STAT3-mediated IGF-2 secretion in the tumour microenvironment elicits innate resistance to anti-IGF-1R antibody View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-10-14

AUTHORS

Ji-Sun Lee, Ju-Hee Kang, Hye-Jin Boo, Su-Jung Hwang, Sungyoul Hong, Su-Chan Lee, Young-Jun Park, Tae-Moon Chung, Hyewon Youn, Seung Mi Lee, Byoung Jae Kim, June-Key Chung, Yeonseok Chung, William N. William, Young Kee Shin, Hyo-Jong Lee, Seung-Hyun Oh, Ho-Young Lee

ABSTRACT

Drug resistance is a major impediment in medical oncology. Recent studies have emphasized the importance of the tumour microenvironment (TME) to innate resistance, to molecularly targeted therapies. In this study, we investigate the role of TME in resistance to cixutumumab, an anti-IGF-1R monoclonal antibody that has shown limited clinical efficacy. We show that treatment with cixutumumab accelerates tumour infiltration of stromal cells and metastatic tumour growth, and decreases overall survival of mice. Cixutumumab treatment stimulates STAT3-dependent transcriptional upregulation of IGF-2 in cancer cells and recruitment of macrophages and fibroblasts via paracrine IGF-2/IGF-2R activation, resulting in the stroma-derived CXCL8 production, and thus angiogenic and metastatic environment. Silencing IGF-2 or STAT3 expression in cancer cells or IGF-2R or CXCL8 expression in stromal cells significantly inhibits the cancer–stroma communication and vascular endothelial cells’ angiogenic activities. These findings suggest that blocking the STAT3/IGF-2/IGF-2R intercellular signalling loop may overcome the adverse consequences of anti-IGF-1R monoclonal antibody-based therapies. More... »

PAGES

8499

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  • Journal

    TITLE

    Nature Communications

    ISSUE

    1

    VOLUME

    6

    Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/ncomms9499

    DOI

    http://dx.doi.org/10.1038/ncomms9499

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1008301521

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/26465273


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