Differential proliferative and cytotoxic effect of selected components of essential oils on human glioblastoma cells

2021 ◽  
Vol 08 ◽  
Author(s):  
Sumbla Sheikh ◽  
Alexander Sturzu ◽  
Hubert Kalbacher ◽  
Thomas Nägele ◽  
Ulrike Ernemann ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Essential Oils ◽  
Cell Lines ◽  
Perillyl Alcohol ◽  
Laser Scanning Microscopy ◽  
Membrane Disruption ◽  
Glioblastoma Cells ◽  
Human Glioblastoma ◽  
Hek Cells ◽  
Acute Cytotoxicity

Background: In the study of bioactive agents from traditional medicine, mono- and sesquiterpenes represent the main ingredients of essential oils. Till now, only thymoquinone and perillyl alcohol have been clinically tested on glioblastoma. Objective: In the present study, we examined the effect of ten different essential oils on three human glioblastoma cell lines and one healthy human cell line. Methods: We used confocal laser scanning microscopy, flow cytometry, and cell growth analysis to evaluate cell morphology changes, membrane disruption effects, acute cytotoxicity and effects on the proliferation rate caused by the essential oils pinene, geraniol, eucalyptol, perillaldehyde, limonene, and linalool, perillyl alcohol, myrcene, bisabolol and valencene on human cells. Caspase 3/7 activity was measured to observe apoptosis induced by the essential oils. Results: We found that the cytotoxicity concentrations varied not only between different essential oils but also among different cell lines. Acute cytotoxicity of essential oils was based on cell membrane disruption and that HEK cells were affected to a much higher degree than the Glioblastoma cells. Vacuoles found in surviving glioblastoma cells appeared to be a factor in this effect. Conclusion: Caspase activity did not correlate with the membrane damage observed in the flow cytometry experiments. This is especially evident in the HEK cells that only showed apoptosis with two out of ten essential oils.

scholarly journals ENHANCED p53-DEPENDENT GROWTH INHIBITION OF HUMAN GLIOBLASTOMA CELLS BY COMBINATORIAL TREATMENT OF TEMOZOLOMIDE AND NOVEL PURIFIED NATURAL CARBOHYDRATE OF PLEUROTUS FLORIDA

2017 ◽  
Vol 9 (6) ◽  
pp. 189
Author(s):  
Priyankar Maji ◽  
Ranodeep Chatterjee ◽  
Biswa P. Choudhury ◽  
Urmi Chatterji ◽  
Jhuma Ganguly
Keyword(s):  
Cell Cycle ◽  
Protein Expression ◽  
Cell Lines ◽  
P53 Protein ◽  
Glioblastoma Cells ◽  
Human Glioblastoma ◽  
Pleurotus Florida ◽  
P53 Protein Expression ◽  
Human Glioblastoma Cells ◽  
Combinatorial Treatment

Objective: This study was designed to analyze the combinatorial chemotherapeutic effect of temozolomide (TMZ), the most common drug in glioblastoma treatment and a purified carbohydrate (Fr-II) from the edible mushroom Pleurotus florida, on human glioblastoma cell lines.Methods: Fr-II was purified by size-exclusion chromatography and characterised by different mass spectroscopy analysis. Human glioblastoma cells were treated with TMZ, Fr-II, and combination of TMZ and Fr-II. Cell cytotoxicity was measured by MTT assay, cell cycle phase distribution was determined by cell cycle analysis and followed by the relative p53 protein expression was analyzed by western blot analysis.Results: Chemical analysis of Fr-II confirmed the glycosidically linked two units of glucose with terminally attached mannitol with mass of 506 Da. Fr-II treatment exhibited cytotoxicity in both the cell lines in a dose-dependent manner with most effective dose at 200µg/ml. When Fr-II (200µg/ml) was combined with a dose range of TMZ it showed a more cellular cytotoxicity compared to the cytotoxicity of TMZ alone with most oppressive combinatorial dose at 400µM (TMZ)+200µg/ml (Fr-II). In compliance, with the above results, both cell lines showed a 10% increase in no. of cells (p<0.05) in G2/M phase indicating an arrest of cell cycle and increased p53 protein expression (p<0.05) at the combinatorial dose than TMZ alone at 400µM, but Fr-II alone didn’t show any cell cycle arrest nor did it show increased p53 expression.Conclusion: Therefore it confirms that Fr-II synergizes with TMZ to significantly intensify its anti-proliferative properties, thereby emerging as an effective element for combinatorial treatment of glioblastoma.

scholarly journals Smarcd1 Inhibits the Malignant Phenotypes of Human Glioblastoma Cells via Crosstalk with Notch1

2020 ◽  
Author(s):  
Yihao Zhu ◽  
Handong Wang ◽  
Maoxing Fei ◽  
Ting Tang ◽  
Wenhao Niu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
High Grade Glioma ◽  
Glioblastoma Cell ◽  
Glioblastoma Cells ◽  
Human Glioblastoma ◽  
Protein Levels ◽  
Enhanced Expression ◽  
Human Glioblastoma Cells ◽  
Glioblastoma Cell Lines

AbstractSmarcd1 is a component of an evolutionary conserved chromatin remodeling complex—SWI/SNF, which is involved in transcription factor recruitment, DNA replication, recombination, and repair. Suppression of the SWI/SNF complex required for cellular differentiation and gene regulation may be inducible for cell proliferation and tumorigenicity. However, the inhibitory role of Smarcd1 in human glioblastoma cells has not been well illustrated. Both U87 and U251 human glioblastoma cell lines were employed in the present study. The lentivirus-mediated gene knockdown and overexpression approach was conducted to determine the function of Smarcd1. The protein levels were tested by western blot, and the relative mRNA contents were detected by quantitative real-time PCR. Cell viability was tested by CCK-8 and colony-forming assay. Transwell assays were utilized to evaluate the motility and invasive ability. Flow cytometry was employed to analyze cell cycle and apoptosis. SPSS software was used for statistical analysis. Low expression of Smarcd1 was observed in glioblastoma cell lines and in patients with high-grade glioma. Importantly, the depletion of Smarcd1 promoted cell proliferation, invasion, and chemoresistance, whereas enhanced expression of Smarcd1 inhibited tumor-malignant phenotypes. Mechanistic research demonstrated that overexpression of Smarcd1 decreased the expression of Notch1, while knockdown of Notch1 increased the expression of Smarcd1 through Hes1 suppression. Hence, the crosstalk between Smarcd1 and Notch1, which formed a feedback loop, was crucial in regulation of glioblastoma malignant phenotypes. Furthermore, targeting Smarcd1 could be a potential strategy for human glioblastoma treatment.

scholarly journals CYTOTOXICITY AND HEMOCOMPATIBILITY OF DOXORUBICIN-LOADED PLGA NANOPARTICLES

2020 ◽  
Vol 19 (1) ◽  
pp. 71-80
Author(s):  
Yu. A. Malinovskaya ◽  
E. I. Kovalenko ◽  
T. S. Kovshova ◽  
N. S. Osipova ◽  
O. O. Maksimenko ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Blood Coagulation ◽  
Hemoglobin Concentration ◽  
Coagulation Cascade ◽  
Coagulation System ◽  
Intracranial Tumour ◽  
Glioblastoma Cells ◽  
Human Glioblastoma ◽  
Human Glioblastoma Cells

Introduction. The use of polymeric biodegradable nanoparticles (NP) as drug delivery systems is a promising approach to overcome histohematomatic barriers. Thus, poloxamer 188-coated poly (lactide-co-glycolide) (PLGA) NP are able to overcome blood-brain barrier and to deliver therapeutic agents, in particular doxorubicin, into intracranial tumour upon intravenous administration. It is important to evaluate NP interaction with blood components in preclinical studies.The objective of the study was to investigate cytotoxicity and hemocompatibility of doxorubicin-loaded PLGA NP (Dox-PLGA NP), to essess NP uptake by glioblastoma cells.Materials and methods. The influence of NP on coagulation cascade was evaluated by prothrombin time measuring before and after plasma incubation with NP. To assess NP thrombogenicity the platelet activation level was determined by flow cytometry. The NP hemolytic activity (released hemoglobin concentration) was measured spectrophotometrically. NP cytotoxicity was determined by MTS assay. NP uptake by human glioblastoma cells was evaluated by flow cytometry.Results. Dox-PLGA NP did not influence blood coagulation time and thrombocyte activity at concentrations up to 100 mcg/mL: PT values were 12–15 s for all tested samples, and P-selectin expression level did not exceed 15 %. All samples were not hemolytic after 3 h of incubation. Cytotoxicity of doxorubicin released from PLGA NP on glioma U87MG cells was comparable to that of free doxorubicin. As shown by flow cytometry Dox-PLGA NP were efficiently internalized into the cells.Conclusion. The study of hemocompatibility confirmed the safety of Dox-PLGA NP: NP did not influence blood coagulation system and did not induce hemolysis. NP were efficiently internalized into the human glioblastoma cells and produced considerable antitumor effect in vitro.

Investigating the Therapeutic Effects of Alginate Nanogel Co-loaded with Gold Nanoparticles and Cisplatin on U87-MG Human Glioblastoma Cells

2018 ◽  
Vol 18 (6) ◽  
pp. 882-890 ◽  
Author(s):  
Ali Neshastehriz ◽  
Maziar Khateri ◽  
Habib Ghaznavi ◽  
Ali Shakeri-Zadeh
Keyword(s):  
Flow Cytometry ◽  
Gold Nanoparticles ◽  
Survival Rate ◽  
Therapeutic Effects ◽  
X Rays ◽  
Glioblastoma Cells ◽  
Pilot Studies ◽  
Human Glioblastoma ◽  
Human Glioblastoma Cells

Background and Purpose: It has been well-known both gold nanoparticles (AuNPs) and cisplatin are potential radiosensitizers for radiotherapy of cancer. In this in vitro study, we investigated the chemoradiotherapeutic effects of alginate nanogel co-loaded with AuNPs and cisplatin (ACA) on U87-MG human glioblastoma cells. Methods: Based on the accomplished pilot studies, U87-MG cells were incubated with ACA and cisplatin at 10% inhibitory concentration (IC10) for 4h. Then, the cells were irradiated to different doses of 6MV X-rays (2 and 10 Gy). MTT assay was performed to evaluate the cell survival rate. Apoptosis was determined by flow cytometry using an annexinV–fluorescein isothiocyanate/propidium iodide apoptosis detection kit. Results: The results showed that ACA at the concentration of 4 µg/ml (per cisplatin) and free cisplatin at concentration of 15 μg/ml have the same effects on U87-MG cells (survival rate: 90%). The combination of ACA with radiation resulted in a significant decrease in cell viability (survival rate: 30%). The flow cytometry assay also showed that such a combination therapy induces more apoptosis than necrosis. Conclusion: It may be concluded that co-delivery of AuNPs and cisplatin with a single nanoplatform like ACA nanocomplex enhances the therapeutic ratio of human glioblastoma radiation therapy.

scholarly journals Attachment of A172 human glioblastoma cells affects calcium signalling: A comparison of image cytometry, flow cytometry, and spectrofluorometry

Cytometry ◽  
1991 ◽  
Vol 12 (8) ◽  
pp. 707-716 ◽  
Author(s):  
Jànos Szöllösi ◽  
Burt G. Feuerstein ◽  
William C. Hyun ◽  
Manoj K. Das ◽  
Laurence J. Marton
Keyword(s):  
Flow Cytometry ◽  
Calcium Signalling ◽  
Image Cytometry ◽  
Glioblastoma Cells ◽  
Human Glioblastoma ◽  
Human Glioblastoma Cells

scholarly journals Synthetic Cannabinoids Induce Autophagy and Mitochondrial Apoptotic Pathways in Human Glioblastoma Cells Independently of Deficiency in TP53 or PTEN Tumor Suppressors

Cancers ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 419
Author(s):  
Aleksandra Ellert-Miklaszewska ◽  
Iwona Anna Ciechomska ◽  
Bozena Kaminska
Keyword(s):  
Cell Lines ◽  
Synthetic Cannabinoids ◽  
Glioma Cells ◽  
Genetic Alterations ◽  
Receptor Expression ◽  
Low Grade ◽  
Glioblastoma Cells ◽  
Apoptosis Resistance ◽  
Human Glioblastoma ◽  
Human Glioblastoma Cells

Glioblastomas (GBMs) are aggressive brain tumors with frequent genetic alterations in TP53 and PTEN tumor suppressor genes rendering resistance to standard chemotherapeutics. Cannabinoid type 1 and 2 (CB1/CB2) receptor expression in GBMs and antitumor activity of cannabinoids in glioma cells and animal models, raised promises for a targeted treatment of these tumors. The susceptibility of human glioma cells to CB2-agonists and their mechanism of action are not fully elucidated. We determined CB1 and CB2 expression in 14 low-grade and 21 high-grade tumor biopsies, GBM-derived primary cultures and established cell lines. The non-selective CB receptor agonist WIN55,212-2 (but not its inactive enantiomer) or the CB2-selective agonist JWH133 induced apoptosis in patient-derived glioma cultures and five established glioma cell lines despite p53 and/or PTEN deficiency. Growth inhibitory efficacy of cannabinoids correlated with CB1/CB2 expression (EC50 WIN55,212-2: 7.36–15.70 µM, JWH133: 12.15–143.20 µM). Treatment with WIN55,212-2 or JWH133 led to activation of the apoptotic mitochondrial pathway and DNA fragmentation. Synthetic cannabinoid action was associated with the induction of autophagy and knockdown of autophagy genes augmented cannabinoid-induced apoptotic cell death. The high susceptibility of human glioblastoma cells to synthetic cannabinoids, despite genetic defects contributing to apoptosis resistance, makes cannabinoids promising anti-glioma therapeutics.

Glioblastoma invasion and NMDA receptors: A novel prospect

2019 ◽  
Vol 106 (3) ◽  
pp. 250-260 ◽  
Author(s):  
DN Nandakumar ◽  
P Ramaswamy ◽  
C Prasad ◽  
D Srinivas ◽  
K Goswami
Keyword(s):  
Glutamate Receptors ◽  
Cell Lines ◽  
Intracellular Signaling ◽  
Transcript Level ◽  
Glioblastoma Cells ◽  
Invasion And Migration ◽  
Matrigel Invasion ◽  
Nmdar Activation ◽  
And Migration

Purpose Glioblastoma cells create glutamate-rich tumor microenvironment, which initiates activation of ion channels and modulates downstream intracellular signaling. N-methyl-D-aspartate receptors (NMDARs; a type of glutamate receptors) have a high affinity for glutamate. The role of NMDAR activation on invasion of glioblastoma cells and the crosstalk with α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) is yet to be explored. Main methods LN18, U251MG, and patient-derived glioblastoma cells were stimulated with NMDA to activate NMDAR glutamate receptors. The role of NMDAR activation on invasion and migration and its crosstalk with AMPAR were evaluated. Invasion and migration of glioblastoma cells were investigated by in vitro trans-well Matrigel invasion and trans-well migration assays, respectively. Expression of NMDARs and AMPARs at transcript level was evaluated by quantitative real-time polymerase chain reaction. Results We determined that NMDA stimulation leads to enhanced invasion in LN18, U251MG, and patient-derived glioblastoma cells, whereas inhibition of NMDAR using MK-801, a non-competitive antagonist of the NMDAR, significantly decreased the invasive capacity. Concordant with these findings, migration was significantly augmented by NMDAR in both cell lines. Furthermore, NMDA stimulation upregulated the expression of GluN2 and GluA1 subunits at the transcript level. Conclusions This study demonstrated the previously unexplored role of NMDAR in invasion of glioblastoma cells. Furthermore, the expression of the GluN2 subunit of NMDAR and the differential overexpression of the GluA1 subunit of AMPAR in both cell lines provide a plausible rationale of crosstalk between these calcium-permeable subunits in the glutamate-rich microenvironment of glioblastoma.

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