Inhibitory effect of human fibroblast interferon (HuIFN-β) on the growth and invasive potential of cultured human melanoma cells in vitro

Fukuzawa, Kumiko; Horikoshi, Takashi

doi:10.1111/j.1365-2133.1992.tb00673.x

Cited by 15 publications

(10 citation statements)

References 21 publications

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“…It has been reported that murine IFN-y was more effective than murine IFN-{3 against BI6-FI0 melanoma (15). In our previous report, we showed that HuIFN-{3 exerted dosedependent inhibitory effects on SK-MEL-1l8 cells (3). In our present comparative study of three types of IFNs, HuIFN-{3 exerted the strongest antiproliferative effects against human melanoma cells!…”

Section: Discussionmentioning

confidence: 81%

In vitro Comparative Study of the Antitumor Effects of Human Interferon‐α, β and γ on the Growth and Invasive Potential of Human Melanoma Cells

Horikoshi¹,

Fukuzawa²,

Hanada³

et al. 1995

The Journal of Dermatology

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We have studied the effects of interferon (IFN)-alpha, beta, and gamma in vitro on the growth and invasive potential of human melanoma SK-MEL-118 cells. The antiproliferative effects of IFNs were assessed by a quantitative regrowth assay in which cells were treated with IFNs at concentrations of 10(2), 10(3) or 10(4) IU/ml for 3 days (until day 4) and then further incubated without IFNs for 7 days (until day 11). The growth inhibitory effect of each IFN on melanoma cells was dose- and time-dependent. Among these three types of IFNs, however, IFN-beta exerted the strongest inhibitory effect on cell growth. To assess the anti-invasive effect of each IFN on melanoma cells, we employed an in vitro assay system using matrigel-coated Transwell chambers. When cells were treated with 10(2), 10(3), or 10(4) IU/ml of the three types of IFNs for 24 hours, the amount of tritiated thymidine incorporated into melanoma cells were treated for 24 hours with 10(4) IU/ml of IFN-beta or gamma prior to the assay, the number of cells that invaded the filter decreased by 40%; this decrease was only 10% with the same amount of IFN-alpha. Simultaneous addition of IFNs during the invasion assay was not effective in any combination. Only when the cells were pretreated with IFNs, antiinvasive effects against melanoma cells were exerted. IFN-alpha was less inhibitory than IFN-beta or gamma on proliferation and not at all inhibitory on invasion. Considering both the antiproliferative and antiinvasive effects of IFNs, our results suggest that IFN-beta has the strongest antitumoral effect on human melanoma cells.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionmentioning

confidence: 81%

In vitro Comparative Study of the Antitumor Effects of Human Interferon‐α, β and γ on the Growth and Invasive Potential of Human Melanoma Cells

Horikoshi¹,

Fukuzawa²,

Hanada³

et al. 1995

The Journal of Dermatology

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“…Of these steps, STAT1 negatively regulates endothelial cell proliferation and tube formation. In contrast to type I IFNs, IFN-a and IFN-h, IFN-g does not inhibit endothelial cell migration (27,28). Endothelial cell proliferation and tube formation was inhibited by IFN-g even in the presence of the potent endothelial cell mitogen and differentiation factor, VEGF, in a STAT1-dependent manner.…”

Section: Discussionmentioning

confidence: 94%

Signal Transducer and Activator of Transcription 1 Activation in Endothelial Cells Is a Negative Regulator of Angiogenesis

Battle

Lynch²,

Frank³

2006

Cancer Research

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“…Treatment of melanoma cells with IFN-␤ elicits antiproliferative effects (35,36) and apoptosis (37). Some early reports noted increased melanogenesis in cultured melanomas in response to IFN-␤ (14, 38), but did not further characterize these effects.…”

Section: Discussionmentioning

confidence: 99%

Enhancement of Human Melanoma Antigen Expression by IFN-β

Dunn

Haggerty

Kono

et al. 2007

The Journal of Immunology

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Although many immunotherapeutic investigations have focused on improving the effector limb of the antitumor response, few studies have addressed preventing the loss of tumor-associated Ag (TAA) expression, associated with immune escape by tumors. We found that TAA loss from human melanomas usually results from reversible gene down-regulation, rather than gene deletion or mutation. Previously, we showed that inhibitors of MAPK-signaling pathways up-regulate TAA expression in melanoma cell lines. We have now identified IFN-β as an additional stimulus to TAA expression, including Melan-A/MART-1, gp100, and MAGE-A1. IFN-β (but neither IFN-α nor IFN-γ) augmented both protein and mRNA expression of melanocytic TAA in 15 melanoma lines (irrespective of initial Ag-expression levels). Treatment of low Ag melanoma lines with IFN-β increased expression of melanocyte-lineage Ags, inducing susceptibility to lysis by specific CTLs. Treatment with IFN-β also enhances expression of class I HLA molecules, thereby inducing both nominal TAA and the presenting HLA molecule. Data from fluorescent cellular reporter systems demonstrated that IFN-β triggers promoter activation, resulting in augmentation of Ag expression. In addition to enhancing TAA expression in melanomas, IFN-β also stimulated expression of the melanocytic Ag gp100 in cells of other neural crest-derived tumor lines (gliomas) and certain unrelated tumors. Because IFN-β is already approved for human clinical use in other contexts, it may prove useful as a cotreatment for augmenting tumor Ag expression during immunotherapy.

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Inhibitory effect of human fibroblast interferon (HuIFN-β) on the growth and invasive potential of cultured human melanoma cells in vitro

Cited by 15 publications

References 21 publications

In vitro Comparative Study of the Antitumor Effects of Human Interferon‐α, β and γ on the Growth and Invasive Potential of Human Melanoma Cells

In vitro Comparative Study of the Antitumor Effects of Human Interferon‐α, β and γ on the Growth and Invasive Potential of Human Melanoma Cells

Signal Transducer and Activator of Transcription 1 Activation in Endothelial Cells Is a Negative Regulator of Angiogenesis

Enhancement of Human Melanoma Antigen Expression by IFN-β

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