CHARACTERIZATION OF AN OXIDATION-RESISTANT TUMOR-CELL LINE AND ITS SENSITIVITY TO IMMUNE-RESPONSE AND CHEMOTHERAPY

被引：6

作者：

SAURI, H ^{[1
]}

KIM, AT ^{[1
]}

SHAU, HY ^{[1
]}

机构：

[1] UNIV CALIF LOS ANGELES, SCH MED, JONSSON COMPREHENS CANC CTR, LOS ANGELES, CA 90024 USA

来源：

JOURNAL OF SURGICAL RESEARCH | 1995年 / 58卷 / 05期

关键词：

D O I：

10.1006/jsre.1995.1083

中图分类号：

R61 [外科手术学];

学科分类号：

摘要：

Aerobic cells have several scavenger systems for protection from reactive oxygen species (ROS). We developed an ROS-resistant variant of the human erythroleukemic cell line K562 by culturing cells in glucose oxidase to produce hydrogen peroxide. Testing the activity of the scavenger systems for ROS showed these cells had a 25- to 28-fold increase in catalase activity. We therefore termed this variant cell line K562-CAT. There was no similar increase in glutathione content or activity of superoxide dismutase and glutathione peroxidase. To determine what effect the increased catalase activity would have on the immune response to these tumor cells, we compared K562 and K562-CAT sensitivity to tumor necrosis factor-alpha (TNF alpha) activated polymorphonuclear neutrophil (PMN), natural killer (NK), and lymphokine-activated killer (LAK) cells. K562-CAT showed a significant increase in resistance to TNF alpha-activated PMN but not to NK or LAK, confirming the role of ROS in the former but not the latter. We also tested K562-CAT sensitivity to cisplatin and mitomycin C, agents known to involve ROS in their cytotoxic mechanism. There was no increased resistance in K562-CAT compared to parental K562, indicating that catalase is not involved in tumor cell resistance to those drugs. Given the characteristics of its resistance to the immune response, K562-CAT or a similar catalase-hyperexpressing cell line could be useful in determining the significance of TNF alpha-activated PMN in antitumor defenses. (C) 1995 Academic Press, Inc.

引用

页码：526 / 535

页数：10

共 60 条

[41]

Hiraishi H., Terano A., Ota S., Mutoh H., Sugimoto T., Razandi M., Antioxidant defenses of cultured gastric cells against oxygen metabolites: Role of GSH redox cycle and endogenous catalase, Am. J. Physiol, 261, (1991)

[42]

Suttorp N., Toepfer W., Roka L., Antioxidant defense mechanisms of endothelial cells: Glutathione redox cycle versus catalase, Am. J. Physiol, 251, (1986)

[43]

Kinnula V.L., Mangum J.B., Chang L.Y., Crapo J.D., Antioxidant defense mechanisms in cultured pleural mesothelial cells, Am. J. Respir. Cell Mol. Biol, 7, (1992)

[44]

Harlan J.M., Levine J.D., Callahan K.S., Schwartz B.R., Harker L.A., Glutathione redox cycle protects cultured endothelial cells against lysis by extracellularly generated hydrogen peroxide, J. Clin. Invest, 73, (1984)

[45]

Zimmerman R.J., Marafino B.J., Chan A., Landre P., Winkelhake J.L., The role of oxidant injury in tumor cell sensitivity to recombinant human tumor necrosis factor in vivo: Implications for mechanisms of action, J. Immunol, 142, (1989)

[46]

Zimmerman R.J., Chan A., Leadon S.A., Oxidative damage in murine tumor cells treated in vitro by recombinant human tumor necrosis factor, Cancer Res, 49, (1989)

[47]

Shau H., Roberts R.L., Tumor necrosis factor stimulation of neutrophils for anti tumor activity, Granulocyte Responses to Cytokines, (1992)

[48]

Russo A., Degraff W., Friedman N., Mitchell J.B., Selective modulation of glutathione levels in human normal versus tumor cells and subsequent differential response to chemotherapy drugs, Cancer Res, 46, (1986)

[49]

Spitz D.R., Phillips J.W., Adams D.T., Sherman C.M., Deen D.F., Li G.C., Cellular resistance to oxidative stress is accompanied by resistance to cisplatin: The significance of increased catalase activity and total glutathione in hydrogen peroxide-resistant fibroblasts, J. Cell. Physiol, 156, (1993)

[50]

Ueta E., Umazume M., Yamamoto T., Osaki T., Enhancement of polymorphonuclear (PMN) function by OK-432, Int. J. Immunopharmacol, 16, (1994)

← 1 2 3 4 5 6 →