Further Studies on the Relationship Between Large Glycoprotein Molecules and Allotransplantability in the TA3 Tumor of the Mouse: Studies on Segregating TA3-Ha Hybrids23

Codington, John F.; Klein, George; Cooper, Amiel G.; Lee, Nora; Brown, Michael C.; Jeanloz, Roger W.

doi:10.1093/jnci/60.4.811

Cited by 35 publications

(21 citation statements)

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“…Indeed, transmembrane proteins with mucin-like domains have a common property: masking other cell surface molecules through steric hindrance. For instance, it has been proposed that masking of MHC molecules by epiglycanin results in a reduced immune response against cells expressing this protein (3,12).…”

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confidence: 99%

Ebolavirus Glycoprotein GP Masks both Its Own Epitopes and the Presence of Cellular Surface Proteins

Reynard

Borowiak

Volchkova

et al. 2009

J Virol

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Ebolavirus (EBOV) is the etiological agent of a severe hemorrhagic fever with a high mortality rate. The spike glycoprotein (GP) is believed to be one of the major determinants of virus pathogenicity. In this study, we demonstrated the molecular mechanism responsible for the downregulation of surface markers caused by EBOV GP expression. We showed that expression of mature GP on the plasma membrane results in the masking of cellular surface proteins, including major histocompatibility complex class I. Overexpression of GP also results in the masking of certain antigenic epitopes on GP itself, causing an illusory effect of disappearance from the plasma membrane.

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mentioning

confidence: 99%

Ebolavirus Glycoprotein GP Masks both Its Own Epitopes and the Presence of Cellular Surface Proteins

Reynard

Borowiak

Volchkova

et al. 2009

J Virol

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“…1B). The different growth rates of these cell sublines may be relevant to the biological function of epiglycanin, including the fact that epiglycanin functions as a barrier against immune attack as reported previously (25,26).…”

Section: Proliferation Of Ta3-ha and Ta3-st Cells In Vitro And In Vivomentioning

confidence: 54%

“…Carbohydrate moieties comprise 75% to 80% of the molecule by weight, essentially all of which comprises short O-glycans. Because of its length and high level of expression, epiglycanin has been suggested to have an immunosuppressive effect, including masking of cell surface molecules, such as class I MHC antigen (25)(26)(27). Epiglycanin is shed from the cell surface and can be detected in the ascites fluid and in the serum of mice.…”

Section: Introductionmentioning

confidence: 99%

Different Progression of Tumor Xenografts between Mucin-Producing and Mucin–Non-Producing Mammary Adenocarcinoma-Bearing Mice

Sugihara¹,

Yoshida²,

T³

et al. 2006

Cancer Research

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Previously, we found that MUC2 mucins could activate monocytes/macrophages through a scavenger receptor leading to cyclooxygenase (COX) 2 induction and overproduction of prostaglandin E 2 (PGE 2 ). To investigate the role of mucins in the tumor-bearing state, we compared s.c. tumor formation by using mucin-producing (TA3-Ha) and mucin-non-producing (TA3-St) cloned variants of mouse mammary adenocarcinomas. Expression of COX2 mRNA and protein and production of PGE 2 were elevated in peritoneal macrophages stimulated with epiglycanin, which is a mucin-like glycoprotein produced by TA3-Ha cells. S.c. tumor tissues comprising TA3-Ha cells grew much faster than tissues comprising TA3-St cells. COX2 protein and vascular endothelial growth factor in TA3-Ha tumor tissues were elevated compared with the TA3-St tumor tissues. Although similar numbers of macrophages were observed immunochemically in the two types of tumor tissues, COX2 was induced prominently in the infiltrating macrophages in TA3-Ha tumor tissues but only faintly in TA3-St tumor tissues. Furthermore, angiogenesis progressed remarkably in TA3-Ha tumor tissues but only slightly in TA3-St tumor tissues. Epiglycanin-induced overproduction of PGE 2 down-regulated interleukin-12 production by macrophages. IFN-;-producing CD4 T cells in spleens obtained from TA3-Ha tumor-bearing mice were significantly reduced compared with TA3-St tumor-bearing mice, suggesting that mucins cause PGE 2 -mediated immune suppression. Actually, the tumor growth of a TA3-Ha cell xenograft was suppressed effectively by oral administration of a COX2 inhibitor but that of a TA3-St cell one was not. These results suggest that mucins play an important role in tumor progression through overproduction of PGE 2 . (Cancer Res 2006; 66(12): 6175-82)

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“…In addition, epiglycanin has been suggested to mask class I major histocompatibility antigens and thus to be responsible for the ability of TA3Ha cells to grow in allogeneic mouse strains [5,6]. MAbs directed against epiglycanin are being used to quantitatively measure an epiglycanin cross-reacting antigen, designated HCA (human carcinoma antigen), in the ascites fluid and serum of carcinoma patients, including carcinomas of breast, lung, colon, prostate and ovaries, where it has been found to correlate with disease progression [32,33].…”

Section: Discussionmentioning

confidence: 99%

“…Epiglycanin has been suggested to mask surface molecules, in particular class I histocompatibility antigens, and thus is considered to be responsible for the ability of TA3Ha cells to grow in allogeneic mouse strains [5,6]. Epiglycanin has also been shown to be extremely potent in preventing cell-cell and cell-matrix adhesion, despite the expression of an intact E-cadherin/catenin complex and the presence of · 6 ß 4 integrins on TA3Ha cells [7].…”

Section: Introductionmentioning

confidence: 99%

Tumor-Host Interactions Regulate Glucocorticoid-Mediated Epiglycanin Expression in TA3Ha Murine Mammary Carcinoma Cells

Thingstad

Hilkens²

2003

Heart Drug

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The mucin-type glycoprotein epiglycanin is highly expressed on the cell surface of TA3Ha mouse mammary carcinoma cells if the cells are maintained by serial intraperitoneal passage in mice. We found that upon transfer of the cells to growth in vitro in medium supplemented with fetal bovine serum, the expression level of epiglycanin slowly diminished to less than 15% of that in vivo. Repassage of the cells in vivo fully restored the expression of epiglycanin. When TA3Ha cells were cultured in media supplemented with ascites fluid obtained from mice bearing these cells, the high expression level of epiglycanin was maintained. Ascites fluid-containing medium also restored the high expression level of epiglycanin in cells cultured for prolonged periods in vitro. Human ascites fluids obtained from patients with mammary and ovary carcinoma were likewise able to induce the expression of epiglycanin, in contrast to ascites fluids obtained from noncarcinoma patients or serum of healthy individuals. The factor responsible for the upregulation of epiglycanin is heat stable and can be removed from ascites fluids by activated charcoal, suggesting that it is a steroid. Indeed, dexamethasone, at a concentration of 10^–7 mol/l, induced maximal epiglycanin expression within 4 days, and upregulation was inhibited by the glucocorticoid receptor antagonist RU486. However, the maximal induction of epiglycanin expression achieved with ascites fluid was higher, while the kinetics of the induction was much slower, but still RU486 sensitive, than upon treatment with dexamethasone. These results suggest that stimulation of epiglycanin expression by ascites also involves a glucocorticoid. However, the induction in vivo is indirect and involves a cascade of events induced by tumor-host interactions that lead to glucocorticoid-mediated induction of epiglycanin.

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Further Studies on the Relationship Between Large Glycoprotein Molecules and Allotransplantability in the TA3 Tumor of the Mouse: Studies on Segregating TA3-Ha Hybrids23

Cited by 35 publications

References 0 publications

Ebolavirus Glycoprotein GP Masks both Its Own Epitopes and the Presence of Cellular Surface Proteins

Ebolavirus Glycoprotein GP Masks both Its Own Epitopes and the Presence of Cellular Surface Proteins

Different Progression of Tumor Xenografts between Mucin-Producing and Mucin–Non-Producing Mammary Adenocarcinoma-Bearing Mice

Tumor-Host Interactions Regulate Glucocorticoid-Mediated Epiglycanin Expression in TA3Ha Murine Mammary Carcinoma Cells

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