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    The calcium-binding protein S100B reduces IL6 production in malignant melanoma via inhibition of RSK cellular signaling

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    Author
    Alasady, Milad J
    Terry, Alexander R
    Pierce, Adam D
    Cavalier, Michael C
    Blaha, Catherine S
    Adipietro, Kaylin A
    Wilder, Paul T
    Weber, David J
    Hay, Nissim
    Date
    2021-08-19
    Journal
    PLoS ONE
    Publisher
    Public Library of Science
    Type
    Article
    
    Metadata
    Show full item record
    See at
    https://doi.org/10.1371/journal.pone.0256238
    Abstract
    S100B is frequently elevated in malignant melanoma. A regulatory mechanism was uncovered here in which elevated S100B lowers mRNA and secreted protein levels of interleukin-6 (IL6) and inhibits an autocrine loop whereby IL6 activates STAT3 signaling. Our results showed that S100B affects IL6 expression transcriptionally. S100B was shown to form a calcium-dependent protein complex with the p90 ribosomal S6 kinase (RSK), which in turn sequesters RSK into the cytoplasm. Consistently, S100B inhibition was found to restore phosphorylation of a nuclear located RSK substrate, CREB, which is a potent transcription factor for IL6 expression. Thus, elevated S100B reduces IL6-STAT3 signaling via RSK signaling pathway in malignant melanoma. Indeed, the elevated S100B levels in malignant melanoma cell lines correspond to low levels of IL6 and p-STAT3.
    Keyword
    autocrine loop
    S100B
    Interleukin 6--antagonists & inhibitors
    Melanoma
    STAT3 Transcription Factor
    Identifier to cite or link to this item
    http://hdl.handle.net/10713/16490
    ae974a485f413a2113503eed53cd6c53
    10.1371/journal.pone.0256238
    Scopus Count
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