The murine Fc-gamma (Fcγ) receptor type II B1 is a tumorigenicity-enhancing factor in polyoma-virus-transformed 3T3 cells

Zusman, Tal; Gohar, Ofra; Eliassi, Ilan; Avivi, Y.; Lisansky, E.; Sautès, Catherine; Even, Jos; Bonnerot, Christian; Fridman, Wolf‐Herman; Witz, Isaac P.; Ran, Maya

doi:10.1002/(sici)1097-0215(19960117)65:2<221::aid-ijc16>3.0.co;2-g

Cited by 28 publications

(7 citation statements)

References 30 publications

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“…In our previous work, we observed that the expression of FcγRIIB in human melanoma was associated to inhibition of tumor development in nude mice and increased the therapeutic effect of anti‐tumor IgG in SCID mice 26. These observations are in apparent contradiction with our current results and previous studies showed that FcγRIIB1 expressed by polyoma‐virus‐transformed nonhematopoietic tumor confers an in vivo growth advantage to tumor cells and increases their malignancy when grafted subcutaneously in immunocompetent mice 36. One hypothesis to explain this discrepancy can be the different nature of the antibodies that mediate the anti‐tumor defenses in these studies.…”

Section: Discussioncontrasting

confidence: 98%

Selective expression of inhibitory Fcγ receptor by metastatic melanoma impairs tumor susceptibility to IgG‐dependent cellular response

Cassard

Cohen-Solal

Fournier

et al. 2008

Intl Journal of Cancer

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During melanoma progression, patients develop anti-tumor immunity including the production of anti-tumor antibodies. Although the strategies developed by malignant cells to escape anti-tumor cellular immunity have been extensively investigated, little is known about tumor resistance to humoral immunity. The main effect of IgG antibodies is to activate the immune response by binding to host Fc gamma receptors (FccR) expressed by immune cells. We previously reported in a limited study that some human metastatic melanoma cells ectopically express the FccRIIB1, an inhibitory isoform of FccR. By analyzing a large panel of different types of human primary and metastatic solid tumors, we report herein that expression of FccRIIB is restricted to melanoma and is acquired during tumor progression. We show that FccRIIB expression prevents the lysis of human metastatic melanoma cells by NK cell-mediated antibody-dependent cellular cytotoxicity (ADCC) in vitro, independently of the intracytoplasmic region of FccRIIB. Using experimental mouse models, we demonstrate that expression of FccRIIB protects B16F0 melanoma tumors from the ADCC induced by monoclonal and polyclonal anti-tumor IgG in vivo. Thus, our results identify FccRIIB as a marker of human metastatic melanoma that impairs the tumor susceptibility to FccR-dependent innate effector responses.

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Section: Discussioncontrasting

confidence: 98%

Selective expression of inhibitory Fcγ receptor by metastatic melanoma impairs tumor susceptibility to IgG‐dependent cellular response

Cassard

Cohen-Solal

Fournier

et al. 2008

Intl Journal of Cancer

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“…One such microenvironment-induced molecule with the capacity to confer a high malignancy phenotype upon mouse tumor cells was identified in our laboratory as an immunoglobulin receptor, the Fc-y receptor type lIB 1 (Ran et al, 1992;Zusman et al, 1996a and1996b). In an unpublished study, we identified the factor capable of inducing the expression of the Fc receptor to be an interferon-y, a cytokine known to be present in the microenvironment of several cancer types (Hess et aI., 2003;Lebel-Binay et aI., 2003).…”

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confidence: 86%

The Link Between Inflammation and Cancer

Dalgleish¹,

Haefner²

2006

Cancer Treatment and Research

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“…The work in our laboratory focuses on tumor-CMF interactions trying to identify genes whose expression is altered (induced/upregulated or silenced/downregulated) by CMF-mediated signaling as low malignancy tumor cells progress to a high malignancy phenotype [Zusman et al, 1996a;Katz et al, 1994Katz et al, , 1994Katz et al, -1995Witz et al, 1996;Halachmi and Witz, 1989;Ben-Baruch et al, 1992;Ran et al, 1991]. The approach undertaken has been to screen for microenvironmentregulated gene-products differentially expressed by tumor cells expressing either a high or a low malignancy phenotype [Katz et al, 1994;Witz et al, 1996;Halachmi and Witz, 1989].…”

Section: Microenvironment-regulated Genes and The Involvement Of Murimentioning

confidence: 99%

“…A comprehensive comparison in gene expression profiles of nonmetastatic and metastatic tumor cells has not been constructed as yet. However, numerous studies focusing on certain gene products that are likely to play a role in tumor progression toward metastasis have demonstrated differences in their expression between less and more progressed tumor cells [Zhang et al, 1997;Zusman et al, 1996a;Katz et al, 1994;Fidler et al, 1996;Witz et al, 1996]. Because tumor progression toward metastasis largely involves genes that control the social behavior of cancer cells such as adhesion, motility, invasiveness, and interaction with growth factors [Hakomori, 1996], these genes should be focused on.…”

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confidence: 99%

Differential expression of genes by tumor cells of a low or a high malignancy phenotype: The case of murine and human Ly-6 proteins

Witz¹

2000

J. Cell. Biochem.

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Progression of tumor cells toward a high malignancy phenotype and metastasis is a multi‐event cascade involving inter alia alterations in the expression of various genes. The focus of our laboratory is on genes whose altered expression may lead, directly or indirectly, to an increased malignancy phenotype. The identification of such genes and the evaluation of the consequences of their altered expression is essential for attempts to halt tumor progression and prevent metastasis formation. Published work originating in our laboratory showed that members of the murine Ly‐6 supergene family are involved in the progression of certain mouse tumors. The expression level of several members of this family was higher on highly malignant cells than on tumor cells expressing a lower malignancy phenotype. Sorting by flow cytometry of tumor cells to subpopulations expressing either high or low levels of Ly‐6E.1 yielded correspondingly cells expressing a high or a low malignancy phenotype. The high malignancy, high Ly‐6E.1‐expressing cells also expressed high levels of the receptor for urokinase plasminogen activator (uPAR), whereas low malignancy, low Ly‐6E.1‐expressing cells also expressed low levels of uPAR. Transfection studies indicated that uPAR was causally involved in conferring a high malignancy phenotype upon tumor cells expressing high levels of Ly‐6E.1. E48 is a human homologue of the murine ThB protein, a member of the Ly‐6 supergene family (but distinct from the Ly‐6E.1 protein mentioned above) and expressed on head and neck squamous carcinoma cells. Experiments currently in progress are aimed to find out whether E48 is involved in the progression of such cancer cells. Using the differential display technology, it was shown that ligation of E48 on tumor cells by the corresponding antibodies (serving as a surrogate for an as yet unidentified E48 ligand) upregulates an enzyme (FX) involved in the biosynthesis of GDP‐L‐fucose. Fucose is an essential component of certain selectin ligands. J. Cell. Biochem. Suppl. 34:61–66, 2000. © 2000 Wiley‐Liss, Inc.

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The murine Fc-gamma (Fcγ) receptor type II B1 is a tumorigenicity-enhancing factor in polyoma-virus-transformed 3T3 cells

Abstract: o 1996 Wiley-Liss, Inc.

Cited by 28 publications

References 30 publications

Selective expression of inhibitory Fcγ receptor by metastatic melanoma impairs tumor susceptibility to IgG‐dependent cellular response

Selective expression of inhibitory Fcγ receptor by metastatic melanoma impairs tumor susceptibility to IgG‐dependent cellular response

The Link Between Inflammation and Cancer

Differential expression of genes by tumor cells of a low or a high malignancy phenotype: The case of murine and human Ly-6 proteins

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