Journal Article

Gut microbiota accelerate tumor growth via c-jun and STAT3 phosphorylation in APC<sup>Min/+</sup> mice

Yinghui Li, Parag Kundu, Shih Wee Seow, Cristina Teixeira de Matos, Linda Aronsson, Keh Chuang Chin, Klas Kärre, Sven Pettersson and Gediminas Greicius

in Carcinogenesis

Volume 33, issue 6, pages 1231-1238
Published in print June 2012 | ISSN: 0143-3334
Published online March 2012 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/bgs137
Gut microbiota accelerate tumor growth via c-jun and STAT3 phosphorylation in APCMin/+ mice

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Chronic inflammation is increasingly recognized as a major contributor of human colorectal cancer (CRC). While gut microbiota can trigger inflammation in the intestinal tract, the precise signaling pathways through which host cells respond to inflammatory bacterial stimulation are unclear. Here, we show that gut microbiota enhances intestinal tumor load in the APCMin/+ mouse model of CRC. Furthermore, systemic anemia occurs coincident with rapid tumor growth, suggesting a role for intestinal barrier damage and erythropoiesis-stimulating mitogens. Short-term stimulation assays of murine colonic tumor cells reveal that lipopolysaccharide, a microbial cell wall component, can accelerate cell growth via a c-Jun/JNK activation pathway. Colonic tumors are also infiltrated by CD11b+ myeloid cells expressing high levels of phospho-STAT3 (p-Tyr705). Our results implicate the role of gut microbiota, through triggering the c-Jun/JNK and STAT3 signaling pathways in combination with anemia, in the acceleration of tumor growth in APCMin/+ mice.

Journal Article.  6562 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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