Association of adriamycin‐induced resistance to NK‐mediated lysis with sialic acid level and immunological reactivity of transferrin receptors and glycophorin A

Benoist, Hervé; Madoulet, Claudie; Trentesaux, Chantal; Carpentier, Y.; Joly, Philippe; Jardillier, Jean‐Claude; Desplaces, A

doi:10.1002/ijc.2910420227

Cited by 12 publications

(10 citation statements)

References 15 publications

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“…This synergy would be useful in clinical practice. Various chemotherapeutics might change sialic acid content, that in turn effect the NK and LAK sensitivity of target cells (Benoist 1988).…”

Section: Discussionmentioning

confidence: 99%

Lymphokine-activated killer cell susceptibility in epirubicin-resistant and parental human non-small cell lung cancer (NSCLC)

Özkan

2007

Biologia

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The aim of this study was to evaluate that: (i) epirubicin-HCl (EPI) and lymphokine-activated killer (LAK) cells cytotoxicity may be mediated by free radical generation; and (ii) resistant H1299 cells may be more sensitive to combined treatment of LAK cells plus EPI than the LAK or EPI treatment alone. Viability of H1299 cells treated with EPI, LAK and LAK plus EPI was measured using the MTT test. Amount of glutathione (GSH), protein content and enzymatic activity were measured by spectrophotometer. Glutathione S-transferase (GST)-pi expression in the cells was determined by western blot analysis. LAK plus EPI combined treatment increased susceptibility of H1299 WT and H1299 EPI(R) (300-fold EPI resistant) cells to LAK cell cytotoxicity. The resistance of H1299 EPI(R) cells to EPI appears to be associated with a developed tolerance to free radicals, most likely because of a 2-fold increase in NADPH-dependentcytochrome-P450 reductase (NADPH-CYP reductase) activity, 11-fold GST activity and 11-and 7-fold augmented selenium dependent and independent glutathione peroxidase (GSH-Px) activity, respectively. Amount of GST-pi in H1299 EPI(R) cells is statistically different from negative control and H1299 WT (p < 0.01). It is proposed that production of reactive oxygen species and hydrogen peroxide by the treatment of EPI and LAK cells can cause cytotoxicity of H1299 WT and H1299 EPI(R) cells. Superoxide dismutase, catalase, GSH-Px, GST, NADPH-CYP reductase and GSH must be considered as part of the intracellular antioxidant defense mechanism of H1299 WT and H1299 EPI(R) cells against reactive oxygen species. Combined treatment of EPI plus LAK cells caused the increasing cytotoxicity on the H1299 EPI(R) cells.

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Section: Discussionmentioning

confidence: 99%

Lymphokine-activated killer cell susceptibility in epirubicin-resistant and parental human non-small cell lung cancer (NSCLC)

Özkan

2007

Biologia

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“…Cytotoxicity Assay-The NK cell activity of PBL from healthy donors was tested in a standard 4-h 51 Cr release assay against target cells labeled with 51 Cr as described previously (20). Briefly, various numbers of PBL (effector cells) were mixed in triplicate with 10 4 labeled target cells in microtiter plates.…”

Section: Methodsmentioning

confidence: 99%

“…Recently, it has been established that resistance of K562 cells to NK cells can be correlated with an increase of glycophorin A on the cell surface (20,21). However, it has never been suggested that this glycoprotein was capable of protecting tumor cells against lysis by NK cells.…”

Section: Natural Killer (Nk)mentioning

confidence: 99%

Glycophorin A Protects K562 Cells from Natural Killer Cell Attack

Ouagari

Teissié

Benoist

1995

Journal of Biological Chemistry

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Glycophorin A is a protein with an abundant glycosylation (60% carbohydrate by weight), and studies have suggested that resistance of target cells to natural killing may be correlated with the level of glycophorin A expression. To assess the role of glycophorin A and of its carbohydrates in sensitivity to lysis by natural killer (NK) cells, the glycoprotein was inserted into the membrane of K562 target cells using electropulsation. Peripheral blood lymphocytes were used as effector cells. When glycophorin A was inserted into the membrane, the level of resistance to NK cell attack increased with the number of glycophorin A molecules electroinserted. The resistance to lysis was not due to a defect in target cell-effector cell binding. Electroassociation of glycophorin A did not cause a decrease in the expression of either "positive signals" for NK cells (such as CD71, CD15, and CD32 antigens) or cellular adhesion molecules (CD18, CD29, CD54, and CD58). Furthermore, electroinsertion of glycophorin A did not trigger any "negative signals," such as class I HLA antigen expression. Finally, it was shown that the sialic acid and O-linked oligosaccharides of glycophorin A did not play any role in its effect against NK cells. Conversely, the unique N-linked oligosaccharide was shown to be essential for resistance to occur.

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“…Erythroid differentiation of K562 cells was assessed by evaluating benzidine staining of the hemoglobinized erythroid cells (6). Glycophorin A (GPA) was detected by a n indirect staining method by using MoAb prepared at Centre Rene Huguenin (St Cloud, F).…”

Section: Methodsmentioning

confidence: 99%

“…Glycophorin A (GPA) was detected by a n indirect staining method by using MoAb prepared at Centre Rene Huguenin (St Cloud, F). FITClabelled F(ab'), goat antibody against mouse F(ab'), IgG (Coulter, Hialeah, FL, USA) was used a s the second-step reagent for indirect staining (6).…”

Section: Methodsmentioning

confidence: 99%

Alterations of growth fraction and DNA content in K562 cells by differentiating agents

et al. 1990

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The growth fraction, estimated by the monoclonal antibody Ki-67 labeling, and DNA content, assessed by ethidium bromide staining, were determined simultaneously in K562 leukemic cells by flow cytometry. A multiparametric analysis enabled the fraction of the cell population with GI, S, and G, + M contents in Ki-67-positive and Ki-67-negative cells to be evaluated.Butyric acid (BUT) was used as positive control. The fraction of Ki-positive cells decreased with the BUT concentration, while the proportion of cells with G, DNA content increased only in the Ki-negative cells.Adriamycin, aclacinomycin A, and fagaronine induced differentiation, as assessed by benzidine staining and glycophorin A expression. These drugs decreased the fraction of Ki-positive cells by more than 50% for both anthracyclines and by 25% for fagaronine. Following treatment, Ki-negative cells displayed a G,, but also a G, and a S DNA content in different proportions, indicating that induction of quiescent cells by differentiating agents is not a uniform process and is worthy of interest.Key terms: FCM, proliferation-associated antibody Ki-67, glycophorin A, erythroid differentiationIn cancer therapy, it is of interest to evaluate the tumour growth fraction (GF). It reflects the rate of tumour growth which is a factor of prognosis (8,16,29) and the fraction of cells sensitive to anticancer agents. Non-cycling cells have been described with a GI but also with a G2 and even an S DNA content, both in vitro (4,13,15) and in vivo (11); "recruitment" and "synchronizing" protocols will be better scheduled if the DNA content distributions of the proliferating and quiescent cells are known. A recent strategy in cancer chemotherapy has been to induce cell maturation and inhibit cell growth (21,23) without cell killing. In this case, it will be interesting to know precisely the cell cycle parameters, i.e., the GF and the DNA distributions of both cycling and non-cycling cells. Classical methods to determine GF by using radioactive DNA precursors (11,311, the bromodeoxyuridine (BrdU) antibody technique (3,27), or dye staining of both DNA and RNA (2,4,13) are difficult and time consuming. Recently, methods using monoclonal antibodies (MoAb) have been described. They are directed against human alpha DNA polymerase (11, a heterochromatin-associated antigen (MoAb 244-7) ( 5 ) , a proliferating cell nuclear matrix antigen (32), a nuclear antigen (M 150,000) (9), nuclear antigen p105 (161, the transferrin receptor (25), the ribonucleotide reductase M1 subunit (20), and especially a nuclear-matrix-associated proliferation-related antigen (MoAb Ki-67) (18,30). Different attempts were carried out to stain simultaneously cells with Ki-67 MoAb and propidium iodide (3,12,24). We used simultaneously Ki-67 and ethidium bromide (EB) and then separately measured the DNA content of cells according to their reactivity with Ki-67 MoAb.

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Association of adriamycin‐induced resistance to NK‐mediated lysis with sialic acid level and immunological reactivity of transferrin receptors and glycophorin A

Cited by 12 publications

References 15 publications

Lymphokine-activated killer cell susceptibility in epirubicin-resistant and parental human non-small cell lung cancer (NSCLC)

Lymphokine-activated killer cell susceptibility in epirubicin-resistant and parental human non-small cell lung cancer (NSCLC)

Glycophorin A Protects K562 Cells from Natural Killer Cell Attack

Alterations of growth fraction and DNA content in K562 cells by differentiating agents

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