Tumour necrosis factor-α induces an increase in susceptibility of human glioblastoma U87-MG cells to natural killer cell-mediated lysis

Kondo, Sciji; Yin, Dali; Takeuchi, Juji; Morimura, Tatsuo; Si, Miyatake; Nakatsu, Shouji; Oda, Yoshifumi; Kikuchi, Hiroe

doi:10.1038/bjc.1994.123

Cited by 18 publications

(11 citation statements)

References 34 publications

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“…First, analysis of HLA-G gene transcriptional activity upon treatment with TNF-α or PMA, both of which stimulate NF-κ B activity, confirms previous data demonstrating that the HLA-G gene is not targeted by the classical NF-κ B pathway, thus excluding the presence of a putative functional target site outside the proximal promoter region of HLA-G. Secondly, we observed a decrease in HLA-G1 at the cell surface of three tumor cell lines treated with either TNF-α or PMA. This effect was specific to HLA-G, since expression of classical HLA class I molecules was enhanced, a result in agreement with previous work showing that TNF-α induces the expression of HLA class I molecules [71,72]. Third, we found an enhancement of intracytoplasmic HLA-G proteins in the three cell lines upon exposure to TNF-α and PMA.…”

Section: Discussionsupporting

confidence: 92%

Increase in HLA-G1 proteolytic shedding by tumor cells: a regulatory pathway controlled by NF-κB inducers

Zidi

Guillard

Marcou

et al. 2006

Cell. Mol. Life Sci.

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HLA-G is expressed by tumors, in which it contributes to the evasion of immunosurveillance. NF-kappaB appears to be a candidate for regulating HLA-G expression, since it is considered to be a hallmark of cancer. We investigated the role of NF-kappaB in modulating HLA-G expression in HLA-G-positive tumor cells, JEG-3 (choriocarcinoma), FON (melanoma), and M8-HLA-G1 (HLAG1-transfected melanoma). The treatment of tumor cells with two NF-kappaB inducers, tumor necrosis factor-alpha and phorbol 12-myristate 13-acetate, decreased HLA-G1 cell surface expression but increased intracytoplasmic HLA-G proteins. Reduction in HLA-G1 cell surface expression is driven by NF-kappaB and involves a proteolytic shedding process dependent on metalloproteinase activity. In contrast, an increase in intracytoplasmic HLA-G proteins involves post-transcriptional mechanisms that are independent of NF-kappaB. These results, and the fact that soluble HLA-G1 reduces the cytotoxicity of the NKL cell line, lead us to propose a novel regulatory pathway for HLA-G expression by tumor cells that may have particular relevance in tumor escape.

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Section: Discussionsupporting

confidence: 92%

Increase in HLA-G1 proteolytic shedding by tumor cells: a regulatory pathway controlled by NF-κB inducers

Zidi

Guillard

Marcou

et al. 2006

Cell. Mol. Life Sci.

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“…TNF treatment induces immune cell migration, 1,2) generates multiple cytokine responses, 3,5) and makes glioma cells susceptible to natural killer cell-mediated lysis. 48) These immunological responses would induce an in vivo bystander effect of Adv-IκBdN infection in the presence of TNF. Further investigations are needed to evaluate the in vivo efficacy of this system, including the bystander effect.…”

Section: U251 T-98gmentioning

confidence: 99%

Adenovirus‐mediated Gene Transduction of IkB or IkB Plus Bax Gene Drastically Enhances Tumor Necrosis Factor (TNF)‐induced Apoptosis in Human Gliomas

Shinoura¹,

Yamamoto²,

Yoshida³

et al. 2000

Japanese Journal of Cancer Research

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Tumor necrosis factor‐α (TNF), which was initially supposed to be a promising cancer therapeutic reagent, does not kill most types of cancer cells partly due to the activation of an anti‐apoptotic gene, NF‐kB. NF‐kB forms an inactive complex with the inhibitor kappa B alpha (IkBα), which is rapidly phosphorylated and degraded in response to various extracellular signals. To disrupt this protective mechanism, we introduced an inhibitor kappa B alpha (IkBdN) gene, a deletion mutant gene lacking the nucleotides for the N‐terminal 36 amino acids of IkBα, into human glioma cells (U251, T‐98G, and U‐373MG) via an adenoviral (Adv) vector in addition to treatment of the glioma cells with recombinant TNF. Immunohistochemical analysis revealed that NF‐kB was translocated to nuclei by TNF treatment in U251 and T‐98G cells, but not in U‐373MG cells. Neither transduction of IkBdN nor treatment with TNF protein alone induced apoptosis in U251 and T‐98G cells, whereas both cell lines underwent drastic TNF‐induced apoptosis after transduction of IkBdN. On the other hand, U‐373MG cells were refractory to TNF‐induced apoptosis even when they were transduced with the IkBdN gene. U‐373MG cells underwent drastically increased apoptosis when co‐transduced with the IkBdN and Bax gene in the presence of TNF. Adv‐mediated transfer of IkBdN or IkBdN plus Bax may be a promising therapeutic approach to treat gliomas through TNF‐mediated apoptosis.

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“…IFN-Á and TNF-· are known as potent inducers of MHC class II and ICAM-1 expression in a variety of normal and malignant cells, including carcinoma, melanoma and glioblastoma cells [8,10,13]. Since MHC and ICAM-1 molecules regulate the generation and recognition of NK and LAK cells, we tested the expression of these molecules on a different tumor, the teratocarcinoma Germa-2, in the present study.…”

Section: Discussionmentioning

confidence: 99%

“…In extensive studies conducted in the last 2 decades, it has been shown that the major histocompatibility complex (MHC) regulates the generation and recognition of cytotoxic T lymphocytes expressing the phenotype CD3+CD8+. The recognition and function of other cytotoxic cells, including natural killer (NK) cells and interleukin (IL)-2-activated NK (LAK) cells [5], are regulated by certain adhesion molecules including CD54/ ICAM-1 [6][7][8]. Furthermore, the expression of ICAM-1 molecules on a variety of normal as well as tumor cells can be increased by incubating cells with the cytokines IL-1, tumor necrosis factor (TNF)-· and interferon (IFN)-Á [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

“…The recognition and function of other cytotoxic cells, including natural killer (NK) cells and interleukin (IL)-2-activated NK (LAK) cells [5], are regulated by certain adhesion molecules including CD54/ ICAM-1 [6][7][8]. Furthermore, the expression of ICAM-1 molecules on a variety of normal as well as tumor cells can be increased by incubating cells with the cytokines IL-1, tumor necrosis factor (TNF)-· and interferon (IFN)-Á [8][9][10]. While adhesion molecules play an important role in the recognition of tumor cells by NK and LAK cells, the expression of MHC molecules on tumor cells reduces their susceptibility to lysis by these effector cells [6].…”

Section: Introductionmentioning

confidence: 99%

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The Effect of Interferon-γ and Tumor Necrosis Factor-α on the Expression of ICAM-1 and HLA-DR Molecules on Cells of a Human Germ Cell Neoplasm and Their Susceptibility to Lysis by Lymphokine-Activated Killer Cells

Eisenthal

Marder²,

Maymon³

et al. 1998

Pathobiology

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The ICAM-1 molecule plays a role in the interaction of NK cells with a variety of tumor cells, including carcinoma, melanoma and glioblastoma cells. In the present study, we analyzed the effect of IFN-γ and TNF-α on both the expression of HLA-DR and ICAM-1 molecules on HGCN (Germa-2), and on their susceptibility to lysis by LAK cells. Our results show that 1,000 U/ml IFN-γ induced a substantial increase in the expression of both ICAM-1 molecules and HLA-DR on the cell surface, while the effect of TNF-α on the expression of these molecules was substantially less prominent. When Germa-2 cells, previously exposed to 1,000 U/ml IFN-γ, were employed as target cells in a 4-hour ⁵¹Cr release assay, a statistically significant increase in the lysis by LAK cells was noted. These results show that in the presence of IFN-γ, Germa-2 tumor cells undergo modulation which affects both the expression of ICAM-1 and HLA-DR molecules as well as their susceptibility to lysis by LAK cells.

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Tumour necrosis factor-α induces an increase in susceptibility of human glioblastoma U87-MG cells to natural killer cell-mediated lysis

Cited by 18 publications

References 34 publications

Increase in HLA-G1 proteolytic shedding by tumor cells: a regulatory pathway controlled by NF-κB inducers

Increase in HLA-G1 proteolytic shedding by tumor cells: a regulatory pathway controlled by NF-κB inducers

Adenovirus‐mediated Gene Transduction of IkB or IkB Plus Bax Gene Drastically Enhances Tumor Necrosis Factor (TNF)‐induced Apoptosis in Human Gliomas

The Effect of Interferon-γ and Tumor Necrosis Factor-α on the Expression of ICAM-1 and HLA-DR Molecules on Cells of a Human Germ Cell Neoplasm and Their Susceptibility to Lysis by Lymphokine-Activated Killer Cells

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