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Cited by 434

The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.

Macrophages Induce Invasiveness of Epithelial Cancer Cells Via NF-κB and JNK

Open access
Hagemann, Thorsten, Wilson, Julia, Kulbe, Hagen, Li, Ningfeng Fiona, Leinster, David A, Charles, Kellie, Klemm, Florian, Pukrop, Tobias, Binder, Claudia, Balkwill, Frances R·2005·The Journal of Immunology
DOI 10.4049/jimmunol.175.2.1197
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Abstract

Tumor-associated macrophages may influence tumor progression, angiogenesis and invasion. To investigate mechanisms by which macrophages interact with tumor cells, we developed an in vitro coculture model. Previously we reported that coculture enhanced invasiveness of the tumor cells in a TNF-α- and matrix metalloprotease-dependent manner. In this report, we studied intracellular signaling pathways and induction of inflammatory genes in malignant cells under the influence of macrophage coculture. We report that coculture of macrophages with ovarian or breast cancer cell lines led to TNF-α-dependent activation of JNK and NF-κB pathways in tumor cells, but not in benign immortalized epithelial cells. Tumor cells with increased JNK and NF-κB activity exhibited enhanced invasiveness. Inhibition of the NF-κB pathway by TNF-α neutralizing Abs, an NF-κB inhibitor, RNAi to RelA, or overexpression of IκB inhibited tumor cell invasiveness. Blockade of JNK also significantly reduced invasiveness, but blockade of p38 MAPK or p42 MAPK had no effect. Cocultured tumor cells were screened for the expression of 22 genes associated with inflammation and invasion that also contained an AP-1 and NF-κB binding site. EMMPRIN and MIF were up-regulated in cocultured tumor cells in a JNK- and NF-κB-dependent manner. Knocking down either MIF or EMMPRIN by RNAi in the tumor cells significantly reduced tumor cell invasiveness and matrix metalloprotease activity in the coculture supernatant. We conclude that TNF-α, via NF-κB, and JNK induces MIF and EMMPRIN in macrophage to tumor cell cocultures and this leads to increased invasive capacity of the tumor cells.

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Metadata

Authors
Hagemann, T., Wilson, J., Kulbe, H., Li, N. F., Leinster, D. A., Charles, K., Klemm, F., Pukrop, T., Binder, C., & Balkwill, F. R.
Venue
The Journal of Immunology
Publisher
Oxford University Press (OUP)
Published
2005-07
Volume
175
Issue
2
Pages
1197-1205
ISSN
  • 0022-1767 (ISSN-L)
  • 1550-6606
DOI
10.4049/jimmunol.175.2.1197
OpenAlex
W2145400898
Cited by
434
References
5
FWCI
7.08
Type
journal article
Language
en
Open access
bronze

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