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Type of publication: Journal Article
Type of document: Full Paper

Year: 2015

Authors: Pathria, P; Gotthardt, D; Prchal-Murphy, M; Putz, EM; Holcmann, M; Schlederer, M; Grabner, B; Crncec, I; Svinka, J; Musteanu, M; Hoffmann, T; Filipits, M; Berger, W; Poli, V; Kenner, L; Bilban, M; Casanova, E; Müller, M; Strobl, B; Bayer, E; Mohr, T; Sexl, V; Eferl, R

Title: Myeloid STAT3 promotes formation of colitis-associated colorectal cancer in mice.

Source: Oncoimmunology. 2015; 4(4):e998529

Authors Vetmeduni Vienna:

Gotthardt Dagmar
Kenner Lukas
Müller Mathias
Prchal-Murphy Michaela
Putz Eva Maria
Sexl Veronika
Strobl Birgit

Vetmed Research Units
Institute of Pharmacology and Toxicology
Institute of Pathology, Pathology of Laboratory Animals
Institute of Animal Breeding and Genetics, Unit of Molecular Genetics

Project(s): Jak Stat - Signalling from Basis to Disease

Myeloid cells lacking STAT3 promote antitumor responses of NK and T cells but it is unknown if this crosstalk affects development of autochthonous tumors. We deleted STAT3 in murine myeloid cells (STAT3(Δm)) and examined the effect on the development of autochthonous colorectal cancers (CRCs). Formation of Azoxymethane/Dextransulfate (AOM/DSS)-induced CRCs was strongly suppressed in STAT3(Δm) mice. Gene expression profiling showed strong activation of T cells in the stroma of STAT3(Δm) CRCs. Moreover, STAT3(Δm) host mice were better able to control the growth of transplanted MC38 colorectal tumor cells which are known to be killed in a T cell-dependent manner. These data suggest that myeloid cells lacking STAT3 control formation of CRCs mainly via cross activation of T cells. Interestingly, the few CRCs that formed in STAT3(Δm) mice displayed enhanced stromalization but appeared normal in size indicating that they have acquired ways to escape enhanced tumor surveillance. We found that CRCs in STAT3(Δm) mice consistently activate STAT3 signaling which is implicated in immune evasion and might be a target to prevent tumor relapse.

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