Interferons Inhibit Tumor Necrosis Factor-α-mediated Matrix Metalloproteinase-9 Activation via Interferon Regulatory Factor-1 Binding Competition with NF-κB

Sancëau, Josiane; Boyd, Douglas D.; Seiki, Motoharu; Bauvois, Brigitte

doi:10.1074/jbc.m202959200

Cited by 99 publications

(84 citation statements)

References 49 publications

(82 reference statements)

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“…Similar data are available for MMPs (26,27), whose control by genetic (29) and pharmacological means (30) has been shown to inhibit the aggressiveness of experimental melanoma. However, information on the control of these proteases by inflammatory cytokines in tumor cells is still limited, and an inconsistency in the trend is seen in the present information (31)(32)(33)(34)(35)(36)(37)(38).…”

Section: Introductionmentioning

confidence: 56%

Cytokine-dependent invasiveness in B16 murine melanoma cells: Role of uPA system and MMP-9

et al. 2006

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Abstract. Proteases are crucial for the spread of cancer cells from a primary tumor to the site of secondary growth. This study examined the ability of IFNÁ and TNF· to stimulate a better invasiveness in B16 murine melanoma cells, and investigated whether this enhanced ability was related to a higher expression of protease activities, such as urokinase plasminogen activator (uPA) and its receptor (uPAR), and matrix metalloproteinases 2 and 9 (MMP-2, MMP-9). We found that murine melanoma cells enhanced their lungcolonizing potential in vivo and invasiveness through Matrigel-coated filters upon costimulation with IFNÁ and TNF·; neither IFNÁ nor TNF· alone, at the dose used in the experiments, was able to elicit a change in the invasive/ metastatic efficiency of melanoma cells. The invasive phenotype of murine melanoma cells stimulated with IFNÁ and TNF· was characterized by an enhanced uPA/uPAR and MMP-9 expression: TNF· promoted MMP-9 mRNA expression and pro-MMP-9 protein secretion, and the costimulation with IFNÁ and TNF· was required to potentiate the expression of mRNA and protein for uPAR, and to induce a redistribution of uPA from the soluble to the cell bodyassociated form. Both monoclonal antibodies, anti-uPAR and anti-MMP-9, caused a significant reduction of invasiveness in IFNÁ/TNF·-stimulated melanoma cells. These results indicate that invasiveness in B16 murine melanoma cells can be regulated in a cytokine-specific fashion and is dependent on the synergism between the uPA/uPAR system and MMP-9.

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Section: Introductionmentioning

confidence: 56%

Cytokine-dependent invasiveness in B16 murine melanoma cells: Role of uPA system and MMP-9

et al. 2006

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“…The cDNAs for human b 2 -microglobulin, ACE and TACE were amplified by PCR, and primers were designed according to published sequences (Costerousse et al, 1993;Satoh et al, 2000;Sanceau et al, 2002). b 2 -Microglobulin cDNA (165 bp) was amplified using the sense primer 5 0 -CAT CCA GCG TAC TCC AAA GA-3 0 and the antisense primer 5 0 -GAC AAG TCT GAA TGC TCC AC-3 0 .…”

Section: Flow Cytometry Analysismentioning

confidence: 99%

“…Following cell stimulation with IFNg (1000 U/ml) for 16 h, total cell extracts were prepared, separated on 12% polyacrylamide-sodium dodecyl sulphate gels, transferred to nitrocellulose and blotted as described (Sanceau et al, 2002). Membranes were hybridized with Abs for IRF1 and actin as described (Sanceau et al, 2002) using chemiluminescence technique developed by Santa Cruz.…”

Section: Western Blot Analysismentioning

confidence: 99%

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Differential regulation of tumor necrosis factor-α-converting enzyme and angiotensin-converting enzyme by type I and II interferons in human normal and leukemic myeloid cells

et al. 2006

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The transmembrane metalloproteases angiotensin-converting enzyme (ACE) and tumor necrosis factor-a (TNF-a)-converting enzyme (TACE/ADAM-17) have been associated with inflammation, cancer progression and angiogenesis. Few investigations into the regulation of these enzymes by physiological stimuli have been reported. In this study, we investigated the influence of interferons (IFNs) type I (a, b) and II (c) on ACE and TACE expression of human leukemic NB4 cells and monocytes.We assessed the expression of proteases by reverse transcriptase-polymerase chain reaction, enzyme-linked immunosorbent assay and immunofluorescence analyses. IFNc, but not type I IFNs, upregulated membrane ACE in a dose-and time-dependency and this was reflected by the increase of ACE enzymatic activity and ACE mRNA. ACE upregulation was dependent on protein synthesis. Treatment of the interferon responsive factor 1 (IRF1)-unresponsive HepG2 cell line with IFNc did not affect ACE expression, thus suggesting the participation of the IRF1 signaling pathway in IFNc-mediated ACE upregulation in myeloid cells. In contrast, both types of IFNs, in a dose-and time-dependent manner, downregulated surface TACE without affecting TACE transcript. Soluble TACE was not detected in the medium of IFN-treated cells. IFNc-mediated decrease of surface TACE in NB4 cells was reversible, and correlated with an increase in intracellular TACE, suggesting that cell surface TACE was internalized in response to IFNs. These findings, showing the presence of IFN-dependent controlled mechanisms by which ACE and TACE levels are regulated in human normal and leukemic myeloid cells, may have implications in the context of current investigations on the therapeutic potential of IFNs.

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“…Although the mechanisms are not clear, it has been reported that IFNs inhibit TNF-a-mediated MMP-9 activation via IFN regulatory factor-1 binding competition with NF-jB. 39 Therefore, TL -pulsed DCs induce CTL in cancer tissues, which produce IFNs, inhibit MMP-9 activation and may lead to apoptosis of cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Combination therapy with tumor‐lysate pulsed dendritic cells and antiangiogenic drug TNP‐470 for mouse pancreatic cancer

Miyazaki

Tsuzuki

Matsuzaki

et al. 2005

Intl Journal of Cancer

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Most cases of pancreatic cancer are inoperable when diagnosed. Since immunotherapy and antiangiogenic therapy have been reported to be promising for pancreatic cancer, we examined whether the combination of immunotherapy with dendritic cells (DCs) and the antiangiogenic drug TNP-470 induces tumor regression. Syngeneic mouse pancreatic adenocarcinoma cells were orthotopically inoculated into C57/BL6 mice. DCs with or without tumor lysate (TL) were administered i.p. at 4 and 5 weeks. TNP-470 was injected s.c. into tumor-bearing mice every other day from 4 weeks to 6 weeks. We compared anticancer effects in 6 groups: NT (no treatment), DC/TL2 (DCs without TL), DC/TL1 (DCs pulsed with TL), TNP (TNP-470 alone), DC/TL-TNP (DC/TL2 plus TNP-470) and DC/TL1TNP (DC/TL1 plus TNP-470). We measured tumor volume, mean vascular density (MVD) and vessel diameter by FITC-dextran using an intravital microscope; degrees of proliferation and apoptosis of cancer cells by PCNA and TUNEL; infiltrating lymphocytes and expression levels of VEGF and MMP-9 by immunohistochemistry and immunoblotting. Tumor volume and MVD were significantly suppressed in the treatment groups with prolonged survival rate, especially in the DC/TL1TNP group. There were no significant differences in apoptosis among the 6 groups except DC/TL1. The number of infiltrating CD4 1 cells in the DC/TL1 group was higher than that in the NT group. VEGF expression was significantly suppressed in the treatment groups containing TNP-470, and MMP-9 was also suppressed in the groups containing DC/TL1. Our data suggested that TL-pulsed DCs combined with TNP-470 induced regression of mouse pancreatic cancer, possibly through induction of immune responses and suppression of angiogenesis. ' 2005 Wiley-Liss, Inc.

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Interferons Inhibit Tumor Necrosis Factor-α-mediated Matrix Metalloproteinase-9 Activation via Interferon Regulatory Factor-1 Binding Competition with NF-κB

Cited by 99 publications

References 49 publications

Cytokine-dependent invasiveness in B16 murine melanoma cells: Role of uPA system and MMP-9

Cytokine-dependent invasiveness in B16 murine melanoma cells: Role of uPA system and MMP-9

Differential regulation of tumor necrosis factor-α-converting enzyme and angiotensin-converting enzyme by type I and II interferons in human normal and leukemic myeloid cells

Combination therapy with tumor‐lysate pulsed dendritic cells and antiangiogenic drug TNP‐470 for mouse pancreatic cancer

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