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.

Escitalopram oxalate, a selective serotonin reuptake inhibitor, exhibits cytotoxic and apoptotic effects in glioma C6 cells

2011 ◽  
Vol 23 (4) ◽  
pp. 173-178 ◽  
Author(s):  
Miriş Dikmen ◽  
Zerrin Cantürk ◽  
Yusuf Öztürk
Keyword(s):  
Selective Serotonin Reuptake Inhibitor ◽  
Serotonin Reuptake ◽  
Glioma Cells ◽  
C6 Glioma ◽  
Selective Serotonin ◽  
C6 Glioma Cells ◽  
C6 Cells ◽  
Glioma C6 ◽  
Apoptotic Effects ◽  
Cell Proliferations

Dikmen M, Cantürk Z, Öztürk Y. Escitalopram oxalate, a selective serotonin reuptake inhibitor, exhibits cytotoxic and apoptotic effects in glioma C6 cells.Objective: Various antidepressants, mainly tricyclic antidepressants (TCAs) and selective serotonin reuptake inhibitors (SSRIs), have been reported to exhibit potent anticancer properties in different cancer cells. In this study, we evaluated the antiproliferative and apoptotic effects of escitalopram oxalate (25, 50, 100 and 200 µM) on rat C6 glioma cells.Methods: Cell proliferations were measured by [3-(4,5-dimethylthiazol-2-yl)-2-5-diphenyltetrazolium bromide] (MTT) assay, apoptosis was observed by flow cytometric analysis on C6 cells.Results: Significant decreases in the proliferation of C6 glioma cells were detected depending on increases in the escitalopram concentrations and incubation periods. When compared to controls, C6 cell proliferations after 24 h incubation were determined with 97.7, 85.9, 74.5 and 67.9% for 25, 50, 100 and 200 µM escitalopram, respectively, while the cell proliferations after 48 h were established as 96.5, 68.0, 50.7 and 39.9% for 25, 50, 100 and 200 µM concentrations, respectively. IC50 value of escitalopram was able to be calculated as 106.97 µM after 48 h. Based on Annexin V-propidium iodide (PI) binding capacity for 25, 50, 100 and 200 µM escitalopram, apoptotic effects were determined as 17.0, 22.3, 12.5 and 7.8%, respectively.Conclusion: Based on our findings, escitalopram oxalate was observed to induce cytotoxic and apoptotic activities in C6 cells.

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.

PROTEOMIC ANALYSIS OF ASTROCYTE CELL LINE BEFORE AND AFTER CO-COCULTIVATION WITH RATTUS NORVEGICUS GLIOMA C6 CELLS

2020 ◽  
pp. 174-176
Author(s):  
A. Chernysheva ◽  
O. Pobeguts ◽  
A. Nosyrev ◽  
G. Pavlova ◽  
O. Gurina
Keyword(s):  
Cell Line ◽  
Proteomic Analysis ◽  
Glioma Cells ◽  
Glioma Cell Line ◽  
C6 Glioma ◽  
C6 Glioma Cells ◽  
Glioma C6 ◽  
Before And After ◽  
Normal Rat ◽  
Rat Astrocytes

We perfomed panoramic proteomic analysis of rat C6 glioma cells, native rat astrocytes and rat astrocytes co- cultivated with C6 glioma cell line. Based on the data, a putative model was present for the diagnostic differentiation of normal rat astrocytes from C6 glioma cells.

scholarly journals Plasmin modulates the thrombin-evoked calcium response in C6 glioma cells

1994 ◽  
Vol 297 (1) ◽  
pp. 175-179 ◽  
Author(s):  
J S Turner ◽  
G T Redpath ◽  
J E Humphries ◽  
S L Gonias ◽  
S R Vandenberg
Keyword(s):  
Binding Sites ◽  
Cellular Response ◽  
Glioma Cells ◽  
C6 Glioma ◽  
C6 Glioma Cells ◽  
Similar Response ◽  
C6 Cells ◽  
Plasmin Activity ◽  
Strong Concentration ◽  
Agonist Peptide

Extracellular proteinases may be selectively targeted to cell surfaces by specific receptors or binding sites. In previous studies, we have characterized cellular binding sites for plasminogen and plasmin on rat C6 glioma cells. In this investigation, we studied the response of C6 cells to alpha-thrombin and plasmin by measuring the rapid kinetics of free intracellular Ca2+ concentrations ([Ca2+]i). Thrombin produced a strong, concentration-dependent rise in [Ca2+]i with an onset within 3 s and peak levels achieved in less than 10 s. A similar response was also evoked by an SFLLRN-containing thrombin-agonist peptide. C6 cells did not respond to plasmin (25 nM-1.5 microM). By contrast, pretreatment of C6 cells with 100 nM plasmin significantly inhibited the [Ca2+]i response to thrombin and the thrombin-agonist peptide. The peak [Ca2+]i response to thrombin, in cells pretreated with plasmin, was reduced by approx. 50%. The effect of plasmin on the cellular response to thrombin was selective, as pretreatment of the cells with plasmin did not affect the [Ca2+]i response to platelet-activating factor. Di-isopropylphosphorylplasmin and plasminogen did not inhibit the cellular response to thrombin, indicating that plasmin activity is required and that occupancy of cellular plasmin(ogen)-binding sites alone is insufficient. These studies demonstrate that plasmin does not directly induce a response in C6 cells, but may affect cellular function by specifically modulating the thrombin response.

scholarly journals TGF-β1 EXPRESSION BY GLIOMA C6 CELLS IN VITRO

2017 ◽  
Vol 39 (4) ◽  
pp. 258-263 ◽  
Author(s):  
L D Liubich ◽  
L M Kovalevska ◽  
M I Lisyany ◽  
V M Semenova ◽  
T A Malysheva ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Rat Brain ◽  
Glioma Cells ◽  
C6 Glioma ◽  
C6 Glioma Cells ◽  
C6 Cells ◽  
Fetal Rat ◽  
Tgf Β1 ◽  
Fetal Rat Brain

The aim of the work was to study the impact of fetal rat brain cell supernatant (FRBCS) on the expression of transforming growth factor β1 (TGF-β1) and p53 in C6 cells of rat glioma in vitro. Materials and Methods: FRBCS was obtained from suspensions of fetal rat brain cells on the 14th (E14) day of gestation. C6 glioma cells were cultured for 48 h in the presence of FRBCS or FRBCS + anti-TGF-β1 monoclonal antibody. Immunocytochemical staining for TGF-β1 and p53 was performed. Results: The proportion of TGF-β1-immunopositive tumor cells in C6 glioma cultures was statistically significantly higher than in the control cell cultures of normal fetal rat brain. FRBCS reduced the proportion of TGF-β1-immunopositive tumor cells and increased the proportion of p53-immunopositive cells in C6 glioma cultures. In cells cultured with FRBCS + anti-TGF-β1 monoclonal antibody, the above effects of FRBCS were abrogated. Conclusion: The obtained results suggest that TGF-β1 seems to be responsible for decrease in TGF-β1 expression and increase in p53 expression in C6 glioma cells treated with FRBCS.

Bioactivatable, Membrane-Permeant Analogs of Cyclic Nucleotides as Biological Tools for Growth Control of C6 Glioma Cells

2003 ◽  
Vol 384 (9) ◽  
pp. 1321-1326 ◽  
Author(s):  
M. Bartsch ◽  
M. Zorn-Kruppa ◽  
N. Kühl ◽  
H.-G. Genieser ◽  
F. Schwede ◽  
...  
Keyword(s):  
Cyclic Nucleotides ◽  
Growth Control ◽  
Glioma Cells ◽  
Glioma Cell Line ◽  
C6 Glioma ◽  
C6 Glioma Cells ◽  
C6 Cells ◽  
Dibutyryl Camp ◽  
Ester Prodrugs ◽  
Rat C6 Glioma

Abstract In the present study, the cAMP analogs 8-bromocAMP (8-Brc-AMP), N6-2'O-dibutyryl-cAMP (DBcAMP) and 8-parachlorophenylthio-cAMP (8-CPT-cAMP), as well as the corresponding cAMP-acetoxymethyl (AM)-ester-prodrugs were tested in a HPLC study for their membrane permeability, intracellular accumulation and biotransformation. Antiproliferative activities of these compounds were studied in the rat C6 glioma cell line. Chromatographic analysis revealed that the AM-ester analogs of the cyclic nucleotides penetrate quantitatively into rat C6 glioma cells and generate high amounts of their parent cyclic nucleotides intracellularly within 60 min; however, longterm growth inhibition tested in C6 cells is only slightly enhanced with the AM-ester prodrugs of 8-Br-cAMP or DBcAMP.

Post-transcriptional induction of β1-adrenergic receptor by retinoic acid, but not triiodothyronine, in C6 glioma cells expressing thyroid hormone receptors

1996 ◽  
Vol 135 (6) ◽  
pp. 709-715 ◽  
Author(s):  
Mònica López-Barahona ◽  
Teresa Iglesias ◽  
Irene García-Higuera ◽  
Federico Mayor ◽  
Angel Zaballos ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Thyroid Hormone ◽  
Adrenergic Receptor ◽  
Hormone Receptors ◽  
Glioma Cells ◽  
C6 Glioma ◽  
High Expression ◽  
Thyroid Hormone Receptors ◽  
C6 Glioma Cells ◽  
C6 Cells

López-Barahona M, Iglesias T, García-Higuera I, Mayor Jr F, Zaballos A, Bernal J, Muñoz A. Posttranscriptional induction of β1 -adrenergic receptor by retinoic acid, but not triiodothyronine, in C6 glioma cells expressing thyroid hormone receptors. Eur J Endocrinol 1996:135:709–15. ISSN 0804–4643 Thyroid hormone (triiodothyronine; T3) has been shown to control the expression of β1 -adrenergic receptors (β1-AR) in cardiac myocytes, but not in C6 glioma cells. This cell specificity has been attributed to low expression of T3 receptors and high expression of the c-erbAα2 splice variant that interferes with the action of T3. To check this hypothesis we have expressed the c-erbA/thyroid hormone receptor (TR) α1 gene in C6 glioma cells and investigated their response to thyroid hormone. Cells expressing TRα1, but not wild-type cells, were responsive to T3 as shown by increased expression of mitochrondrial hydroxymethylglutaryl CoA synthase after T3 exposure. However, T3 had no effect on β1-AR gene expression in either set of cells. The β1-AR mRNA concentrations were, however, altered by retinoic acid (RA) treatment. Retinoic acid caused a rapid up-regulation of β1-AR mRNA levels that was blocked by cycloheximide. Retinoic acid did not increase the β1-AR gene transcription rate in run-on experiments. These results indicate an indirect post-transcriptional effect of RA. Control of β1-AR expression in C6 cells is also exerted at the translational level, because there was no correlation between mRNA and protein induction, as determined by radioligand binding studies. We conclude that lack of responsiveness of the β1-AR gene in C6 cells to T3 is not due to high expression of c-erbAα2 but to undefined cell-specific factors. Alberto Muñoz, Instituto Investigaciones Biomedicas, Arturo Duperier 4, 28029 Madrid, Spain

Exogenous hydrogen sulfide exhibits anti-cancer effects though p38 MAPK signaling pathway in C6 glioma cells

2015 ◽  
Vol 396 (11) ◽  
pp. 1247-1253 ◽  
Author(s):  
Lanfu Zhao ◽  
Yuan Wang ◽  
Quan Yan ◽  
Wenhai Lv ◽  
Yufu Zhang ◽  
...  
Keyword(s):  
Protein Expression ◽  
P38 Mapk ◽  
Caspase 3 ◽  
Glioma Cells ◽  
Cell Number ◽  
Mapk Signaling ◽  
C6 Glioma ◽  
C6 Glioma Cells ◽  
C6 Cells ◽  
Anti Cancer

Abstract It has been documented that H2S, in some types of cancer, promotes tumor proliferation, whereas, in the other types, it inhibits the tumor cell growth. In the present study, we investigated the anti-cancer effects and relevant mechanisms of NaHS in C6 glioma cells. C6 cells were subjected to different concentrations of NaHS, then cell viability and morphological changes were examined by MTT assay and Hoechst staining. The protein expression of Caspase-3, Bcl-2, Bax, p38 MAPK (mitogen-activated protein kinase), and p53 was measured by Western blotting. This work demonstrated that NaHS could reduce cell number and induce apoptosis of C6 gliomas cells. The protein expression of Caspase-3 and Bax was up-regulated, while the protein expression of Bcl-2 was down-regulated. Additionally, p38 MAPK and p53 were activated in response to NaHS. Moreover, p38 MAPK inhibitor, SB203580, counteracted the inhibitory effect of NaHS on C6 glioma cells. These data suggest that NaHS can effectively reduce cell number of C6 cells by triggering the apoptosis via Caspase-dependent pathway. p38 MAPK and p53 play an important role in NaHS-induced apoptosis in C6 cells. These findings imply that administration of NaHS may represent a new strategy for the treatment of glioma.

Isoflurane Enhances the Expression and Activity of Glutamate Transporter Type 3 in C6 Glioma Cells

2003 ◽  
Vol 99 (6) ◽  
pp. 1346-1353 ◽  
Author(s):  
Yueming Huang ◽  
Zhiyi Zuo
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Glutamate Transporter ◽  
Glioma Cells ◽  
C6 Glioma ◽  
C6 Glioma Cells ◽  
C6 Cells ◽  
Phosphatidylinositol 3 Kinase ◽  
Kinase C ◽  
Type 3

Background Glutamate transporters play an important role in maintaining extracellular glutamate homeostasis. Volatile anesthetics have been shown to affect glutamate transporter activity acutely (within minutes after the exposure). It is not known whether volatile anesthetics affect the expression of glutamate transporters. Methods Rat cultured C6 glioma cells that express excitatory amino acid transporter type 3 (EAAT3) were exposed to isoflurane at various concentrations (0.5-4.0%) or for different periods (1-24 h) at 37 degrees C. EAAT3 mRNA, proteins, and activity were quantified. Results Isoflurane induced a time- and concentration-dependent increase in the mRNA and protein levels of EAAT3 in C6 cells. The maximal increase was induced by 2% isoflurane, and the cells incubated with 2% isoflurane for 3 and 7 h expressed the highest levels of EAAT3 mRNA and proteins, respectively. Similarly, glutamate uptake was higher in C6 cells exposed to 2% isoflurane for 7 h than in control cells. Actinomycin D and cycloheximide, inhibitors for mRNA and protein synthesis, respectively, did not affect the isoflurane-induced increase in EAAT3 mRNA and protein expression. Phorbol 12-myristate 13-acetate, a protein kinase C activator, also enhanced EAAT3 expression. The combination of 2% isoflurane and phorbol 12-myristate 13-acetate caused a higher level of EAAT3 expression than that induced by 2% isoflurane alone. Neither staurosporine, a protein kinase C inhibitor, nor wortmannin, a phosphatidylinositol 3 kinase inhibitor, inhibited the isoflurane-induced increase in EAAT3 expression. Conclusions The results of this study suggest that isoflurane increases the expression and activity of EAAT3 by stabilizing EAAT3 mRNA and proteins via protein kinase C- and phosphatidylinositol 3 kinase-independent pathways.

scholarly journals Oleic Acid and Hydroxytyrosol Inhibit Cholesterol and Fatty Acid Synthesis in C6 Glioma Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Paola Priore ◽  
Antonio Gnoni ◽  
Francesco Natali ◽  
Mariangela Testini ◽  
Gabriele V. Gnoni ◽  
...  
Keyword(s):  
Oleic Acid ◽  
Fatty Acid ◽  
Olive Oil ◽  
Fatty Acid Synthase ◽  
Lipid Synthesis ◽  
Glioma Cells ◽  
C6 Glioma ◽  
Lipid Lowering ◽  
C6 Glioma Cells ◽  
C6 Cells

Recently, the discovery of natural compounds capable of modulating nervous system function has revealed new perspectives for a healthier brain. Here, we investigated the effects of oleic acid (OA) and hydroxytyrosol (HTyr), two important extra virgin olive oil compounds, on lipid synthesis in C6 glioma cells. OA and HTyr inhibited both de novo fatty acid and cholesterol syntheses without affecting cell viability. The inhibitory effect of the individual compounds was more pronounced if OA and HTyr were administered in combination. A reduction of polar lipid biosynthesis was also detected, while triglyceride synthesis was marginally affected. To clarify the lipid-lowering mechanism of these compounds, their effects on the activity of key enzymes of fatty acid biosynthesis (acetyl-CoA carboxylase-ACC and fatty acid synthase-FAS) and cholesterologenesis (3-hydroxy-3-methylglutaryl-CoA reductase-HMGCR) were investigated in situ by using digitonin-permeabilized C6 cells. ACC and HMGCR activities were especially reduced after 4 h of 25 μM OA and HTyr treatment. No change in FAS activity was observed. Inhibition of ACC and HMGCR activities is corroborated by the decrease of their mRNA abundance and protein level. Our results indicate a direct and rapid downregulatory effect of the two olive oil compounds on lipid synthesis in C6 cells.

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