Both interferon (IFN) α and IFN γ inhibit histidine decarboxylase expression in the HT168 human melanoma cell line

Héninger, Erika; Falus, András; Darvas, Zsuzsanna; Szalai, Csaba; Zsinkó, M.; Pós, Zoltán; Hegyesi, Hargita

doi:10.1007/s000110050606

Cited by 14 publications

(6 citation statements)

References 24 publications

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“…The results are consistent with a previous report showing that IFN-g inhibited the expression of histidine decarboxylase in melanoma (Heninger et al, 2000).…”

Section: Resultssupporting

confidence: 93%

Histamine Inhibits the Production of Interferon-induced Protein of 10 kDa in Human Squamous Cell Carcinoma and Melanoma

Kanda

Watanabe

2002

Journal of Investigative Dermatology

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Interferon-induced protein of (IP-10) inhibits tumor progression. Tumor cells can produce interferon-induced protein of IP-10 in response to interferon-g. Histamine in the vicinity of tumor cells may sustain the tumor progression. We examined the in vitro effects of histamine on interferon-induced protein of IP-10 production in human squamous cell carcinoma and melanoma. Histamine suppressed interferon-g-mediated interferon-induced protein of IP-10 secretion and mRNA expression in SV40-transformed keratinocytes, SCC15, SCC4, and melanoma WM115, WM266-4, and C32. Histamine suppressed interferon-g-induced interferon-mediated protein of IP-10 promoter activation in these cells, and the interferon-stimulated response element on the promoter was responsible for the suppression. Histamine suppressed interferon-g-mediated transcription through the interferon-stimulated response element and signal transducer and activator of transcription 1alpha binding to the interferon-stimulated response element. Histamine suppressed interferon-g-induced tyrosine phosphorylation of the signal transducer and activator of transcription 1alpha, Janus tyrosine kinase 1, and Janus tyrosine kinase 2. Histamine-mediated suppression on the interferon-g-induced interferon-mediated protein of IP-10 synthesis was counteracted by the H2 receptor antagonist cimetidine, adenylate cyclase inhibitor SQ22536, and protein kinase A inhibitor H-89, but were not affected by H1 receptor antagonist mepyramine. Cimetidine, SQ22536, and H-89 also counteracted histamine-mediated suppression on the interferon-g-induced transcription through the interferon-stimulated response element, signal transducer and activator of transcription 1alpha binding to the interferon-stimulated response element, and tyrosine phosphorylation of the signal transducer and activator of transcription 1alpha, Janus tyrosine kinase 1, and Janus tyrosine kinase 2. Histamine increased intracellular 3',5'-adenosine cyclic monophosphate level and protein kinase A activity in squamous cell carcinoma and melanoma, and the effects of histamine were blocked by cimetidine. These results suggest that histamine may interact with H2 receptor on squamous cell carcinoma and melanoma and generate 3',5'-adenosine cyclic monophosphate, which may activate protein kinase A. The cyclic 3',5'-adenosine monophosphate/protein kinase A signaling pathway induced by histamine may inhibit interferon-g-induced signal transducer and activator of transcription 1alpha activation and suppress interferon-induced protein of IP-10 synthesis.

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“…The results are consistent with a previous report showing that IFN-g inhibited the expression of histidine decarboxylase in melanoma (Heninger et al, 2000).…”

Section: Resultssupporting

confidence: 93%

Histamine Inhibits the Production of Interferon-induced Protein of 10 kDa in Human Squamous Cell Carcinoma and Melanoma

Kanda

Watanabe

2002

Journal of Investigative Dermatology

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“…A more indirect way of in¯uencing melanoma growth by locally produced histamine is by its suppression of the production of IFN-g by surrounding immune cells (e.g., T lymphocytes and natural killer cells; Horva Âth et al, 1999), which effectively impairs their antitumor activity and contributes to escape of melanoma cells from immunosurveillance. Interestingly, IFN-g in turn decreases HDC expression (Heninger et al, 2000). These reciprocal effects re¯ect a highly complex regulatory network acting in the close microenvironment of melanoma cells.…”

Section: Resultsmentioning

confidence: 99%

Suppression of Melanoma Cell Proliferation by Histidine Decarboxylase Specific Antisense Oligonucleotides

Hegyesi

Somlai²,

Varga

et al. 2001

Journal of Investigative Dermatology

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Histidine decarboxylase (HDC) is expressed by the cells of melanoma, in which the histamine content tends to be relatively high. This study shows that elevated expression of HDC was found by western blot analysis of primary and metastatic melanoma tissue using a polyclonal HDC specific antibody. The specificity of anti-HDC antibody was confirmed by inhibition of HDC translation (i.e., immunopositivity) in melanoma cells by HDC-specific antisense oligonucleotide. Moreover, the decrease in proliferation caused by HDC antisense oligonucleotides indicates considerable functional relevance of histamine synthesis in melanoma growth and suggests a possible in situ application of specific antisense oligonucleotides for HDC in melanoma therapy.

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“…It has been shown that there is a regulation loop between interleukin 6 (IL-6) and histamine: histamine increased IL-6 expression and secretion in metastatic lines via the H 1 R, and IL-6 treatment increased the HDC and histamine content in primary melanoma lines (Lázar-Molnar et al, 2002). Interferon-gamma (IFN-gamma) produced by surrounding immune cells decreases HDC expression, affecting melanoma growth and also impairs antitumour activity of the immune system, then contributing to the escape of melanoma cells from immunosurveillance (Horváth et al, 1999;Heninger et al, 2000). Furthermore, www.intechopen.com mast cell activation initiates upon ultraviolet-B irradiation, which triggers histamine secretion acts as a cellular immunity suppressor (Chang et al, 2006).…”

Section: Histamine Receptors In Melanomamentioning

confidence: 99%

Histamine Receptors as Potential Therapeutic Targets for Cancer Drug Development

Medina¹,

Lamas²,

Brenzoni³

et al. 2011

Drug Development - A Case Study Based Insight Into Modern Strategies

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Both interferon (IFN) α and IFN γ inhibit histidine decarboxylase expression in the HT168 human melanoma cell line

Abstract: Since previously the inhibitory effect of histamine on gene expression of interferon gamma was detected, a reciprocal inhibition between histamine and IFNgamma is proposed.

Cited by 14 publications

References 24 publications

Histamine Inhibits the Production of Interferon-induced Protein of 10 kDa in Human Squamous Cell Carcinoma and Melanoma

Histamine Inhibits the Production of Interferon-induced Protein of 10 kDa in Human Squamous Cell Carcinoma and Melanoma

Suppression of Melanoma Cell Proliferation by Histidine Decarboxylase Specific Antisense Oligonucleotides

Histamine Receptors as Potential Therapeutic Targets for Cancer Drug Development

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