Hyperactivation of STAT3 is involved in abnormal differentiation of dendritic cells in cancer

Abnormal differentiation of myeloid cells is one of the hallmarks of cancer. However, the molecular mechanisms of this process remain elusive. In this study, we investigated the effect of tumor-derived factors on Janus kinase (Jak)/STAT signaling in myeloid cells during their differentiation into de...

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Vydáno v:	The Journal of immunology (1950) Ročník 172; číslo 1; s. 464
Hlavní autoři:	Nefedova, Yulia, Huang, Mei, Kusmartsev, Sergei, Bhattacharya, Raka, Cheng, Pingyan, Salup, Raoul, Jove, Richard, Gabrilovich, Dmitry
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States 01.01.2004
Témata:	Animals Cell Aggregation - immunology Cell Differentiation - immunology Cell Division - immunology Cell Line, Tumor Colonic Neoplasms - enzymology Colonic Neoplasms - immunology Colonic Neoplasms - metabolism Colonic Neoplasms - pathology Dendritic Cells - enzymology Dendritic Cells - metabolism Dendritic Cells - pathology DNA-Binding Proteins - metabolism DNA-Binding Proteins - physiology Female Growth Inhibitors - physiology Hematopoietic Stem Cells - immunology Hematopoietic Stem Cells - pathology Janus Kinase 2 Mice Mice, Inbred BALB C Mice, Inbred C57BL Myeloid Cells - metabolism Myeloid Cells - pathology Neoplasm Proteins - physiology NIH 3T3 Cells Protein-Tyrosine Kinases - metabolism Proto-Oncogene Proteins Signal Transduction - immunology STAT3 Transcription Factor Trans-Activators - metabolism Trans-Activators - physiology Up-Regulation - immunology
ISSN:	0022-1767
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Shrnutí:	Abnormal differentiation of myeloid cells is one of the hallmarks of cancer. However, the molecular mechanisms of this process remain elusive. In this study, we investigated the effect of tumor-derived factors on Janus kinase (Jak)/STAT signaling in myeloid cells during their differentiation into dendritic cells. Tumor cell conditioned medium induced activation of Jak2 and STAT3, which was associated with an accumulation of immature myeloid cells. Jak2/STAT3 activity was localized primarily in these myeloid cells, which prevented the differentiation of immature myeloid cells into mature dendritic cells. This differentiation was restored after removal of tumor-derived factors. Inhibition of STAT3 abrogated the negative effects of these factors on myeloid cell differentiation, and overexpression of STAT3 reproduced the effects of tumor-derived factors. Thus, this is a first demonstration that tumor-derived factors may affect myeloid cell differentiation in cancer via constitutive activation of Jak2/STAT3.
Bibliografie:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0022-1767
DOI:	10.4049/jimmunol.172.1.464