Tumor-associated macrophage-induced invasion and angiogenesis of human basal cell carcinoma cells by cyclooxygenase-2 induction
Journal
Journal of Investigative Dermatology
Journal Volume
129
Journal Issue
4
Pages
1016-1025
Date Issued
2009
Author(s)
Tjiu J.-W.
Inoue H.
Kuo M.-L.
Jee S.-H.
Abstract
Tumor-associated macrophages (TAMs) and cyclooxygenase-2 (COX-2) are associated with invasion, angiogenesis, and poor prognosis in many human cancers. However, the role of TAMs in human basal cell carcinoma (BCC) remains elusive. We found that the number of TAMs infiltrating the tumor is correlated with the depth of invasion, microvessel density, and COX-2 expression in human BCC cells. TAMs also aggregate near COX-2 expressing BCC tumor nests. We hypothesize that TAMs might activate COX-2 in BCC cells and subsequently increase their invasion and angiogenesis. TAMs are a kind of M2 macrophage derived from macrophages exposed to Th2 cytokines. M2-polarized macrophages derived from peripheral blood monocytes were cocultured with BCC cells without direct contact. Coculture with the M2 macrophages induced COX-2-dependent invasion and angiogenesis of BCC cells. Human THP-1 cell line cells, after treated with phorbol myristate acetate (PMA), differentiated to macrophages with M2 functional profiles. Coculture with PMA-treated THP-1 macrophages induced COX-2-dependent release of matrix metalloproteinase-9 and subsequent increased invasion of BCC cells. Macrophages also induced COX-2-dependent secretion of basic fibroblast growth factor and vascular endothelial growth factor-A, and increased angiogenesis in BCC cells. ? 2009 The Society for Investigative Dermatology.
SDGs
Other Subjects
cyclooxygenase 2; fibroblast growth factor; gelatinase B; immunoglobulin enhancer binding protein; mitogen activated protein kinase p38; phorbol 13 acetate 12 myristate; vasculotropin A; angiogenesis; article; basal cell carcinoma; carcinoma cell; cell invasion; controlled study; enzyme activation; human; human cell; major clinical study; priority journal; protein expression; tumor associated leukocyte
Publisher
Nature Publishing Group
Type
journal article