Copper transport and kinetics in cultured C6 rat glioma cells

1995 ◽  
Vol 269 (4) ◽  
pp. C892-C898 ◽  
Author(s):  
Y. Qian ◽  
E. Tiffany-Castiglioni ◽  
E. D. Harris
Keyword(s):  
Membrane Fraction ◽  
Glioma Cells ◽  
Maximum Velocity ◽  
C6 Cells ◽  
Michaelis Constant ◽  
Rat Glioma ◽  
Saturation Kinetics ◽  
Efflux Mechanism ◽  
Import And Export ◽  
P Type

C6 rat glioma cells accumulate and efflux 67Cu. Both processes showed saturation kinetics with increasing 67Cu concentration. The Michaelis constant (Km) for uptake was 0.63 +/- 0.14 microM; maximum velocity (Vmax) was 3.29 +/- 0.57 pmol Cu.mg protein-1.min-1. The Km for efflux was 0.15 +/- 0.06 microM; Vmax was 1.08 +/- 0.71 pmol Cu.mg protein-1.min-1. p-Chloromercuribenzoate (p-CMB) totally blocked 67Cu efflux but had no effect on Km or Vmax of uptake. Total 67Cu in the cell after 50 min was partitioned equally between particulate and soluble fractions. p-CMB-treated cells accumulated more 67Cu, but < 10% was bound to the particulate (membrane) fraction. Pb also increased 67Cu accumulation without affecting Km and Vmax of 67Cu uptake. These data suggest that carriers for import and export of Cu in C6 cells are distinct or operate in two different cellular environments. Efflux is a sulfhydryl-dependent process subject to inhibition by Pb. The data are consistent with a P-type ATPase in the efflux of Cu from cells and the potential for Pb to inhibit the efflux mechanism.

Invading C6 glioma cells maintaining tumorigenicity

1995 ◽  
Vol 83 (4) ◽  
pp. 665-671 ◽  
Author(s):  
Michael R. Chicoine ◽  
Daniel L. Silbergeld
Keyword(s):  
Cell Line ◽  
Tumor Cells ◽  
Frontal Lobe ◽  
Glioma Cells ◽  
C6 Glioma Cells ◽  
C6 Cells ◽  
Contralateral Hemisphere ◽  
Rat Glioma ◽  
C6 Cell Line ◽  
Cells Cultured

✓ To characterize rat glioma cell invasion, 2 × 106 fluorophore-labeled or transfection-labeled C6 rat glioma cells were implanted in the rat frontal lobe. Eighty percent of the rats implanted formed bulk tumors (3–4 mm in diameter). Two weeks after implantation, fluorescence microscopy revealed single tumor cells in sites over 16 mm from the bulk brain tumor. Tumor cells distant from the bulk tumor remained single without mass formation and invaded primarily along white matter tracts. Two weeks after tumor implantation, three cell lines were created from each brain by disaggregation and initiation in culture of 1) bulk tumor, 2) contralateral hemisphere, and 3) cerebellum; all disaggregated specimens generated viable cultures. Cells cultured from the contralateral hemisphere were morphologically indistinguishable from cells from the bulk tumor and from the original C6 cell line. Cells cultured from the cerebellum were morphologically quite distinct from the C6 cell line. Cells from disaggregated specimens obtained from the tumor, contralateral hemisphere, and cerebellum were implanted in the frontal lobe of naive rats to test tumorgenicity. Bulk tumor formed in 58% of the rats implanted with specimens from tumor, in 75% of the rats implanted with specimens from contralateral hemisphere, and in only 12.5% of the rats implanted with specimens from the cerebellar hemispheres. Experiments using C6 cells labeled by transfection with the p3′ss DNA vector prior to implantation confirmed that the cells cultured from the contralateral hemisphere were derived from the implanted C6 cells. Experiments with C6 cells anchored in agar served to verify that movement to the contralateral hemisphere was secondary to parenchymal invasion rather than dispersion in the cerebrospinal fluid.

Quantitative Analysis of Glutathione S-Transferase in Human Brain Tumors, C6 Rat Glioma Cells, and Drug Resistant C6 Cells

1991 ◽  
pp. 281-287 ◽  
Author(s):  
Yoshihito Matsumoto ◽  
Noboru Sasaoka ◽  
Takahiro Tsuchida ◽  
Takashi Fujiwara ◽  
Takashi Ohmoto
Keyword(s):  
Quantitative Analysis ◽  
Brain Tumors ◽  
Human Brain ◽  
Glioma Cells ◽  
Drug Resistant ◽  
C6 Cells ◽  
Glutathione S Transferase ◽  
Rat Glioma ◽  
Human Brain Tumors

Zinc Induces Apoptosis That Can Be Suppressed by Lanthanum in C6 Rat Glioma Cells

2001 ◽  
Vol 382 (8) ◽  
pp. 1227-1234 ◽  
Author(s):  
Hajo Haase ◽  
Wim Wätjen ◽  
Detmar Beyersmann
Keyword(s):  
Membrane Potential ◽  
Protein Kinase ◽  
Mitochondrial Membrane Potential ◽  
Mammalian Cells ◽  
Mitochondrial Membrane ◽  
Glioma Cells ◽  
Zinc Uptake ◽  
Zinc Toxicity ◽  
C6 Cells ◽  
Rat Glioma

Abstract Zinc ions have both essential and toxic effects on mammalian cells. Here we report the ability of zinc to act as an inducer of apoptosis in C6 rat glioma cells. Incubation with 150 to 300 M ZnCl2 caused cell death that was characterized as apoptotic by internucleosomal DNA fragmentation, formation of apoptotic bodies, nuclear fragmentation and breakdown of the mitochondrial membrane potential. On the other hand, zinc deprivation by the membrane permeable chelator TPEN [N,N,N,N,tetrakis (2-pyridylmethyl)ethylenediamine] also induced programmed death in this cell line, indicating the existence of intracellular zinc levels below and above which apoptosis is induced. Zincinduced apoptosis in C6 cells was independent of major signaling pathways (protein kinase C, mitogen activated protein kinase and guanylate cyclase) and protein synthesis, but was increased by facilitating zinc uptake with the ionophore pyrithione. Lanthanum(III)chloride was also able to increase the net zinc uptake, but nevertheless apoptotic features and zinc toxicity were reduced. Remarkably, lanthanum suppressed the zincinduced breakdown of the mitochondrial membrane potential. We conclude that in C6 cells lanthanum acts in two different ways, as a promoter of net zinc uptake and as a suppressor of zincinduced apoptosis.

Radiosensitivity of glioma to Gamma Knife treatment enhanced in vitro and in vivo by RNA interfering Ku70 that is mediated by a recombinant adenovirus

2010 ◽  
Vol 113 (Special_Supplement) ◽  
pp. 228-235 ◽  
Author(s):  
Qiang Jia ◽  
Yanhe Li ◽  
Desheng Xu ◽  
Zhenjiang Li ◽  
Zhiyuan Zhang ◽  
...  
Keyword(s):  
Western Blot ◽  
Gamma Knife ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Glioma Cells ◽  
C6 Glioma ◽  
C6 Glioma Cells ◽  
C6 Cells

Object The authors sought to evaluate modification of the radiation response of C6 glioma cells in vitro and in vivo by inhibiting the expression of Ku70. To do so they investigated the effect of gene transfer involving a recombinant replication-defective adenovirus containing Ku70 short hairpin RNA (Ad-Ku70shRNA) combined with Gamma Knife treatment (GKT). Methods First, Ad-Ku70shRNA was transfected into C6 glioma cells and the expression of Ku70 was measured using Western blot analysis. In vitro, phenotypical changes in C6 cells, including proliferation, cell cycle modification, invasion ability, and apoptosis were evaluated using the MTT (3′(4,5-dimethylthiazol-2-yl)2,5-diphenyltetrazolium bromide) assay, Western blot analysis, and cell flow cytometry. In vivo, parental C6 cells transfected with Ad-Ku70shRNA were implanted stereotactically into the right caudate nucleus in Sprague-Dawley rats. After GKS, apoptosis was analyzed using the TUNEL (terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick-end labeling) method. The inhibitory effects on growth and invasion that were induced by expression of proliferating cell nuclear antigen and matrix metalloproteinase–9 were determined using immunohistochemical analyses. Results The expression of Ku70 was clearly inhibited in C6 cells after transfection with Ad-Ku70shRNA. In vitro following transfection, the C6 cells showed improved responses to GKT, including suppression of proliferation and invasion as well as an increased apoptosis index. In vivo following transfection of Ad-Ku70shRNA, the therapeutic efficacy of GKT in rats with C6 gliomas was greatly enhanced and survival times in these animals were prolonged. Conclusions Our data support the potential for downregulation of Ku70 expression in enhancing the radiosensitivity of gliomas. The findings of our study indicate that targeted gene therapy–mediated inactivation of Ku70 may represent a promising strategy in improving the radioresponsiveness of gliomas to GKT.

scholarly journals α-Conotoxins and α-Cobratoxin Promote, while Lipoxygenase and Cyclooxygenase Inhibitors Suppress the Proliferation of Glioma C6 Cells

Marine Drugs ◽  
2021 ◽  
Vol 19 (2) ◽  
pp. 118
Author(s):  
Tatiana I. Terpinskaya ◽  
Alexey V. Osipov ◽  
Elena V. Kryukova ◽  
Denis S. Kudryavtsev ◽  
Nina V. Kopylova ◽  
...  
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Glioma Cells ◽  
Nordihydroguaiaretic Acid ◽  
C6 Glioma ◽  
Cyclooxygenase Inhibitors ◽  
C6 Glioma Cells ◽  
C6 Cells ◽  
Lipoxygenase Inhibitor ◽  
Glioma C6

Among the brain tumors, glioma is the most common. In general, different biochemical mechanisms, involving nicotinic acetylcholine receptors (nAChRs) and the arachidonic acid cascade are involved in oncogenesis. Although the engagement of the latter in survival and proliferation of rat C6 glioma has been shown, there are practically no data about the presence and the role of nAChRs in C6 cells. In this work we studied the effects of nAChR antagonists, marine snail α-conotoxins and snake α-cobratoxin, on the survival and proliferation of C6 glioma cells. The effects of the lipoxygenase and cyclooxygenase inhibitors either alone or together with α-conotoxins and α-cobratoxin were studied in parallel. It was found that α-conotoxins and α-cobratoxin promoted the proliferation of C6 glioma cells, while nicotine had practically no effect at concentrations below 1 µL/mL. Nordihydroguaiaretic acid, a nonspecific lipoxygenase inhibitor, and baicalein, a 12-lipoxygenase inhibitor, exerted antiproliferative and cytotoxic effects on C6 cells. nAChR inhibitors weaken this effect after 24 h cultivation but produced no effects at longer times. Quantitative real-time polymerase chain reaction showed that mRNA for α4, α7, β2 and β4 subunits of nAChR were expressed in C6 glioma cells. This is the first indication for involvement of nAChRs in mechanisms of glioma cell proliferation.

effect of ginsenoside Rd on nitric oxide system induced by lipopolysaccharide plus TNF-α in C6 rat glioma cells

2003 ◽  
Vol 26 (5) ◽  
pp. 375-382 ◽  
Author(s):  
Seong-Soo Choi ◽  
Jin-Koo Lee ◽  
Eun-Jung Han ◽  
Ki-Jung Han ◽  
Han-Kyu Lee ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Glioma Cells ◽  
Oxide System ◽  
Rat Glioma ◽  
Ginsenoside Rd ◽  
Tnf Α ◽  
Nitric Oxide System

Growth inhibition by sialosyl cholesterol of rat glioma cells

1990 ◽  
Vol 17 (1) ◽  
pp. 93-100 ◽  
Author(s):  
Sumiko Abe-Dohmae ◽  
Jin-Ichi Ito ◽  
Taiji Kato ◽  
Ryo Tanaka
Keyword(s):  
Growth Inhibition ◽  
Glioma Cells ◽  
Rat Glioma
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