Browsing by Author "Nisamanee Charoenchon"

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    BRN2 is a non-canonical melanoma tumor-suppressor
    (2021-12-01) Michael Hamm; Pierre Sohier; Valérie Petit; Jérémy H. Raymond; Véronique Delmas; Madeleine Le Coz; Franck Gesbert; Colin Kenny; Zackie Aktary; Marie Pouteaux; Florian Rambow; Alain Sarasin; Nisamanee Charoenchon; Alfonso Bellacosa; Luis Sanchez-del-Campo; Laura Mosteo; Martin Lauss; Dies Meijer; Eirikur Steingrimsson; Göran B. Jönsson; Robert A. Cornell; Irwin Davidson; Colin R. Goding; Lionel Larue; Université PSL; Universite Paris-Saclay; Læknadeild Háskóla Íslands; Institut de Cancerologie Gustave Roussy; The University of Edinburgh; Skånes universitetssjukhus; Mahidol University; University of Iowa Carver College of Medicine; Fox Chase Cancer Center; Nuffield Department of Medicine; CNRS Centre National de la Recherche Scientifique; Equipe Labellisée Ligue Contre le Cancer
    While the major drivers of melanoma initiation, including activation of NRAS/BRAF and loss of PTEN or CDKN2A, have been identified, the role of key transcription factors that impose altered transcriptional states in response to deregulated signaling is not well understood. The POU domain transcription factor BRN2 is a key regulator of melanoma invasion, yet its role in melanoma initiation remains unknown. Here, in a BrafV600EPtenF/+ context, we show that BRN2 haplo-insufficiency promotes melanoma initiation and metastasis. However, metastatic colonization is less efficient in the absence of Brn2. Mechanistically, BRN2 directly induces PTEN expression and in consequence represses PI3K signaling. Moreover, MITF, a BRN2 target, represses PTEN transcription. Collectively, our results suggest that on a PTEN heterozygous background somatic deletion of one BRN2 allele and temporal regulation of the other allele elicits melanoma initiation and progression.
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    Differential reorganisation of cutaneous elastic fibres: A comparison of the: In vivo effects of broadband ultraviolet B versus solar simulated radiation
    (2018-01-01) Nisamanee Charoenchon; Lesley E. Rhodes; Suzanne M. Pilkington; Mark D. Farrar; Rachel E.B. Watson; NHS Foundation Trust; Mahidol University; University of Manchester
    © 2018 The Royal Society of Chemistry and Owner Societies. Long-term exposure of human skin to ultraviolet radiation (UVR) in sunlight negatively impacts its appearance and function with photoaged skin having a characteristic leathery, rough appearance, with deep wrinkles. These clinical features of photodamage are thought to result from UVR-induced remodelling of the dermal extracellular matrix, particularly the elastic fibre system. There are few in vivo human data on the impact of acute UVR exposure on this fibre system and particularly solar-simulated radiation (SSR)-mediated effects. We examined the differential effect of broadband UVB and SSR on the human dermal elastic fibre system, and specifically the microfibrillar components fibrillin-1, fibulin-2 and fibulin-5. Healthy white Caucasian adults (skin type II-III) were recruited and irradiated with 3× their minimal erythema dose of broadband UVB (n = 6) or SSR (n = 6) on photoprotected buttock skin. Punch biopsies were taken 24 h after irradiation and from unirradiated control skin. Overall, histological assessment of elastic fibres revealed significantly less elastic fibre staining in broadband UVB (P = 0.004) or SSR (P = 0.04) irradiated skin compared to unirradiated control skin. Significantly less staining of fibrillin-1-positive microfibrils was also observed in the papillary dermis of UVB irradiated skin (P = 0.02) but not skin exposed to SSR. Conversely, immunohistochemistry for fibulin-5-positive microfibrils revealed significantly less expression in skin exposed to SSR (P = 0.04) but not to broadband UVB. There was no significant change in fibulin-2-positive microfibrils following either broadband UVB or SSR irradiation. Thus, broadband UVB and SSR mediate differential effects on individual components of the dermal elastic fibre network in human skin. Further human studies are required to explore the mechanisms underlying these findings and the impact of potential photoprotective agents.
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    Oxyresveratrol inhibits cellular tyrosinase-related oxidative stress-induced melanogenesis in B16 melanoma cells
    (2020-01-01) Teerapat Rodboon; Sarawoot Palipoch; Seiji Okada; Nisamanee Charoenchon; Yaowarin Nakornpakdee; Prasit Suwannalert; Graduate School of Medical Sciences; Walailak University; Mahidol University
    © 2020, Open Science Publishers LLP Inc.. Cellular oxidative stress is caused by an imbalance in the redox status and manifests as hyperpigmentation disorders. Reactive oxygen species, particularly hydrogen peroxide (H2O2) as the highly reactive hydroxyl radicals, promote the melanin production through the induction of tyrosinase enzyme activity. In this study, the antioxidant activity of oxyresveratrol was investigated by 2,2'-azino-bis-3-ethylbenzothiazoline-6-sulfonic acid (ABTS) and 2,2-dipheny l-1-picrylhydrazyl (DPPH) assays. In addition, melanin biosynthesis, tyrosinase activity, and cellular oxidants due to the bioactive component, oxyresveratrol, were determined in B16 cells by melanin content assay, cellular tyrosinase activity assay, and the dichloro-dihydro-fluorescein diacetate (DCFH-DA) assay, respectively. Hydrogen peroxide induced the melanogenesis through tyrosinase activity-related cellular oxidants, whereas oxyresveratrol showed a potent antioxidant activity by DPPH and ABTS assays. At the concentrations of 10 and 12.5 μg/ml, oxyresveratrol significantly inhibited melanogenesis in B16 melanoma cells and also suppressed tyrosinase activity and cellular oxidants. Effective doses of oxyresveratrol inhibit melanogenesis through bioactivity of cellular tyrosinase-related oxidative stress.