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    Oncogenic KRAS regulates tumor cell signaling via stromal reciprocation.

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    Authors
    Tape, C
    Ling, S
    Dimitriadi, M
    McMahon, Kelly M
    Worboys, Jonathan D
    Leong, Hui Sun
    Norrie, Ida C
    Miller, Crispin J
    Poulogiannis, G
    Lauffenburger, D
    Jørgensen, Claus
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    Affiliation
    The Institute ofCancer Research, 237 Fulham Road, London SW3 6JB,
    Issue Date
    2016-05-05
    
    Metadata
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    Abstract
    Oncogenic mutations regulate signaling within both tumor cells and adjacent stromal cells. Here, we show that oncogenic KRAS (KRAS(G12D)) also regulates tumor cell signaling via stromal cells. By combining cell-specific proteome labeling with multivariate phosphoproteomics, we analyzed heterocellular KRAS(G12D) signaling in pancreatic ductal adenocarcinoma (PDA) cells. Tumor cell KRAS(G12D) engages heterotypic fibroblasts, which subsequently instigate reciprocal signaling in the tumor cells. Reciprocal signaling employs additional kinases and doubles the number of regulated signaling nodes from cell-autonomous KRAS(G12D). Consequently, reciprocal KRAS(G12D) produces a tumor cell phosphoproteome and total proteome that is distinct from cell-autonomous KRAS(G12D) alone. Reciprocal signaling regulates tumor cell proliferation and apoptosis and increases mitochondrial capacity via an IGF1R/AXL-AKT axis. These results demonstrate that oncogene signaling should be viewed as a heterocellular process and that our existing cell-autonomous perspective underrepresents the extent of oncogene signaling in cancer. VIDEO ABSTRACT.
    Citation
    Oncogenic KRAS regulates tumor cell signaling via stromal reciprocation. 2016, 165 (4):910-20 Cell
    Journal
    Cell
    URI
    http://hdl.handle.net/10541/610741
    DOI
    10.1016/j.cell.2016.03.029
    PubMed ID
    27087446
    Type
    Article
    Language
    en
    ISSN
    1097-4172
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.cell.2016.03.029
    Scopus Count
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    All Paterson Institute for Cancer Research

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