Effects of different alcoholic beverages on human glioblastoma cell lines

2021 ◽  
Vol 17 ◽  
Author(s):  
Sumbla Sheikh ◽  
Alexander Sturzu ◽  
Thomas Nägele ◽  
Ulrike Ernemann ◽  
Stefan Heckl
Keyword(s):  
Cell Proliferation ◽  
White Wine ◽  
Alcoholic Beverages ◽  
Membrane Disruption ◽  
Glioblastoma Cell ◽  
Proliferation Inhibition ◽  
Red Wines ◽  
Glioblastoma Cells ◽  
Glioblastoma Cell Lines

Background: Anecdotal reports from neurosurgeons suggested that patients with glioblastoma who consumed a moderate amount of alcoholic beverages after glioblastoma surgery presented with improved vitality. Objective: This study aimed to investigate that if any evidence for these anecdotal reports can be reproduced experimentally. We also studied the effects of different alcoholic beverages on glioblastoma cells. Methods: GOS-3 glioblastoma cells and PC3 prostate carcinoma cells as control were incubated with beer, red wine, white wine, vodka, and whiskey at different concentrations. Membrane disruption by acute cytotoxicity and apoptosis induction was evaluated via Annexin-V-FITC flow cytometry and confocal laser scanning microscopy. Long-term effects on cell proliferation were studied by the XTT test. Results: There was no increase in membrane disruption even at physiologically high alcohol concentrations of 1 ‰. Cell proliferation was significantly inhibited by vodka and beer. Among the wines, the white wine caused slight proliferation inhibition in GOS-3 glioblastoma cells while inducing slightly enhanced proliferation in PC3 prostate cancer cells. After these results, more different brands of vodka and additional white and red wines from different grapes were used. While confirming the initial results, no additional differences between the different brands of vodka were observed. In the wine investigations, all the wines showed cell proliferation inhibition during long-term incubation of three different glioblastoma cell lines. Consistently, the inhibition from red wines was lower than the inhibition from white and rosé wines. Conclusion: In conclusion, alcoholic beverages at different concentrations used during the ingestion have both cytotoxic and antiproliferative effects on glioblastoma cells in vitro which could not be found in the controls with pure ethanol.

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 SNHG9/miR-199a-5p/Wnt2 Axis Regulates Cell Growth and Aerobic Glycolysis in Glioblastoma

2019 ◽  
Vol 78 (10) ◽  
pp. 939-948 ◽  
Author(s):  
Han Zhang ◽  
Danxia Qin ◽  
Zhixian Jiang ◽  
Jinning Zhang
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Mrna Expression ◽  
Cell Lines ◽  
Aerobic Glycolysis ◽  
Stress Test ◽  
Glioblastoma Cell ◽  
Glioblastoma Cells ◽  
Qrt Pcr ◽  
Glioblastoma Cell Lines

Abstract Aerobic glycolysis is a characteristic in cancers that is important for cancer cell proliferation. Emerging evidence shows that long non-coding RNA (LncRNA) participates in glucose metabolism and cell proliferation in cancer. This study explored the effect of LncRNA: SNHG9 in glioblastoma. The mRNA expression of SNHG9 in human glioma tissues and glioblastoma cell lines was measured by qRT-PCR. Glioblastoma cell lines (U87 and U251) were transfected with miR-199a-5p or SNHG9-expressing plasmid and cell viability as well as concentrations of glucose and lactate were measured. The extracellular acidification was evaluated by glycolysis stress test. The Wnt2 levels were determined by qRT-PCR and Western blot. Results showed that the mRNA expression of SNHG9 was elevated in glioblastoma tissues. The elevated SNHG9 expression was related to lower survival rate in patients with glioma. SNHG9 could downregulate miR-199a-5p and upregulate Wnt2 in glioblastoma cells. Overexpression of SNHG9 in glioblastoma cells promoted aerobic glycolysis and cell proliferation, which could be attenuated by miR-199a-5p. Results of this study indicated an effect of SNHG9/miR-199a-5p/Wnt2 axis in regulating cell growth and aerobic glycolysis in glioblastoma.

Arctigenin upregulates apoptosis through the AKT/MTOR pathway, inhibiting the proliferation of glioma

2019 ◽  
Author(s):  
jiang yongan ◽  
Liu Jia yu ◽  
Hong Wangwang ◽  
Fei Xiaowei ◽  
Liu ru'en
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Glioma Cells ◽  
Mtor Pathway ◽  
Migration And Invasion ◽  
Glioblastoma Cell ◽  
Caspase 9 ◽  
Arctium Lappa ◽  
Dose Dependent ◽  
Glioblastoma Cell Lines

Abstract Arctigenin (ARG) is a natural lignan compound extracted from arctium lappa and has displayed anticancer functions and effective treatments in a variety of cancers.Studies had shown that Arctigenin(ARG) inhibits tumors through the AKT/MTOR pathway and mediates autophagy.However,the role in glioma cellshave not still fully understood.This study was designed to investigate whether Arctigenin(ARG) can mediateAKT/mTOR pathway in glioma to regulate autophagy,and affected glioma cells growth and survival.We found that the dose-dependent downregulation of Arctigenin(ARG),reducing cell proliferation,migration and invasion in two human glioblastoma cell lines (U87, T98G),These phenomena were reversed after the administration of the AKT agonist (SC79). Arctigenin(ARG) also affected other autophagy markers such as p62, LC3B.In addition, the apoptotic molecules cleaved-PARP,caspase-9, and cleaved-caspase3 were also dose-dependently altered.

scholarly journals CSIG-18. NERVE/GLIAL ANTIGEN (NG)2 EXPRESSION IN GLIOBLASTOMA IS REGULATED BY miR-29b-3p

2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi47-vi48
Author(s):  
Beate Schmitt ◽  
Anne Boewe ◽  
Yuan Gu ◽  
Christoph Sippl ◽  
Steffi Urbschat ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Cell Lines ◽  
Therapeutic Strategy ◽  
Mrna Levels ◽  
Glioblastoma Cell ◽  
Glioblastoma Cells ◽  
Qrt Pcr ◽  
Glioblastoma Patient ◽  
Low Levels ◽  
Glioblastoma Cell Lines

Abstract Overexpression of NG2 in human glioblastoma cells is associated with an elevated drug resistance and thereby worsens clinical outcome. However, the regulatory mechanisms of NG2 expression are largely unknown. In this study, we identified miR-29b-3p as a posttranscriptional factor of NG2 expression. The basal mRNA levels of miR-29b-3p and NG2 were detected in the NG2-positive glioblastoma cell lines A1207 and U87 by qRT-PCR. The cells were transfected with miR-29b-3p-mimic or scrambled-miR (control) and the expression of NG2 was analyzed by qRT-PCR, flow cytometry and Western blot. Reporter gene analyses of the NG2 promotor region and 3’UTR were performed to study the effect of miR-29b-3p on NG2 expression. Finally, we analyzed the mRNA levels of NG2 and miR-29b-3p in samples from glioblastoma patients. We found that the two NG2-positive glioblastoma cell lines A1207 and U87 are positive for miR-29b-3p. Transfection with miR-29b-3p-mimic reduced NG2 mRNA levels in A1207 (29%±9.9; Mean±SD) and U87 (6%±2.8), resulting in a significantly decreased NG2 protein expression in A1207 (67%±6.4) and U87 (75%±4) when compared to controls. The analysis of the 3’UTR revealed that miR-29b-3p is a posttranscriptional regulator of NG2 expression. Moreover, miR-29b-3p affects the pretranscriptional NG2 expression by diminishing SP-1-dependent NG2 promotor activity. These results were confirmed by the analysis of glioblastoma patient-derived samples, demonstrating that a high NG2 expression is associated with low levels of miR-29b-3p. In conclusion, we identified miR-29b-3p as a crucial regulator of NG2 expression in glioblastoma. Hence, targeting NG2 expression by miR-29b-3p may provide a novel therapeutic strategy to overcome drug resistance in NG2-positive glioblastoma cells.

scholarly journals Anti-vimentin, anti-TUFM, anti-NAP1L1 and anti-DPYSL2 nanobodies display cytotoxic effect and reduce glioblastoma cell migration

2020 ◽  
Vol 12 ◽  
pp. 175883592091530 ◽  
Author(s):  
Alja Zottel ◽  
Ivana Jovčevska ◽  
Neja Šamec ◽  
Jernej Mlakar ◽  
Jernej Šribar ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cell Migration ◽  
Cell Lines ◽  
Water Soluble ◽  
Glioblastoma Cell ◽  
Glioblastoma Cells ◽  
Mitochondrial Translation ◽  
Cytotoxic Effects ◽  
Glioblastoma Stem Cells ◽  
Glioblastoma Cell Lines

Background: Glioblastoma is a particularly common and very aggressive primary brain tumour. One of the main causes of therapy failure is the presence of glioblastoma stem cells that are resistant to chemotherapy and radiotherapy, and that have the potential to form new tumours. This study focuses on validation of eight novel antigens, TRIM28, nucleolin, vimentin, nucleosome assembly protein 1-like 1 (NAP1L1), mitochondrial translation elongation factor (EF-TU) (TUFM), dihydropyrimidinase-related protein 2 (DPYSL2), collapsin response mediator protein 1 (CRMP1) and Aly/REF export factor (ALYREF), as putative glioblastoma targets, using nanobodies. Methods: Expression of these eight antigens was analysed at the cellular level by qPCR, ELISA and immunocytochemistry, and in tissues by immunohistochemistry. The cytotoxic effects of the nanobodies were determined using AlamarBlue and water-soluble tetrazolium tests. Annexin V/propidium iodide tests were used to determine apoptotsis/necrosis of the cells in the presence of the nanobodies. Cell migration assays were performed to determine the effects of the nanobodies on cell migration. Results: NAP1L1 and CRMP1 were significantly overexpressed in glioblastoma stem cells in comparison with astrocytes and glioblastoma cell lines at the mRNA and protein levels. Vimentin, DPYSL2 and ALYREF were overexpressed in glioblastoma cell lines only at the protein level. The functional part of the study examined the cytotoxic effects of the nanobodies on glioblastoma cell lines. Four of the nanobodies were selected in terms of their specificity towards glioblastoma cells and protein overexpression: anti-vimentin (Nb79), anti-NAP1L1 (Nb179), anti-TUFM (Nb225) and anti-DPYSL2 (Nb314). In further experiments to optimise the nanobody treatment schemes, to increase their effects, and to determine their impact on migration of glioblastoma cells, the anti-TUFM nanobody showed large cytotoxic effects on glioblastoma stem cells, while the anti-vimentin, anti-NAP1L1 and anti-DPYSL2 nanobodies were indicated as agents to target mature glioblastoma cells. The anti-vimentin nanobody also had significant effects on migration of mature glioblastoma cells. Conclusion: Nb79 (anti-vimentin), Nb179 (anti-NAP1L1), Nb225 (anti-TUFM) and Nb314 (anti-DPYSL2) nanobodies are indicated for further examination for cell targeting. The anti-TUFM nanobody, Nb225, is particularly potent for inhibition of cell growth after long-term exposure of glioblastoma stem cells, with minor effects seen for astrocytes. The anti-vimentin nanobody represents an agent for inhibition of cell migration.

scholarly journals miR-548x and miR-4698 controlled cell proliferation by affecting the PI3K/AKT signaling pathway in Glioblastoma cell lines

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Mohammad Reza kalhori ◽  
Ehsan Arefian ◽  
Fereshteh Fallah Atanaki ◽  
Kaveh Kavousi ◽  
Masoud Soleimani
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Akt Signaling ◽  
Glioblastoma Cell ◽  
Akt Signaling Pathway ◽  
Glioblastoma Cell Lines

scholarly journals Knockdown of BCL6 Inhibited Malignant Phenotype and Enhanced Sensitivity of Glioblastoma Cells to TMZ through AKT Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-11
Author(s):  
Wen Song ◽  
Zhenling Wang ◽  
Pengcheng Kan ◽  
Zhuolin Ma ◽  
Yaru Wang ◽  
...  
Keyword(s):  
Cell Lines ◽  
Mapk Signaling ◽  
Migration And Invasion ◽  
Phenotypic Change ◽  
Glioblastoma Cell ◽  
Glioblastoma Cells ◽  
Protein Levels ◽  
Normal Tissues ◽  
Enhanced Sensitivity ◽  
Glioblastoma Cell Lines

Background. BCL6 was a critical prooncogene of human B-cell lymphomas which promoted tumor progress and contributed to malignant behavior in several kinds of cancers. This study was to detect the expression of BCL6 and its biological effect on glioma. Methods. RT-PCR and Western blot were used to detect the expression of BCL6 mRNA and protein in tissues and glioblastoma cell lines. The expression of BCL6 was knockdown in two glioblastoma cell lines (U87 and U251) using BCL6 shRNA. The CCK8, colony-formation, flow cytometry, Transwell, and wound-healing assays were used to evaluate the malignant phenotypic change of glioblastoma cells. Results. The expression of BCL6 was higher in glioma tissues and glioblastoma cell lines than normal tissues. Knockdown of BCL6 expression reduced the proliferation, migration, and invasion of glioblastoma cells. Moreover, knockdown of BCL6 changed expression of proteins related to malignant behaviors of glioblastoma cells. The suppression of BCL6 could increase chemosensitivity of U87 and U251 to temozolomide. Downregulation of BCL6 levels suppressed the expression of BCL2, cyclin D1, MMP2, and MMP9 proteins as well as two classic signaling pathway proteins p-AKT and p-ERK. Simultaneously, BAX and p21 protein levels were upregulated along with knockdown of BCL6. Conclusions. Our results indicated that BCL6 may be a tumor oncogene involved in the progression of glioma via affecting AKT and MAPK signaling pathways.

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