In:
European Journal of Immunology, Wiley, Vol. 44, No. 1 ( 2014-01), p. 173-183
Abstract:
Nodal, a member of the TGF ‐β superfamily, is an embryonic morphogen that is upregulated in different types of tumors. Nodal increases the tumorigenesis by inducing angiogenesis and promoting metastasis. Importantly, N odal inhibition suppresses the growth and invasion of tumor. Since tumor‐associated macrophages ( TAM s) are the major infiltrating leukocytes in most cancers, we investigated whether N odal is involved in the differentiation of TAM s. Our results revealed that N odal inhibition in tumor microenvironment upregulated the production of IL ‐12 in macrophages and reversed TAM s to classically activated macrophage phenotype. In contrast, treatment with recombinant N odal (r N odal) decreased the expression of IL ‐12 in murine macrophages. Furthermore, r N odal promoted macrophage polarization to an alternatively activated macrophage‐like/ TAM phenotype and modulated its function. These results suggest that N odal may play an important role in macrophage polarization and downregulation of IL ‐12. The rescued antitumor function of TAM s via the inhibition of N odal expression could be a new therapeutic strategy for cancer treatment.
Type of Medium:
Online Resource
ISSN:
0014-2980
,
1521-4141
DOI:
10.1002/eji.201343535
Language:
English
Publisher:
Wiley
Publication Date:
2014
detail.hit.zdb_id:
1491907-2
