Tumor-associated macrophage-secreted 14-3-3ζ signals via AXL to promote pancreatic cancer chemoresistance View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2019-04-01

AUTHORS

Gabriele D’Errico, Marta Alonso-Nocelo, Mireia Vallespinos, Patrick C. Hermann, Sonia Alcalá, Coral Pedrero García, Laura Martin-Hijano, Sandra Valle, Julie Earl, Chiara Cassiano, Luis Lombardia, Jaime Feliu, Maria Chiara Monti, Thomas Seufferlein, Laura García-Bermejo, Paola Martinelli, Alfredo Carrato, Bruno Sainz

ABSTRACT

Pancreatic ductal adenocarcinoma (PDAC) is an inherently chemoresistant tumor. Chemotherapy leads to apoptosis of cancer cells, and in previous studies we have shown that tumor-associated macrophage (TAM) infiltration increases following chemotherapy in PDAC. Since one of the main functions of macrophages is to eliminate apoptotic cells, we hypothesized that TAMs phagocytose chemotherapy-induced apoptotic cells and secrete factors, which favor PDAC chemoresistance. To test this hypothesis, primary human PDAC cultures were treated with conditioned media (CM) from monocyte-derived macrophage cultures incubated with apoptotic PDAC cells (MØApopCM). MØApopCM pretreatment rendered naïve PDAC cells resistant to Gemcitabine- or Abraxane-induced apoptosis. Proteomic analysis of MØApopCM identified YWHAZ/14-3-3 protein zeta/delta (14-3-3ζ), a major regulator of apoptotic cellular pathways, as a potential mediator of chemoresistance, which was subsequently validated in patient transcriptional datasets, serum samples from PDAC patients and using recombinant 14-3-3ζ and inhibitors thereof. Moreover, in mice bearing orthotopic PDAC tumors, the antitumor potential of Gemcitabine was significantly enhanced by elimination of TAMs using clodronate liposomes or by pharmacological inhibition of the Axl receptor tyrosine kinase, a 14-3-3ζ interacting partner. These data highlight a unique regulatory mechanism by which chemotherapy-induced apoptosis acts as a switch to initiate a protumor/antiapoptotic mechanism in PDAC via 14-3-3ζ/Axl signaling, leading to phosphorylation of Akt and activation of cellular prosurvival mechanisms. The data presented therefore challenge the idea that apoptosis of tumor cells is therapeutically beneficial, at least when immune sensor cells, such as macrophages, are present. More... »

PAGES

1-17

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41388-019-0803-9

DOI

http://dx.doi.org/10.1038/s41388-019-0803-9

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1113175276

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30936462


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