Enhanced metastases of a mouse carcinoma after <i>in vitro</i> treatment with murine interferon gamma

Ramani, P.; Balkwill, Frances R.

doi:10.1002/ijc.2910400621

Cited by 46 publications

(26 citation statements)

References 17 publications

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“…Consistent results were obtained in repeated experiments on LAK cells generated from patients with RCC, as well as those from [32]. On the other hand, it has also been reported that IFN-induced protection is observed without any increase in class I molecules [15,21]. Correlation between susceptibility to LAK cells and class I antigen expression on target cells is still controversial.…”

Section: Discussionsupporting

confidence: 70%

Interferon γ but not tumor necrosis factor α decreases susceptibility of human renal cell cancer cell lines to lymphokine-activated killer cells

Tomita

Watanabe

Kobayashi

et al. 1992

Cancer Immunol Immunother

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Human renal cell cancer (RCC) cell lines, ACHN and KRC/Y, with or without exposure to cytokines, were examined for their susceptibility to lymphokine-activated killer (LAK) cells. Flow-cytometric analysis demonstrated constitutional expression of class I antigen on both cell lines, which was enhanced by interferon alpha (IFN alpha), IFN gamma and tumor necrosis factor alpha (TNF alpha). A 4-h 51Cr-release cytotoxicity assay demonstrated that pretreatment of both cell lines with IFN gamma or IFN alpha, but not with TNF alpha, decreased their susceptibility to LAK cells. IFN gamma also decreased susceptibility to natural killer cells in a 16-h 51Cr-release cytotoxicity assay. IFN gamma treatment decreased the susceptibility of ACHN cells in a dose-dependent manner. "Cold"-target competition assay clearly showed that IFN gamma- but not TNF alpha-pretreated cells compete less effectively than do untreated target cells. Pretreatment with IFN gamma, however, increased expression of intercellular adhesion molecule-1 (ICAM-1) to a degree comparable to that with TNF alpha. Northern blot analyses using a 520-base-pair ICAM-1 cDNA as a probe demonstrated that more 3.3-kb mRNA is expressed in IFN gamma- and TNF alpha-pretreated cells. These results suggest that IFN gamma-treated RCC cell lines may reduce their ability to be recognized by LAK cells, and that IFN-induced protection of RCC cell lines against LAK cells may depend upon a mechanism independent of the expression of class I antigens or ICAM-1 on tumor cells.

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Section: Discussionsupporting

confidence: 70%

Interferon γ but not tumor necrosis factor α decreases susceptibility of human renal cell cancer cell lines to lymphokine-activated killer cells

Tomita

Watanabe

Kobayashi

et al. 1992

Cancer Immunol Immunother

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“…Although IFN-␥ should contribute to tumor-suppressive actions of IL-18 in vivo, antitumor functions of IL-18 have been observed in an IFN-␥-independent manner (31,32,34). It is noteworthy that under defined conditions, IFN-␥ in fact appears to be capable of enhancing growth of colon carcinomas (36). Induction of IL-18BP by IFN-␥ might contribute to this observation.…”

Section: Discussionmentioning

confidence: 94%

Expression and Release of IL-18 Binding Protein in Response to IFN-γ

Paulukat

Bosmann

Nold

et al. 2001

The Journal of Immunology

124

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IL-18 and IL-18 binding protein (IL-18BP) are two newly described opponents in the cytokine network. Local concentrations of these two players may determine biological functions of IL-18 in the context of inflammation, infection, and cancer. As IL-18 appears to be involved in the pathogenesis of Crohn’s disease and may modulate tumor growth, we investigated the IL-18/IL-18BPa system in the human colon carcinoma/epithelial cell line DLD-1. In this study, we report that IFN-γ induces expression and release of IL-18BPa from DLD-1 cells. mRNA induction and secretion of IL-18BPa immunoreactivity were associated with an activity that significantly impaired release of IFN-γ by IL-12/IL-18-stimulated PBMC. Inducibility of IL-18BPa by IFN-γ was also observed in LoVo, Caco-2, and HCT116 human colon carcinoma cell lines and in the human keratinocyte cell line HaCaT. Induction of IL-18BPa in colon carcinoma/epithelial cell lines was suppressed by coincubation with sodium butyrate. IFN-γ-mediated IL-18BPa and its suppression by sodium butyrate were confirmed in organ cultures of intestinal colonic biopsy specimens. In contrast, sodium butyrate did not modulate expression of IL-18. The present data suggest that IFN-γ may limit biological functions of IL-18 at sites of colonic immune activation by inducing IL-18BPa production. Down-regulation of IL-18BPa by sodium butyrate suggests that reinforcement of local IL-18 activity may contribute to actions of this short-chain fatty acid in the colonic microenvironment.

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“…IFN-γ inhibits metastasis of mouse ovarian and lung tumour cells (Ossina et al, 1997), renal adenocarcinoma cells (Yanagihara et al, 1994) and human non-small-cell lung cancer cells (Masumori et al, 1995). By contrast, it enhances experimental metastatic potential of colon 26 adenocarcinoma cells and B16 melanoma cells (Ramani and Balkwill, 1987). These results may be due to the time of treatment of the cells with IFN-γ, as suggested by some investigators (McMillan et al, 1987), or the properties of each cell line.…”

Section: Discussionmentioning

confidence: 96%

Suppression of metastasis-associated S100A4 gene expression by gamma-interferon in human colon adenocarcinoma cells

Takenaga

1999

Br J Cancer

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Summary S100A4 belongs to the S100 subfamily of calcium-binding proteins and has been suggested to be directly involved in invasion and metastasis of rodent and human tumour cells. The present study demonstrates that interferon gamma (IFN-γ), but not IFN-α and IFN-β, downregulates the S100A4 mRNA level in colon adenocarcinoma WiDr cells in time-and dose-dependent manners. The effect was not associated with any cytotoxicity and was specific for the S100A4 mRNA, since the levels of the S100A6 and GAPDH mRNAs were not significantly affected by the treatment. IFN-γ also strongly suppressed the S100A4 mRNA expression in HT-29 cells, but weakly in Colo201 cells. Flow cytometric analysis revealed that the level of the IFN-γ receptor expression in Colo201 cells was lower than that in WiDr and HT-29 cells, suggesting that the suppression of the S100A4 expression by IFN-γ depends on the amount of cell surface IFN-γ receptor protein. IFN-γ had no effect on the transcription rate of the S100A4 gene but reduced the stability of the S100A4 mRNA. WiDr cells treated with IFN-γ showed reduced motile ability, further supporting the assumption that the S100A4 gene product is involved in controlling cell motility.

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Enhanced metastases of a mouse carcinoma after in vitro treatment with murine interferon gamma

Cited by 46 publications

References 17 publications

Interferon γ but not tumor necrosis factor α decreases susceptibility of human renal cell cancer cell lines to lymphokine-activated killer cells

Interferon γ but not tumor necrosis factor α decreases susceptibility of human renal cell cancer cell lines to lymphokine-activated killer cells

Expression and Release of IL-18 Binding Protein in Response to IFN-γ

Suppression of metastasis-associated S100A4 gene expression by gamma-interferon in human colon adenocarcinoma cells

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