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Changes in tumor microenvironments in high‐fat diet‐fed mice: role of macrophages and adipocytes (37.5)
Author(s) -
Park Jung,
Cho Han Jin,
Jung Jae In,
Kwon Gyoo Taik,
Lee Ki Won
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.37.5
Subject(s) - lymphangiogenesis , angiogenesis , tumor microenvironment , adipose tissue , paracrine signalling , cancer research , medicine , metastasis , endocrinology , chemokine , adipose tissue macrophages , biology , chemistry , receptor , white adipose tissue , cancer , tumor cells
Using several mouse tumor models, we have shown that the chronic consumption of a high‐fat diet (HFD) stimulates solid tumor growth and metastasis and thereby reduces the survival rate. The present study examined the mechanisms by which HFD stimulates tumor promotion. Angiogenesis and lymphangiogenesis in tumor tissues and lymph node (LN)s are markedly increased in HFD‐fed mice. HFD feeding increases adipocytes and M2‐macrophage (M2‐MΦ)s in tumor tissues and M2‐MΦs in adipose tissues of tumor‐bearing mice. Results from in vivo and in vitro co‐culture studies revealed that the crosstalk between adipocytes, tumor cells, M2‐MΦs, and/or lymphatic endothelial cell (LEC)s stimulates the production of several factors which stimulate tumor cell/monocyte migration, angiogenesis, and lymphangiogenesis via endocrine and paracrine mechanisms. In HFD‐fed mice, increased chemokine ligands in LECs recruit tumor cells expressing high levels of their receptors, thereby increasing LN metastasis. Our results indicate that increased adipocytes in HFD‐fed mice play important roles in the recruitment of M2‐MΦs in tumor tissues and lymphangiogenesis as well as tumor cell migration, thereby stimulating tumor metastasis.