Prostaglandins Regulate Melanoma-Induced Cytokine Production in Macrophages

Eisengart, Charles A.; Mestre, Juan R.; Naama, Hassan A.; Mackrell, Peter J.; Rivadeneira, David E.; Murphy, Erin M.; Stapleton, Philip P.; Daly, J.M.

doi:10.1006/cimm.2000.1686

Cited by 36 publications

(13 citation statements)

References 26 publications

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“…3E) or surrounding tumor lesions. This is in accordance with recent findings that describe the production of murine TNF-␣ after stimulation with melanoma-conditioned medium (56) or IL-18 (57). TNF-␣ production by monocytes/macrophages after activation is well known (51).…”

Section: Discussionsupporting

confidence: 92%

Low-Level Monocyte Chemoattractant Protein-1 Stimulation of Monocytes Leads to Tumor Formation in Nontumorigenic Melanoma Cells

Nesbit

Schaider

Miller

et al. 2001

The Journal of Immunology

206

162

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Tumors commonly produce chemokines for recruitment of host cells, but the biological significance of tumor-infiltrating inflammatory cells, such as monocytes/macrophages, for disease outcome is not clear. Here, we show that all of 30 melanoma cell lines secreted monocyte chemoattractant protein-1 (MCP-1), whereas normal melanocytes did not. When low MCP-1-producing melanoma cells from a biologically early, nontumorigenic stage were transduced to overexpress the MCP-1 gene, tumor formation depended on the level of chemokine secretion and monocyte infiltration; low-level MCP-1 secretion with modest monocyte infiltration resulted in tumor formation, whereas high secretion was associated with massive monocyte/macrophage infiltration into the tumor mass, leading to its destruction within a few days after injection into mice. Tumor growth stimulated by monocytes/macrophages was due to increased angiogenesis. Vessel formation in vitro was inhibited with mAbs against TNF-α, which, when secreted by cocultures of melanoma cells with human monocytes, induced endothelial cells under collagen gels to form branching, tubular structures. These studies demonstrate that the biological effects of tumor-derived MCP-1 are biphasic, depending on the level of secretion. This correlates with the degree of monocytic cell infiltration, which results in increased tumor vascularization and TNF-α production.

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Section: Discussionsupporting

confidence: 92%

Low-Level Monocyte Chemoattractant Protein-1 Stimulation of Monocytes Leads to Tumor Formation in Nontumorigenic Melanoma Cells

Nesbit

Schaider

Miller

et al. 2001

The Journal of Immunology

206

162

View full text Add to dashboard Cite

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“…COX-2 is upregulated in a high percentage of common human cancers and is associated with invasive and metastatic tumor behavior [1]. Studies have shown that COX-2 promotes carcinogenesis and growth of established tumors [2] by PG-induced immunosuppression, affecting mitogenesis, regulating cellular adhesion and tumor cell growth, inhibiting apoptosis, promoting angiogenesis, converting procarcinogens to carcinogens, modulating inflammation, and increasing tumor cell invasiveness [1,[5][6][7]. Increased levels of COX-2 have been identified in malignancies such as colon, lung, breast, brain, gastric, prostate, cervix, head, and neck cancers and in pancreatic adenocarcinomas.…”

Section: Introductionmentioning

confidence: 99%

Cyclooxygenase-2 expression in human irradiated uveal melanomas

et al. 2007

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“…Growing evidence suggests that COX-2-derived PGE 2 augments synthesis of IL-6 in activated macrophages [13 -15], monocytes [16], smooth muscle cells [17], human gingival fibroblasts [18], and human osteoblasts [19]. Since COX-2 has been shown to be upregulated by CD40-CD154 interactions in other cell types and IL-6 is a known product of the CD40-mediated signaling pathway in endothelial cells, we asked whether CD40-CD154 interactions could trigger COX-2 protein expression in HUVEC and more importantly whether COX-2 derived prostanoids, such as PGE 2 , could be responsible for the accompanying IL-6 induction in this in vitro cell system.…”

Section: Introductionmentioning

confidence: 99%