Insulin-like growth factor-I-induced migration of melanoma cells is mediated by interleukin-8 induction

Kapaettu Satyamoorthy, Gang Li, Bhavesh Vaidya, Jiri Kalabis, Meenhard Herlyn

    Research output: Contribution to journalArticle

    50 Citations (Scopus)

    Abstract

    Successive events of growth factor-induced autocrine and paracrine activation promote tumor growth and metastasis. Insulin-like growth factor-I (IGF-I) stimulates melanoma cells to grow, survive, and migrate. Interleukin-8 (IL-8) is produced by melanoma cells and has been correlated with melanoma metastasis, but the biological functions of this cytokine have not been elucidated. We show here that IGF-I-induced migration of melanoma cells could be inhibited by neutralizing antibody against IL-8. IGF-I overexpression induced IL-8 production in melanoma cells, especially in biologically early melanomas by accelerating its transcription rate via activation of mitogen-activated protein kinase pathway. IGF-I treatment phosphorylated c-Jun and stimulated the binding of AP-1 but not NF-κB to the IL-8 promoter. These data identify IL-8 as a new target of IGF-I in melanoma and suggest that some of the biological functions of IGF-I are mediated by IL-8.

    Original languageEnglish
    Pages (from-to)87-93
    Number of pages7
    JournalCell Growth and Differentiation
    Volume13
    Issue number2
    Publication statusPublished - 2002

    Fingerprint

    Interleukin-8
    Insulin-Like Growth Factor I
    Cell Movement
    Melanoma
    Neoplasm Metastasis
    Transcription Factor AP-1
    Mitogen-Activated Protein Kinases
    Neutralizing Antibodies
    Intercellular Signaling Peptides and Proteins
    Cytokines
    Growth
    Neoplasms

    All Science Journal Classification (ASJC) codes

    • Cell Biology
    • Molecular Biology

    Cite this

    Satyamoorthy, Kapaettu ; Li, Gang ; Vaidya, Bhavesh ; Kalabis, Jiri ; Herlyn, Meenhard. / Insulin-like growth factor-I-induced migration of melanoma cells is mediated by interleukin-8 induction. In: Cell Growth and Differentiation. 2002 ; Vol. 13, No. 2. pp. 87-93.
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    abstract = "Successive events of growth factor-induced autocrine and paracrine activation promote tumor growth and metastasis. Insulin-like growth factor-I (IGF-I) stimulates melanoma cells to grow, survive, and migrate. Interleukin-8 (IL-8) is produced by melanoma cells and has been correlated with melanoma metastasis, but the biological functions of this cytokine have not been elucidated. We show here that IGF-I-induced migration of melanoma cells could be inhibited by neutralizing antibody against IL-8. IGF-I overexpression induced IL-8 production in melanoma cells, especially in biologically early melanomas by accelerating its transcription rate via activation of mitogen-activated protein kinase pathway. IGF-I treatment phosphorylated c-Jun and stimulated the binding of AP-1 but not NF-κB to the IL-8 promoter. These data identify IL-8 as a new target of IGF-I in melanoma and suggest that some of the biological functions of IGF-I are mediated by IL-8.",
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    Insulin-like growth factor-I-induced migration of melanoma cells is mediated by interleukin-8 induction. / Satyamoorthy, Kapaettu; Li, Gang; Vaidya, Bhavesh; Kalabis, Jiri; Herlyn, Meenhard.

    In: Cell Growth and Differentiation, Vol. 13, No. 2, 2002, p. 87-93.

    Research output: Contribution to journalArticle

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    AU - Satyamoorthy, Kapaettu

    AU - Li, Gang

    AU - Vaidya, Bhavesh

    AU - Kalabis, Jiri

    AU - Herlyn, Meenhard

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    AB - Successive events of growth factor-induced autocrine and paracrine activation promote tumor growth and metastasis. Insulin-like growth factor-I (IGF-I) stimulates melanoma cells to grow, survive, and migrate. Interleukin-8 (IL-8) is produced by melanoma cells and has been correlated with melanoma metastasis, but the biological functions of this cytokine have not been elucidated. We show here that IGF-I-induced migration of melanoma cells could be inhibited by neutralizing antibody against IL-8. IGF-I overexpression induced IL-8 production in melanoma cells, especially in biologically early melanomas by accelerating its transcription rate via activation of mitogen-activated protein kinase pathway. IGF-I treatment phosphorylated c-Jun and stimulated the binding of AP-1 but not NF-κB to the IL-8 promoter. These data identify IL-8 as a new target of IGF-I in melanoma and suggest that some of the biological functions of IGF-I are mediated by IL-8.

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