Targeting STAT3 affects melanoma on multiple fronts View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2005-06

AUTHORS

Marcin Kortylewski, Richard Jove, Hua Yu

ABSTRACT

As a point of convergence for numerous oncogenic signaling pathways, STAT3 is constitutively-activated at 50 to 90% frequency in diverse human cancers, including melanoma. A critical role of STAT3 in tumor cell survival, proliferation, angiogenesis, metastasis and immune evasion has been recently demonstrated. STAT3 contributes to tumor cell growth by regulating the expression of genes that are involved in cell survival and proliferation. STAT3 promotes metastasis and angiogenesis by inducing expression of the metastatic gene, MMP-2, and the potent angiogenic gene, VEGF. STAT3 participates in the regulation of tumor immune evasion by inhibiting expression of proinflammatory mediators while promoting expression of immune-suppressing factors, which in turn activates STAT3 signaling in dendritic cells leading to immune tolerance. Thus, targeting STAT3 for therapy assaults cancer on multiple fronts. Many of the studies that defined STAT3’s role in oncogenesis were carried out in melanoma cells and tumor models. In this review, we summarize the key role of STAT3 in cancer in general and melanoma in particular. With the emergence of small-molecule drugs that directly inhibit STAT3 or the oncogenic signaling pathways upstream of STAT3 in melanoma, a promising novel approach for melanoma therapy is emerging. More... »

PAGES

315-327

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    URI

    http://scigraph.springernature.com/pub.10.1007/s10555-005-1580-1

    DOI

    http://dx.doi.org/10.1007/s10555-005-1580-1

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1047575709

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/15986140


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