pharmacology; D008543:Melanins / Q000378:metabolism*; D051379:Mice; D051739:Microphthalmia-Associated Transcription Factor / Q000037:antagonists & inhibitors* / Q000378:metabolism; D014442:Monophenol Monooxygenase / Q000187:drug effects; D009025:Morpholines / Q000494:pharmacology; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D010766:Phosphorylation / Q000187:drug effects; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D000521:alpha-MSH / Q000378:metabolism*
chemical_list: D002867:Chromones; D017362:Cyclic AMP Response Element-Binding Protein; D003839:Deoxyadenosines; D005419:Flavonoids; D008543:Melanins; D051739:Microphthalmia-Associated Transcription Factor; D009025:Morpholines; C085911:2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; D000521:alpha-MSH; D014442:Monophenol Monooxygenase; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D048049:Extracellular Signal-Regulated MAP Kinases; C058120:cordycepin; C093973:2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; D015056:1-Methyl-3-isobutylxanthine