Detection of human glioma-associated antigen by rat monoclonal antibody raised against syngeneic rat glioma cells

1986 ◽  
Vol 65 (4) ◽  
pp. 495-502 ◽  
Author(s):  
Hideyuki Saya ◽  
Takashi Masuko ◽  
Takashi Kokunai ◽  
Hideo Yagita ◽  
Akihiro Ijichi ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Cultured Cells ◽  
Periodic Acid ◽  
Glioma Cells ◽  
Immunoperoxidase Staining ◽  
Low Grade ◽  
Human Tissues ◽  
Human Glioma ◽  
Content Type ◽  
Rat Glioma

✓ A monoclonal antibody termed “FR77” was obtained from a hybridoma clone established by fusion between P3x63Ag8.653 mouse myeloma cells and spleen cells of a Fischer F344 rat hyperimmune to syngeneic 9L/R3 glioma cells. Immunoperoxidase staining of various cultured cells showed that FR77 was reactive to both rat and human glioma cells, but was not reactive with other nonglioma cells. Immunohistochemical examination of paraffin-embedded or cryostat-frozen sections of various human tissues revealed that FR77 was strongly reactive with glioblastoma, grade III astrocytoma, and craniopharyngioma; partially reactive with intracerebral primitive neuroectodermal tumor, pineoblastoma, and desmoplastic medulloblastoma; and weakly reactive with low-grade astrocytoma. It was not reactive with other types of brain tumors and normal human tissues tested. The FR77-defined antigen was observed to be predominantly localized in the cytoplasm of antigen-bearing cells as suggested by the immunostaining pattern, but part of it was also expressed on the cell surface of glioma cells as demonstrated by a complement-mediated cytotoxic test. Fractionation of the antigenic component and periodic acid treatment of tumor tissue bearing the FR77-defined antigen indicated that the antigen is of a neutral glycolipid nature and that the antigenic determinant to FR77 is present on its sugar portion.

Antigen related to cell proliferation in malignant gliomas recognized by a human monoclonal antibody

1990 ◽  
Vol 73 (6) ◽  
pp. 901-908 ◽  
Author(s):  
Takashi Kokunai ◽  
Norihiko Tamaki ◽  
Satoshi Matsumoto
Keyword(s):  
Monoclonal Antibody ◽  
Cell Proliferation ◽  
Cultured Cells ◽  
Human Monoclonal Antibody ◽  
Malignant Gliomas ◽  
Fetal Brain ◽  
Glioma Cells ◽  
Normal Brain ◽  
Human Glioma ◽  
Brain Tissues

✓ A human monoclonal antibody (CLN-IgG) was produced from a human-human hybridoma derived from lymphocytes of a patient with cervical carcinoma. The reactivities of this antibody with various human glioma tissues and cultured glioma cells and the characterization of the antigen recognized by CLN-IgG on malignant glioma cells were analyzed and reported. CLN-IgG reacted with various human glioma cells and glioma tissues, especially glioblastoma, but did not react with normal brain tissues or fetal brain tissues. A large amount of antigen recognized by CLN-IgG was expressed on cell membranes of undifferentiated glioma cells and of glioma cells at the G2/M tumor growth phase in cycling cells. Antigen recognized by CLN-IgG was detected in only one of seven samples of cyst fluid, and was not detected in 27 serum samples or 18 samples of cerebrospinal fluid from glioma patients. CLN-IgG exhibited antibody-dependent cell cytotoxicity against U-251MG glioma cells and primary cultured cells of glioblastomas and anaplastic astrocytomas. These data suggest that the antigen recognized by CLN-IgG might be related to cell proliferation in malignant gliomas. Thus, CLN-IgG might be useful for immunotherapy or immunoimaging of malignant gliomas.

Cell cycle arrest and astrocytic differentiation resulting from PTEN expression in glioma cells

1999 ◽  
Vol 91 (5) ◽  
pp. 822-830 ◽  
Author(s):  
Jun-ichi Adachi ◽  
Katsumi Ohbayashi ◽  
Tomonari Suzuki ◽  
Tomio Sasaki
Keyword(s):  
Expression System ◽  
Biological Significance ◽  
Glioma Cells ◽  
Genetic Alterations ◽  
Pten Expression ◽  
Human Glioma ◽  
Wild Type ◽  
Content Type ◽  
Astrocytic Differentiation ◽  
Fine Print

Object. Genetic alterations of the PTEN gene (also known as MMAC1 or TEP1) have frequently been identified in high-grade gliomas, indicating that inactivation of PTEN plays a crucial role in human glioma progression. The aim of this study was to assess the biological significance of PTEN inactivation in the development of glioma.Methods. The authors introduced wild-type PTEN complementary DNA into four human glioma cell lines (T98G, U-251MG, U-87MG, and A172) containing endogenous aberrant PTEN alleles. The number of colonies transfected with the wild-type PTEN was reduced to 15 to 32% of those found after transfection of a control vector, suggesting growth suppression by the exogenous PTEN. To analyze phenotypic alterations produced by PTEN expression, T98G-derived clones with inducible PTEN expression were further established using a tetracycline-regulated inducible gene expression system. Induction of PTEN expression suppressed the in vitro growth of T98G cells with accumulation of G1 phase cells. Furthermore, when cells were cultured in the presence of the extracellular matrix (ECM), PTEN expression caused distinct morphological changes, with multiple and elongated cytoplasmic processes similar to those of normal astrocytes. The level of glial fibrillary acidic protein, an intermediate protein specifically expressed in differentiated astrocytes, was upregulated concomitantly.Conclusions. These findings strongly indicate that exogenous PTEN expression inhibits the proliferation of glioma cells by inducing G1 arrest and elicits astrocytic differentiation in the presence of the ECM. Inactivation of PTEN would play an important role in the enhancement of unregulated growth of undifferentiated glioma cells.

scholarly journals Establishment of a Monoclonal Antibody against CD81 that Decreases the Proliferation of Rat Glioma Cells

2014 ◽  
Vol 23 (1) ◽  
pp. 131-134 ◽  
Author(s):  
Erika Fujimoto ◽  
Hiroki Mori ◽  
Motoharu Takehara ◽  
Miyuki Tanaka ◽  
Toshitaka Ohashi ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Glioma Cells ◽  
Rat Glioma

Differential effects of vincristine and phenytoin on the proliferation, migration, and invasion of human glioma cell lines

1995 ◽  
Vol 82 (6) ◽  
pp. 1035-1043 ◽  
Author(s):  
Jörg-Christian Tonn ◽  
Hans Kristian Haugland ◽  
Jaakko Saraste ◽  
Klaus Roosen ◽  
Ole Didrik Laerum
Keyword(s):  
Cell Lines ◽  
Glioma Cell ◽  
Glioma Cells ◽  
Migration And Invasion ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Content Type ◽  
Glioma Cell Lines ◽  
Dose Dependent ◽  
Fine Print

✓ The aim of this study was to investigate the antimigratory and antiinvasive potential of vincristine sulfate (VCR) on human glioma cells and to analyze whether phenytoin (5,5-diphenylhydantoin; DPH) might act synergistically with VCR. Vincristine affects the cytoplasmic microtubules; DPH has been reported to enhance VCR cytotoxicity in murine cells. In two human glioma cell lines, GaMG and D-37MG, we found VCR to reduce monolayer growth and colony formation in a dose-dependent fashion at concentrations of 10 ng/ml and above. Phenytoin increased the cytotoxic and cystostatic effects of VCR in monolayer cells but not in spheroids. Multicellular spheroids were used to investigate directional migration. A coculture system of GaMG and D-37MG spheroids with fetal rat brain aggregates was used to analyze and quantify tumor cell invasion. A dose-dependent inhibition of migration and invasion by VCR was observed in both cell lines without further enhancement by DPH. Immunofluorescence microscopy with antibodies against α-tubulin revealed dose-dependent morphological alterations in the microtubules when the cells were exposed to VCR but not after incubation with DPH. Based on the combination of standardized in vitro model systems currently in use and the present data, the authors strongly suggest that VCR inhibits migration and invasion of human glioma cells. This is not altered by DPH, which inhibits cell proliferation in combination with VCR.

scholarly journals Enhanced apoptosis following treatment with TRA-8 anti-human DR5 monoclonal antibody and overexpression of exogenous Bax in human glioma cells

Gene Therapy ◽  
2004 ◽  
Vol 11 (8) ◽  
pp. 658-667 ◽  
Author(s):  
S Kaliberov ◽  
M A Stackhouse ◽  
L Kaliberova ◽  
T Zhou ◽  
D J Buchsbaum
Keyword(s):  
Monoclonal Antibody ◽  
Glioma Cells ◽  
Human Glioma ◽  
Human Glioma Cells

TAMI-47. MIR-542-3P CONTRIBUTES TO THE HK2-MEDIATED HIGH GLYCOLYTIC PHENOTYPE IN HUMAN GLIOMA CELLS

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi208-vi208
Author(s):  
Junhyung Kim ◽  
Min Woo Park ◽  
Ju Won Ahn ◽  
Jeong Min Sim ◽  
Suwan Kim ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Cellular Proliferation ◽  
Glioma Cells ◽  
Low Grade ◽  
High Grade ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Glycolytic Activity ◽  
High Grade Gliomas ◽  
Glycolytic Phenotype

Abstract BACKGROUND The elevation of glucose metabolism is linked to high-grade gliomas such as glioblastoma multiforme (GBM). The high glycolytic phenotype is associated with cellular proliferation and resistance to treatment with chemotherapeutic agents in GBM. MicroRNA-542-3p (miR-542-3p) has been implicated in several tumors including gliomas. However, the role of miR-542-3p in glucose metabolism in human gliomas remains unclear. METHODS We measured the levels of cellular proliferation in human glioma cells. We measured the glycolytic activity in miR-542-3p knockdown and over-expressed human glioma cells. We measured the levels of miR-542-3p and HK2 in glioma tissues from patients with low- and high-grade gliomas using imaging analysis. RESULTS We show that knockdown of miR-542-3p significantly suppressed cellular proliferation in human glioma cells. Knockdown of miR-542-3p suppressed HK2-induced glycolytic activity in human glioma cells. Consistently, over-expression of miR-542-3p increased HK2-induced glycolytic activity in human glioma cells. The levels of miR-542-3p and HK2 were significantly elevated in glioma tissues of patients with high-grade gliomas relative to that in low-grade gliomas. The elevation of HK2 levels in patients with high-grade gliomas were positively correlated with the high levels of miR-542-3p in GBM and low-grade gliomas (LGG) based on the datasets from the Cancer Genome Atlas (TCGA) database. Moreover, the high levels of miR-542-3p were associated with poor survival rate in the TCGA database. CONCLUSIONS miR-542-3p contributes to the HK2-mediated high glycolytic phenotype in human glioma cells.

Enhancement of C2-ceramide antitumor activity by small interfering RNA on X chromosome—linked inhibitor of apoptosis protein in resistant human glioma cells

2004 ◽  
Vol 101 (1) ◽  
pp. 119-127 ◽  
Author(s):  
Manabu Hatano ◽  
Masaaki Mizuno ◽  
Jun Yoshida
Keyword(s):  
Small Interfering Rna ◽  
Glioma Cells ◽  
Inhibitor Of Apoptosis ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Content Type ◽  
Inhibitor Of Apoptosis Protein ◽  
Apoptosis Protein ◽  
Interfering Rna ◽  
Fine Print

Object. Many human glioma cells are resistant to ceramide. In this study the authors investigated the mechanisms of that resistance and considered ways to overcome it. Methods. The authors first administered C2-ceramide (N-acetylsphingosine) to human glioma cells from rare cell lines susceptible to C2-ceramide (SKMG1 and U87MG) and other cell lines resistant to it (U251SP, T98G, SKAO2, and U251MG). Following this, the authors analyzed the statuses of transduction signals such as cell viability, morphological changes, caspases, mitochondrial membrane potential, apoptosis-inducing factor, oligonucleosomal DNA fragmentation, and the inhibitor of apoptosis protein (IAP) family. Conclusions. Ceramide resistance was found to arise from the inhibition of caspase-7 induced by IAPs, especially X chromosome—linked IAP (XIAP). Small interfering RNA (siRNA) on XIAP quenched that resistance in ceramide-resistant human glioma cells (U251SP, T98G, SKAO2, U251MG), indicating that a siRNA for XIAP may be a useful tool for overcoming the resistance to ceramide in human glioma cells.

Specific induction of ACNU-resistance in V79 Chinese hamster cells and C6 rat glioma cells

1987 ◽  
Vol 67 (4) ◽  
pp. 553-557 ◽  
Author(s):  
Yukio Horie ◽  
Kenji Arai ◽  
Shunro Endoh ◽  
Toshio Kuroki ◽  
Akira Takaku
Keyword(s):  
Alkylating Agents ◽  
Lethal Dose ◽  
Chinese Hamster ◽  
Glioma Cells ◽  
Specific Effect ◽  
Cellular Level ◽  
Content Type ◽  
Chinese Hamster Cells ◽  
Rat Glioma ◽  
Resistant Mutants

✓ The antitumor compound ACNU (1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride) is widely used for treatment of malignant brain tumors. The authors have investigated the mechanism of acquisition of ACNU resistance at the cellular level by isolating ACNU-resistant mutants from V79 Chinese hamster cells and C6 rat glioma cells after treatment of the cells with ACNU or other alkylating agents. In V79 Chinese hamster cells, ACNU at 1 to 4 µg/ml caused dose-dependent induction of drug-resistant mutants to ACNU (10 µg/ml) and 8-azaguanine (20 µg/ml), but not to ouabain (1 mM). Values for the mean lethal dose of ACNU-resistant mutants were 2.4 to 17.2 times those of the parent V79 cells. The ACNU-resistant phenotype was stable during an observation period of 13 weeks. The ACNU seemed to have a specific effect in inducing ACNU-resistant mutations, because no ACNU-resistant mutations were induced by treatment of the cells with other known mutagens, such as N-methyl-N′-nitro-N-nitrosoguanidine, methylmethanesulfonate, and ethylmethanesulfonate. The C6 rat glioma cells also showed a significant mutagenic response to ACNU, producing ACNU- and 5-fluorouracil-resistant mutants. The present results have the important therapeutic and mechanistic implication that ACNU is a potent mutagen and induces mutants that are resistant to ACNU and to other drugs.

The studies on monoclonal antibody SZ-39 against human glioma cells

1989 ◽  
Vol 1 (4) ◽  
pp. 5-10
Author(s):  
Yang Weilian ◽  
Du Ziwei ◽  
Li Peixia ◽  
Ruan Changgeng
Keyword(s):  
Monoclonal Antibody ◽  
Glioma Cells ◽  
Human Glioma ◽  
Human Glioma Cells

Characterization of neuroectodermal antigen by a monoclonal antibody and its application in CSF diagnosis of human glioma

1988 ◽  
Vol 68 (3) ◽  
pp. 449-455 ◽  
Author(s):  
Toshihiko Wakabayashi ◽  
Jun Yoshida ◽  
Hisao Seo ◽  
Kyoto Kazo ◽  
Yoshiharu Murata ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Monoclonal Antibody ◽  
Brain Tumors ◽  
Cell Lines ◽  
Glioma Cell ◽  
Glioma Cell Line ◽  
Human Glioma ◽  
Content Type ◽  
Sds Page ◽  
Fine Print

✓ Monoclonal antibodies were produced by immunization of the human glioma cell line SK-MG-4. One of the antibodies, designated G-22, reacted with 18 of 20 glioma cell lines, two melanoma cell lines, and three lung cancer cell lines, but not with 39 cell lines derived from sarcoma, carcinoma, or hematopoietic tumors. The antigen was expressed in the brain of human fetuses in early gestation (9 weeks) but not in late gestation (8 months) or in normal adult brain, suggesting that the antibody recognizes neural differentiation antigens expressed by neuroectodermal origin. A high incidence of positive antigens has been observed in gliomas but not in the other neural tumors, such as ependymomas, meningiomas, and neuroblastomas. Thus, the antigen defined by the G-22 monoclonal antibody could be defined as glioma-associated antigen. Pulse-labeling with tritiated leucine and subsequent immunoprecipitation of the solubilized cell membrane revealed that the antigen recognized by this antibody had a molecular weight of 67 kD on sodium dodecyl sulfate-poly-acrylamide gel electrophoresis (SDS-PAGE). It was shown by dot-blot enzyme-linked immunospecific assay (ELISA) that the antigen could be detected in the cerebrospinal fluid (CSF) from patients with gliomas. From analysis of affinity chromatography and SDS-PAGE, the antigen present in the CSF had a molecular weight similar to that of a 1% Nonidet P-40 (NP-40) extract from a glioma cell line. When the antigen in CSF was quantitatively assayed by ELISA, the mean antigen level (expressed as optical density at 450 nm) in the CSF of seven patients was 0.8 ± 0.28 (mean ± standard deviation), which was significantly higher than the 0.38 ± 0.14 level observed in the CSF of 15 patients with nonglioma brain tumors and the 0.23 ± 0.09 level in the CSF of four patients without brain tumors. These results indicate that the monoclonal antibody G-22 is useful for the diagnosis of glioma.

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