BIOMAT Database Logo BIOMAT Database Logo

Modulation of the growth of transformed cells by human tumor necrosis factor-alpha and interferon-gamma. 1987

G D Lewis, and B B Aggarwal, and T E Eessalu, and B J Sugarman, and H M Shepard
Department of Pharmacological Sciences, Genentech, Inc., South San Francisco, California 94080.

Recombinant human tumor necrosis factor-alpha (rHuTNF-alpha) inhibited growth of the cervical carcinoma cell line, ME-180neo, at doses greater than 50 units/ml, but stimulated the growth of these cells at low doses (0.1-10 units/ml). ME-180neo variants selected for resistance to the cytotoxic effects of rHuTNF-alpha retained the ability to be growth stimulated at all concentrations tested. ME-180neo cells and the rHuTNF-alpha-resistant ME-180neo variants possessed equivalent steady state numbers of TNF-alpha receptors with similar Kd values. Recombinant human interferon-gamma (rHuIFN-gamma) augmented the rHuTNF-alpha-induced cytotoxic response of ME-180neo cells and overcame the resistance of the ME-180neo variants to rHuTNF-alpha cytotoxicity. In separate experiments we were able to show that the number of TNF-alpha binding sites on both rHuTNF-alpha-sensitive and -resistant ME-180neo cells was similar and was increased by treatment with rHuIFN-gamma. These results suggest that the growth stimulation of tumor cells mediated by rHuTNF-alpha can be dissociated from the cytotoxic response and that these responses are not related to the number or affinity of TNF-alpha binding sites.

UI MeSH Term Description Entries
D007371 Interferon-gamma The major interferon produced by mitogenically or antigenically stimulated LYMPHOCYTES. It is structurally different from TYPE I INTERFERON and its major activity is immunoregulation. It has been implicated in the expression of CLASS II HISTOCOMPATIBILITY ANTIGENS in cells that do not normally produce them, leading to AUTOIMMUNE DISEASES. Interferon Type II,Interferon, Immune,gamma-Interferon,Interferon, gamma,Type II Interferon,Immune Interferon,Interferon, Type II
D007700 Kinetics The rate dynamics in chemical or physical systems.
D011956 Receptors, Cell Surface Cell surface proteins that bind signalling molecules external to the cell with high affinity and convert this extracellular event into one or more intracellular signals that alter the behavior of the target cell (From Alberts, Molecular Biology of the Cell, 2nd ed, pp693-5). Cell surface receptors, unlike enzymes, do not chemically alter their ligands. Cell Surface Receptor,Cell Surface Receptors,Hormone Receptors, Cell Surface,Receptors, Endogenous Substances,Cell Surface Hormone Receptors,Endogenous Substances Receptors,Receptor, Cell Surface,Surface Receptor, Cell
D011994 Recombinant Proteins Proteins prepared by recombinant DNA technology. Biosynthetic Protein,Biosynthetic Proteins,DNA Recombinant Proteins,Recombinant Protein,Proteins, Biosynthetic,Proteins, Recombinant DNA,DNA Proteins, Recombinant,Protein, Biosynthetic,Protein, Recombinant,Proteins, DNA Recombinant,Proteins, Recombinant,Recombinant DNA Proteins,Recombinant Proteins, DNA
D002455 Cell Division The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION. M Phase,Cell Division Phase,Cell Divisions,Division Phase, Cell,Division, Cell,Divisions, Cell,M Phases,Phase, Cell Division,Phase, M,Phases, M
D002460 Cell Line Established cell cultures that have the potential to propagate indefinitely. Cell Lines,Line, Cell,Lines, Cell
D002471 Cell Transformation, Neoplastic Cell changes manifested by escape from control mechanisms, increased growth potential, alterations in the cell surface, karyotypic abnormalities, morphological and biochemical deviations from the norm, and other attributes conferring the ability to invade, metastasize, and kill. Neoplastic Transformation, Cell,Neoplastic Cell Transformation,Transformation, Neoplastic Cell,Tumorigenic Transformation,Cell Neoplastic Transformation,Cell Neoplastic Transformations,Cell Transformations, Neoplastic,Neoplastic Cell Transformations,Neoplastic Transformations, Cell,Transformation, Cell Neoplastic,Transformation, Tumorigenic,Transformations, Cell Neoplastic,Transformations, Neoplastic Cell,Transformations, Tumorigenic,Tumorigenic Transformations
D002583 Uterine Cervical Neoplasms Tumors or cancer of the UTERINE CERVIX. Cancer of Cervix,Cancer of the Cervix,Cancer of the Uterine Cervix,Cervical Cancer,Cervical Neoplasms,Cervix Cancer,Cervix Neoplasms,Neoplasms, Cervical,Neoplasms, Cervix,Uterine Cervical Cancer,Cancer, Cervical,Cancer, Cervix,Cancer, Uterine Cervical,Cervical Cancer, Uterine,Cervical Cancers,Cervical Neoplasm,Cervical Neoplasm, Uterine,Cervix Neoplasm,Neoplasm, Cervix,Neoplasm, Uterine Cervical,Uterine Cervical Cancers,Uterine Cervical Neoplasm
D005260 Female Females
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man

Related Publications

G D Lewis, and B B Aggarwal, and T E Eessalu, and B J Sugarman, and H M Shepard
Growth inhibition of human endothelial cells by human recombinant tumor necrosis factor alpha and interferon-gamma.
August 1994, Tumori,
G D Lewis, and B B Aggarwal, and T E Eessalu, and B J Sugarman, and H M Shepard
Protein myristoylation in human mononclear phagocytes: modulation by interferon-gamma and tumor necrosis factor-alpha.
December 1991, Journal of cell science,
G D Lewis, and B B Aggarwal, and T E Eessalu, and B J Sugarman, and H M Shepard
Modulation of human melanoma cells by interleukin-4 and in combination with gamma-interferon or alpha-tumor necrosis factor.
April 1991, Cancer research,
G D Lewis, and B B Aggarwal, and T E Eessalu, and B J Sugarman, and H M Shepard
Modulation of fibronectin production in normal human melanocytes and malignant melanoma cells by interferon-gamma and tumor necrosis factor-alpha.
April 1989, The American journal of pathology,
G D Lewis, and B B Aggarwal, and T E Eessalu, and B J Sugarman, and H M Shepard
Inhibition of growth of normal and human papillomavirus-transformed keratinocytes in monolayer and organotypic cultures by interferon-gamma and tumor necrosis factor-alpha.
March 1995, The American journal of pathology,
G D Lewis, and B B Aggarwal, and T E Eessalu, and B J Sugarman, and H M Shepard
Rat liver macrophages express the 55 kDa tumor necrosis factor receptor: modulation by interferon-gamma, lipopolysaccharide and tumor necrosis factor-alpha.
April 1994, Biological chemistry Hoppe-Seyler,
G D Lewis, and B B Aggarwal, and T E Eessalu, and B J Sugarman, and H M Shepard
Inhibition of chlamydia trachomatis growth by human interferon-alpha: mechanisms and synergistic effect with interferon-gamma and tumor necrosis factor-alpha.
August 2005, Biomedical research (Tokyo, Japan),
G D Lewis, and B B Aggarwal, and T E Eessalu, and B J Sugarman, and H M Shepard
Tumor necrosis factor-alpha and interferon-gamma modulation of nitric oxide and allograft survival.
July 1995, The Journal of surgical research,
G D Lewis, and B B Aggarwal, and T E Eessalu, and B J Sugarman, and H M Shepard
[Apoptosis of cultured human trophoblasts induced by tumor necrosis factor-alpha and interferon-gamma].
August 1999, Zhonghua fu chan ke za zhi,
G D Lewis, and B B Aggarwal, and T E Eessalu, and B J Sugarman, and H M Shepard
Effect of interferon alpha, interferon gamma and tumor necrosis factor on the procoagulant activity of human cancer cells.
January 1993, Haematologica,
Copied contents to your clipboard!