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Image Search Results
Journal: Bioengineering & Translational Medicine
Article Title: Utilizing induced neural stem cell‐based delivery of a cytokine cocktail to enhance chimeric antigen receptor‐modified T‐cell therapy for brain cancer
doi: 10.1002/btm2.10538
Figure Lengend Snippet: RANTES/IL‐15‐secreting GBM tumor cells enhance T‐cell trafficking and expansion. (a) RANTES and IL‐15 were detected in culture supernatant collected from transduced U87 tumor cells. (b) U87 or U87 RANTES‐IL‐15 were seeded and cultured for 24 or 48 h. Transwell inserts were added and CSPG4‐CAR‐T or control T cells were seeded therein. T cells were allowed to migrate through inserts for 5 h. Afterward, inserts were removed and media was collected for flow cytometry. (c) Migration of CSPG4‐CAR‐T or control T cells toward U87 or U87 RANTES‐IL‐15 cultured for 24 or 48 h was evaluated by flow cytometry ( n = 3). (d) NSG mice were implanted i.c. with U87, U87 RANTES‐IL‐15 , or PBS in the right hemisphere of the brain. Five days later, mice were infused i.v. with CSPG4‐CAR‐T. Mice were sacrificed 1, 4, or 7 days following CSPG4‐CAR‐T infusion. Brains were harvested, bisected along the interhemispheric fissure, and processed for flow cytometry ( n = 3). (e) CSPG4‐CAR‐T concentrations in single cell suspensions generated from bisected mouse brains (contralateral hemisphere vs tumor hemisphere) were analyzed by flow cytometry. Schematic(s) created with BioRender.com . * p < 0.05, ** p < 0.01, *** p < 0.001. CAR‐T, chimeric antigen receptor‐modified T cell; CSPG4‐CAR‐T, CAR‐T cells targeting chondroitin sulfate proteoglycan 4 antigen; GBM, glioblastoma; IL‐15, interuekin 15; NSG, NOD.Cg‐ Prkdc scid Il2rg tm1Wjl /SzJ.
Article Snippet: The
Techniques: Cell Culture, Control, Flow Cytometry, Migration, Generated, Modification
Journal: Bioengineering & Translational Medicine
Article Title: Utilizing induced neural stem cell‐based delivery of a cytokine cocktail to enhance chimeric antigen receptor‐modified T‐cell therapy for brain cancer
doi: 10.1002/btm2.10538
Figure Lengend Snippet: Development and characterization of hiNeuroS RANTES‐IL‐15 . (a) Schematic representation of lentivirus encoding human RANTES and IL‐15. (b) Human fibroblasts were transduced with LV‐RANTES‐IL‐15‐GFP, LV‐Sox2, and LV‐rtTA in succession. Reprogramming and primary hiNeuroS formation were initiated by switching to NSC growth media supplemented with growth factors and tetracycline. Three rounds of cell cluster selection were performed by serial seeding on laminin‐coated plates. After each round of selection, nonadhering cells were collected and expanded to yield secondary hiNeuroS. (c) Fluorescence imaging of hiNeuroS RANTES‐IL‐15 confirms successful LV‐RANTES‐IL‐15‐GFP transduction. Scale bar represents 100 μm. (d) RANTES and IL‐15 were detected in culture supernatant collected from transduced hiNeuroS. (e) Migration of CSPG4‐CAR‐T toward U87 ± NS‐CM or control media using a transwell migration assay was evaluated by flow cytometry ( n = 3). (f) CSPG4‐CAR‐T counts after 3 days in co‐culture with U87 ± NS‐CM ( n = 3). (g) Anti‐tumor activity of CSPG4‐CAR‐T after 3 days in co‐culture with U87 ± NS‐CM was assessed by bioluminescence ( n = 8–10). Schematic(s) created with BioRender.com . * p < 0.05, ** p < 0.01, *** p < 0.001. CAR‐T, chimeric antigen receptor‐modified T cell; CSPG4‐CAR‐T, CAR‐T cells targeting chondroitin sulfate proteoglycan 4 antigen; NSC, neural stem cell.
Article Snippet: The
Techniques: Transduction, Selection, Fluorescence, Imaging, Migration, Control, Transwell Migration Assay, Flow Cytometry, Co-Culture Assay, Activity Assay, Modification
Journal: Bioengineering & Translational Medicine
Article Title: Utilizing induced neural stem cell‐based delivery of a cytokine cocktail to enhance chimeric antigen receptor‐modified T‐cell therapy for brain cancer
doi: 10.1002/btm2.10538
Figure Lengend Snippet: Combination hiNeuroS RANTES‐IL‐15 + CAR‐T therapy increases CAR‐T infiltration and eradicates non‐invasive GBM. (a) Schematic representation of study design. NSG mice were implanted i.c. with FLuc + U87 ± hiNeuroS RANTES‐IL‐15 in the right hemisphere of the brain. Four days later, mice were infused i.v. with CSPG4‐CAR‐T or PBS ( n = 5–7). (b) Representative bioluminescent images depict U87 tumor growth. (c) Luminescence was quantified by calculating total flux within a region of interest centered on the head, then normalizing to Day 0 values. Dotted line signifies CAR‐T infusion. (d) Kaplan–Meier survival curves. (e) AUC was calculated for each normalized tumor growth curve. (f) CAR‐T tumor infiltration (brown) was assessed by immunohistochemistry. Schematic(s) created with BioRender.com . *** p < 0.001. CAR‐T, chimeric antigen receptor‐modified T cell; CSPG4‐CAR‐T, CAR‐T cells targeting chondroitin sulfate proteoglycan 4 antigen; GBM, glioblastoma; NSG, NOD.Cg‐ Prkdc scid Il2rg tm1Wjl /SzJ.
Article Snippet: The
Techniques: Immunohistochemistry, Modification
Journal: Journal of neurosurgery
Article Title: Resveratrol Targets AKT and p53 in Glioblastoma and Glioblastoma Stem-like Cells to Suppress Growth and Infiltration
doi: 10.3171/2016.1.JNS152077
Figure Lengend Snippet: Resveratrol inhibits the growth of GBM cells and GSCs. (A) Decreased U87 glioma cell and (B) 44-GSC proliferation upon resveratrol treatment compared to vehicle control (mean±S.D.; *p≤0.05; **p≤0.01; ***p≤0.001 using Student’s two-tailed t-Test, n=3 in each of 3 independent experiments). (C) Likewise, as little as 5 μM resveratrol inhibited sphere formation in multiple patient-derived GSC lines compared to the vehicle control (mean±S.D.; *p≤0.05 compared to 0 μM RES by ANOVA followed by post-hoc Tukey test, n = 3 in each of 3 independent experiments). RES, resveratrol.
Article Snippet: The
Techniques: Two Tailed Test, Derivative Assay
Journal: Journal of neurosurgery
Article Title: Resveratrol Targets AKT and p53 in Glioblastoma and Glioblastoma Stem-like Cells to Suppress Growth and Infiltration
doi: 10.3171/2016.1.JNS152077
Figure Lengend Snippet: Resveratrol inhibits tumor cell invasion in a Matrigel transwell assay. (A) U87 glioma cell invasion as a function of RES concentration; DAPI nuclear stain: white. (B): U87 glioma cell line invasion; mean±S.D.; p<0.05, n=3 in each of 3 independent experiments. (C) 44 GSC invasion; mean±S.D.; p<0.05, n=3 in each of 3 independent experiments). Res, resveratrol.
Article Snippet: The
Techniques: Transwell Assay, Concentration Assay, Staining
Journal: Journal of neurosurgery
Article Title: Resveratrol Targets AKT and p53 in Glioblastoma and Glioblastoma Stem-like Cells to Suppress Growth and Infiltration
doi: 10.3171/2016.1.JNS152077
Figure Lengend Snippet: Resveratrol decreases AKT activity in GBM cells and GSCs. (A) Top panel: Resveratrol treatment resulted in reduced AKT phosphorylation (ser473) in U87 glioma cells and the 44 GSC cell line (bottom panel), 48 hrs post-treatment, while minimally affecting total AKT protein. (B) Triciribine, a specific AKT inhibitor, did not affect U87 glioma cell growth up to 24 hrs post-treatment, although (C) it significantly suppressed migration as early as 4 hrs after treatment, compared to vehicle controls (mean±S.D.; p<0.05, n=3 in each of 3 independent experiments), and demonstrated synergistic anti-invasion effects with resveratrol (mean±S.D.; p<0.05, n=3 in each of 3 independent experiments). Res: resveratrol; Tri: triciribine.
Article Snippet: The
Techniques: Activity Assay, Migration
Journal: Journal of neurosurgery
Article Title: Resveratrol Targets AKT and p53 in Glioblastoma and Glioblastoma Stem-like Cells to Suppress Growth and Infiltration
doi: 10.3171/2016.1.JNS152077
Figure Lengend Snippet: Resveratrol activates p53 and p53 pathway genes. (A) Administration of 100 μM resveratrol to U87 glioma cells (top panel) or 44-GSCs (bottom panel) increased expression and phosphorylation of p53 tumor suppressor protein. (B) P53 activation was reduced by co-administration of a calcium chelator (BAPTA) in U87 glioma cells (top panel) but not in 44-GSCs (bottom panel). Resveratrol activation of p53 in U87 cells (C) and GSCs (D) resulted in expression of multiple downstream genes of p53 suppressor network, compared to vehicle control and detected by quantitative PCR.
Article Snippet: The
Techniques: Expressing, Activation Assay, Real-time Polymerase Chain Reaction
Journal: Journal of neurosurgery
Article Title: Resveratrol Targets AKT and p53 in Glioblastoma and Glioblastoma Stem-like Cells to Suppress Growth and Infiltration
doi: 10.3171/2016.1.JNS152077
Figure Lengend Snippet: Resveratrol inhibits U87 xenograft growth. (A) Resveratrol administered in water ad libitum to mice harboring U87 flank xenografts resulted in significantly reduced tumor growth compared to vehicle-treated controls (p<0.05, mean±S.D.; n=10 mice per group). Similar results were obtained with intragastric delivery of resveratrol; see Results. (B) Direct intra-tumoral injection of resveratrol (b, H&E) significantly decreased tumor volume in mice harboring U87 flank xenografts, compared to vehicle controls (a) (c: p<0.05, mean±S.D.; n=3 mice per group). (C) Brain concentrations of resveratrol were measured 5, 30, and 60 mins after either intravenous (IV) tail vein injection or intracranial (IC) delivery. Resveratrol molar concentrations [μM] are whole brain values for intravenous delivery and localized concentration for intracranial infusion, calculated as described in Materials and Methods.
Article Snippet: The
Techniques: Injection, Concentration Assay
Journal: Biochemistry and Biophysics Reports
Article Title: NF-κB signaling pathway mediates the anti-tumor effect of Ginsenoside Rg1 in glioblastoma
doi: 10.1016/j.bbrep.2026.102548
Figure Lengend Snippet: Evaluation of GS Rg1 Effect on the Viability and Proliferation of Human Glioblastoma U87-MG and U251-MG Cells using MTT and BrdU assays, Respectively. U87-MG(A and B) and U251-MG (C and D) cells were treated with 0, 5, 10 and 20 μM of GS Rg1 for 48 h, respectively. The viabilities were determined as percent compared to the controls. GS Rg1 inhibits proliferative properties of U87-MG and U251-MG cells in a concentration-dependent manner. The results are presented as mean ± SD from three independent experiments. (∗: p < 0.05, ∗∗: p < 0.01,and ∗∗∗: p < 0.001).
Article Snippet: The
Techniques: Concentration Assay
Journal: Biochemistry and Biophysics Reports
Article Title: NF-κB signaling pathway mediates the anti-tumor effect of Ginsenoside Rg1 in glioblastoma
doi: 10.1016/j.bbrep.2026.102548
Figure Lengend Snippet: Inhibition of MMP-2 and MMP-9 mRNA expression and activity of Extracellular Cathepsin B by GS Rg1 in U87-MG and U251-MG Cells. MMP2 (A and D) and MMP9 (B and E) expression levels were evaluated by reverse transcription-quantitative PCR. GS Rg1 at concentrations 5, 10 and 20 μM inhibited mRNA expression of MMP-2 and MMP-9, respectively. (C and F) Evaluation of GS Rg1 effect on proteolytic activity of extracellular Cathepsin B secreted from U87-MG and U251-MG cell line. GS Rg1 at concentrations 5, 10 and 20 μM inhibited activity of cathepsin, respectively. The values are given as mean ± SD compared with the control (∗: p < 0.05, ∗∗: p < 0.01, ∗∗∗: p < 0.001 and ∗∗∗∗: p < 0.0001).
Article Snippet: The
Techniques: Inhibition, Expressing, Activity Assay, Reverse Transcription, Real-time Polymerase Chain Reaction, Control
Journal: Biochemistry and Biophysics Reports
Article Title: NF-κB signaling pathway mediates the anti-tumor effect of Ginsenoside Rg1 in glioblastoma
doi: 10.1016/j.bbrep.2026.102548
Figure Lengend Snippet: Stimulation of Caspase-3 and Caspase-9 activity by GS Rg1 in U87-MG and U251-MG cells. (A and C) GS Rg1 increased activity of Caspase-3 in a concentration-dependent manner. (B and D) GS Rg1 increased activity of Caspase-9 in a concentration-dependent manner. The values are given as mean ± SD compared with the control (∗: p < 0.05, ∗∗: p < 0.01, and ∗∗∗: p < 0.001).
Article Snippet: The
Techniques: Activity Assay, Concentration Assay, Control
Journal: Biochemistry and Biophysics Reports
Article Title: NF-κB signaling pathway mediates the anti-tumor effect of Ginsenoside Rg1 in glioblastoma
doi: 10.1016/j.bbrep.2026.102548
Figure Lengend Snippet: Effect of GS Rg1 on transcriptional expression of proteins involved in Survival of Glioblastoma Cells. Transcriptional expression of IKK2(A and G), survivin (B and H), c-Myc (C and I), hTERT (D and J), NEMO (NF-κB regulators) (E and K), STAT3(F and L) in U87-MG and U251-MG cell line, after treatment with GS Rg1 for 48 h. Data are shown as fold change in relative expression compared with HPRT1 on the basis of comparative Ct (2-ΔΔCt) method. Values are shown as mean ± SD. Statistically different values of ∗: p < 0.05, ∗∗: p < 0.01, ∗∗∗: p < 0.001 and ∗∗∗∗: p < 0.0001 are determined compared with the control.
Article Snippet: The
Techniques: Expressing, Control
Journal: Biochemistry and Biophysics Reports
Article Title: NF-κB signaling pathway mediates the anti-tumor effect of Ginsenoside Rg1 in glioblastoma
doi: 10.1016/j.bbrep.2026.102548
Figure Lengend Snippet: Effect of GS Rg1 on transcriptional expression of proteins involved in apoptosis of Glioblastoma Cells. Transcriptional expression of Bax (A and I), Caspase-3 (B and J), Caspase-9 (C and K), Bcl-2 (D and L), Bax/Bcl-2 (E and M), Blf-1(F and N), Bcl-xl (G and O) and p21(H and P) in U87-MG and U251-MG cell line, after treatment with GS Rg1 for 48 h. Data are shown as fold change in relative expression compared with HPRT1 on the basis of comparative Ct (2-ΔΔCt) method. Values are shown as mean ± SD. Statistically different values of ∗: p < 0.05, ∗∗: p < 0.01, ∗∗∗: p < 0.001 and ∗∗∗∗: p < 0.0001 are determined compared with the control.
Article Snippet: The
Techniques: Expressing, Control
Journal: Biochemistry and Biophysics Reports
Article Title: NF-κB signaling pathway mediates the anti-tumor effect of Ginsenoside Rg1 in glioblastoma
doi: 10.1016/j.bbrep.2026.102548
Figure Lengend Snippet: Effect of GS Rg1 on transcriptional expression of proteins involved in invasion and media pH change of Glioblastoma Cells. Transcriptional expression of MMP14 (A and G), Cathepsin B (B and H), uPA (C and I), uPAR (D and J), CA9 (E and K) and NHE1(F and L) in U87-MG and U251-MG cell line, after treatment with GS Rg1 for 48 h. Data are shown as fold change in relative expression compared with HPRT1 on the basis of comparative Ct (2-ΔΔCt) method. Values are shown as mean ± SD. Statistically different values of ∗: p < 0.05, ∗∗: p < 0.01, ∗∗∗: p < 0.001 and ∗∗∗∗: p < 0.0001 are determined compared with the control.
Article Snippet: The
Techniques: Expressing, Control
Journal: Cancer cell international
Article Title: Circular RNA circPTPRF promotes the progression of GBM via sponging miR-1208 to up-regulate YY1.
doi: 10.1186/s12935-022-02753-1
Figure Lengend Snippet: Fig. 2 Overexpression of circPTPRF promoted proliferation and invasion of glioma in vitro. a: The expression of circPTPRF in U87 and GSC15 after transfec tion of the circPTPRF overexpression plasmids measured by qPCR. b, c: CircPTPRF overexpression increased the proliferation of U87 and GSC15 in MTS assays. d, e: Proliferation of tumor cells was promoted after circPTPRF overexpression as measured by Edu assays. Scale bar = 50 μm. f, g: Representative im ages of transwell assay to demonstrate invasion capacity can be promoted after circPTPRF overexpression. Scale bar = 50 μm. h-k: Representative images of neurospheres (k, l) and extreme limiting dilution assays (m, n) showed tumor formation rate up-regulated after circPTPRF overexpression in U87-GSCs and GSC15. Scale bar = 50 μm. All data are shown as the mean ± SD (three independent experiments). *P < 0.05; **P < 0.01; ***P < 0.001
Article Snippet: Cell treatment and
Techniques: Over Expression, In Vitro, Expressing, Transwell Assay
Journal: Cancer cell international
Article Title: Circular RNA circPTPRF promotes the progression of GBM via sponging miR-1208 to up-regulate YY1.
doi: 10.1186/s12935-022-02753-1
Figure Lengend Snippet: Fig. 3 CircPTPRF knockdown suppressed the proliferation and invasion of glioma in vitro. a: The expression of circPTPRF in LN229 and GSC17 after trans fection of circPTPRF -KD1, circPTPRF -KD2 or negative control measured by qPCR. b, c: CircPTPRF knockdown significantly decreased the proliferation of LN229 and GSC17 in MTS assays. d, e: CircPTPRF knockdown can greatly reduce the proliferative capacity of LN229 and GSC17 measured by Edu assays. Scale bar = 50 μm. f, g: Representative images of transwell assay to demonstrate invasion capacity can be suppressed after circPTPRF knockdown. Scale bar = 50 μm. h-k: Neurospheres formation assays and extreme limiting dilution assays showed that the tumor formation rates decreased after circPTPRF knockdown in LN229-GSCs and GSC17. Scale bar = 50 μm. All data are shown as the mean ± SD (three independent experiments). *P < 0.05; **P < 0.01; ***P < 0.001
Article Snippet: Cell treatment and
Techniques: Knockdown, In Vitro, Expressing, Negative Control, Transwell Assay
Journal: PLoS ONE
Article Title: DMA, a Bisbenzimidazole, Offers Radioprotection by Promoting NFκB Transactivation through NIK/IKK in Human Glioma Cells
doi: 10.1371/journal.pone.0039426
Figure Lengend Snippet: (A) Structure of the DNA minor groove binding ligand DMA –5-(4-methylpiperazin-1-yl)-2-[2′-(3,4-dimethoxyphenyl)-5′-benzimidazolyl] benzimidazole.(B) Effect of varying concentrations of DMA on metabolic viability studied by MTT assay in exponential growing HDF,MCF10A and U87 cells at 24 h, (C) At 48 h (D) At 72 h.Values are mean (±SD) of three independent experiments.Statistical significance by T-test p<0.05.
Article Snippet: The
Techniques: Binding Assay, MTT Assay
Journal: PLoS ONE
Article Title: DMA, a Bisbenzimidazole, Offers Radioprotection by Promoting NFκB Transactivation through NIK/IKK in Human Glioma Cells
doi: 10.1371/journal.pone.0039426
Figure Lengend Snippet: List of pathways and number of genes in each pathway identified in U87 cells in three different treatment conditions DMA (50 µM), radiation (8.5 Gy) and DMA+ radiation (50 µM +8.5 Gy) after 4 h by Microarray hybridization studies.
Article Snippet: The
Techniques: Microarray, Hybridization, Ubiquitin Proteomics
Journal: PLoS ONE
Article Title: DMA, a Bisbenzimidazole, Offers Radioprotection by Promoting NFκB Transactivation through NIK/IKK in Human Glioma Cells
doi: 10.1371/journal.pone.0039426
Figure Lengend Snippet: List of genes differentially regulated in U87 cells 4 h after treatment with DMA (50 µM), radiation (8.5 Gy) and DMA + radiation (50 µM+8.5 Gy).
Article Snippet: The
Techniques: Binding Assay, Activation Assay, Protein Binding, Activity Assay, Histone Deacetylase Assay
Journal: PLoS ONE
Article Title: DMA, a Bisbenzimidazole, Offers Radioprotection by Promoting NFκB Transactivation through NIK/IKK in Human Glioma Cells
doi: 10.1371/journal.pone.0039426
Figure Lengend Snippet: U87 cells were treated with 50 µM DMA and/or 8.5 Gy ionizing radiation. RNA samples were prepared 4 h after treatments. YWHAZ (14-3-3 zeta), MAP3K3 (Mitogen activated protein kinase kinasekinase 3), MAP3K7 (Mitogen activated protein kinase kinasekinase 7), MAP3K14 (Mitogen activated protein kinase kinase 14), MAPK10 (Mitogen activated protein kinase 10) and NFκB (Nuclear Factor Kappa B/Rel A subunit) were quantitated by Real Time PCRusing RNA samples from U87 glioma cell line. Values represent Mean±S.D.(*indicates statistical significance by T-test, *p<0.05).
Article Snippet: The
Techniques:
Journal: PLoS ONE
Article Title: DMA, a Bisbenzimidazole, Offers Radioprotection by Promoting NFκB Transactivation through NIK/IKK in Human Glioma Cells
doi: 10.1371/journal.pone.0039426
Figure Lengend Snippet: U87, human glioma cells were transiently transfected with control-siRNA. Cells were induced with 10 ng/ml TNF-α for 0,5,10,20,40,60 min and treated with DMA (50 µM) and/or irradiated at 8.5 Gy. Phosphorylation of IKKα, IKKβ was observed in DMA treated cells, alone or in combination with IR.
Article Snippet: The
Techniques: Transfection, Control, Irradiation, Phospho-proteomics
Journal: PLoS ONE
Article Title: DMA, a Bisbenzimidazole, Offers Radioprotection by Promoting NFκB Transactivation through NIK/IKK in Human Glioma Cells
doi: 10.1371/journal.pone.0039426
Figure Lengend Snippet: U87, human glioma cells were transiently transfected with siRNA-NIK. Phosphorylation of IKKα, IKKβ was absent concurrent with equivalent expression of IκBα in response to both DMA and radiation treatment.
Article Snippet: The
Techniques: Transfection, Phospho-proteomics, Expressing
Journal: PLoS ONE
Article Title: DMA, a Bisbenzimidazole, Offers Radioprotection by Promoting NFκB Transactivation through NIK/IKK in Human Glioma Cells
doi: 10.1371/journal.pone.0039426
Figure Lengend Snippet: U87, human glioma cells were transiently transfected with p3XFLAG CMV10 NIK. Phosphorylation of IKKα, IKKβ was advanced in NIK overexpressing cells as compared to siRNA transfected cells in response to DMA treatment, alone or in combination with IR.
Article Snippet: The
Techniques: Transfection, Phospho-proteomics
Journal: PLoS ONE
Article Title: DMA, a Bisbenzimidazole, Offers Radioprotection by Promoting NFκB Transactivation through NIK/IKK in Human Glioma Cells
doi: 10.1371/journal.pone.0039426
Figure Lengend Snippet: (A) U87 cells (Control siRNA transfected) were treated with 50 µM DMA and 8.5 Gy Radiation. Post treatment cells were seeded in 6 well plates seeded at 8000 cells/cm2, and their proliferation kinetics was studied at 24 h intervals following trypsinization and counting total cells per well using a hemocytometer. (B) U87 Cells post siRNA-NIK oligonucleotide transfection were treated with 50 µM DMA and 8.5 Gy Radiation. Post treatment cells were seeded in 6 well plates seeded at 8000 cells/cm2, and their proliferation kinetics was studied at 24 h intervals following trypsinization and counting total cells per well using a hemocytometer. Values are mean (±SD) of three independent experiments.Statistical significance by T-test p<0.05.
Article Snippet: The
Techniques: Control, Transfection
Journal: PLoS ONE
Article Title: DMA, a Bisbenzimidazole, Offers Radioprotection by Promoting NFκB Transactivation through NIK/IKK in Human Glioma Cells
doi: 10.1371/journal.pone.0039426
Figure Lengend Snippet: (A) Apoptosis analysis of control siRNA transfected U87 cells at 3 h, 6 h in different treatment condition i.e. 50 µM DMA, radiation (8.5 Gy) and DMA (50 µM) + Radiation (8.5 Gy). Percentage of apoptosis is defined by % of cells that are Annexin V + and Annexin V + PI + . (B) Apoptosis analysis of siRNA-NIK transfected U87 cells at 3 h, 6 h in different treatment condition i.e. 50 µM DMA, radiation (8.5 Gy) and DMA (50 µM) + Radiation (8.5 Gy). Percentage of apoptosis is defined by % of cells that are Annexin V + and Annexin V + PI + . (C) Percentage of Annexin V + and Annexin V + PI + .positive cells in control siRNA transfected U87 cells at, 3 h,6 h, and 24 h in different treatment condition i.e. 50 µM DMA, radiation (8.5 Gy) and DMA (50 µM) + Radiation(8.5 Gy). (Data Not shown for 6 h and 12 h for only DMA and only radiation treatment condition). (D) Percentage of ofAnnexin V + and Annexin V + PI + .positive cellssiRNA-NIK transfected U87 cells at 3 h, 6 h, and 24 h in different treatment condition i.e. 50 µM DMA, radiation (8.5 Gy) and DMA (50 µM) + Radiation (8.5 Gy).(Data Not shown for 6 h and 12 h for only DMA and only radiation treatment condition). (E) Time course graphs showing the progression of cell cycle of control siRNA transfected U87 cells at 0, 3, 6, 12, 18 and 24 h in different treatment condition i.e. 50 µM DMA, radiation (8.5 Gy) and DMA (50 µM) + Radiation(8.5 Gy). (F) Time course graphs showing the progression of cell cycle of siRNA-NIK transfected U87 cells at 0, 3, 6, 12, 18 and 24 h in different treatment condition i.e. 50 µM DMA, radiation (8.5 Gy) and DMA (50 µM) + Radiation(8.5 Gy). (G) Cell cycle progression of control siRNA transfected U87 cells showing % G2-M fraction at 0, 3, 6, 12, 18 and 24 h in different treatment condition i.e. 50 µM DMA, radiation (8.5 Gy) and DMA (50 µM) + Radiation(8.5 Gy). (H) Cell cycle progression of siRNA-NIK transfected U87 cells showing % G2-M fraction at 0, 3, 6, 12, 18 and 24 h in different treatment condition i.e. 50 µM DMA, radiation (8.5 Gy) and DMA (50 µM) + Radiation(8.5 Gy).
Article Snippet: The
Techniques: Control, Transfection
Journal: Cancers
Article Title: Paliperidone Inhibits Glioblastoma Growth in Mouse Brain Tumor Model and Reduces PD-L1 Expression
doi: 10.3390/cancers13174357
Figure Lengend Snippet: DRD2 involved in the PD-L1 expression in GBM cells in the GBM-macrophage co-culture system. ( A ) U87-GFP and U251-GFP cells were co-cultured with the THP-1 differentiated macrophage for 48 h. PD-L1 expression was determined by flow cytometry analysis. ( B ) U87-GFP and U251-GFP cells were treated with paliperidone (20 μM, PAL) for 30 min, and cells were then co-cultured with THP-1 macrophages (HM) after wash-out of paliperidone for 48 h. PD-L1 expression on GBM was determined by flow cytometry analysis. * p < 0.05 compared with GBM alone group. # p < 0.05 compared with THP-1 group. ( C ) THP-1 macrophages (HM) were treated with paliperidone (20 μM, PAL) for 30 min, washed out for 48 h, and then co-cultured with U87-GFP and U251-GFP cells. PD-L1 expression on cell surface of HM was determined by flow cytometry analysis. * p < 0.05 compared with THP-1 alone group. # p < 0.05 compared with U87 or U251 groups ( n = 3–4).
Article Snippet:
Techniques: Expressing, Co-Culture Assay, Cell Culture, Flow Cytometry
Journal: Cancers
Article Title: Paliperidone Inhibits Glioblastoma Growth in Mouse Brain Tumor Model and Reduces PD-L1 Expression
doi: 10.3390/cancers13174357
Figure Lengend Snippet: GBM primed macrophage potentiates PD-L1 expression in GBMs. Human U87 ( A , C , E ) and U251 ( B , D , F ) GBM were incubated with GBM cultured medium, THP-1 cultured medium, HM CM, or HM/GCM CM for 48 h. PD-L1 expression was determined by flow cytometry analysis ( A , B ), Western blot ( C and D ), and real time-PCR ( E , F ). * p < 0.05 compared with GBM alone group. # p < 0.05 compared with HM CM group. ( n = 3–4).
Article Snippet:
Techniques: Expressing, Incubation, Cell Culture, Flow Cytometry, Western Blot, Real-time Polymerase Chain Reaction
Journal: Journal of Korean Medical Science
Article Title: Silencing of Long Non-Coding RNA MALAT1 Promotes Apoptosis of Glioma Cells
doi: 10.3346/jkms.2016.31.5.688
Figure Lengend Snippet: MALAT1 was highly expressed in glioma patients and cell lines. ( A ) 37 glioma tissue samples and adjacent normal brain samples were selected, and then qRT-PCR assay was employed to detect the relative expression level of MALAT1 in glioma patients. The adjacent normal brain tissues (paracancer group) were used as the negative control. ( B ) Human malignant glioma cell lines U87 and U251 cells were cultured, and then qRT-PCR assay was employed to detect the relative expression level of MALAT1 in both cells. The normal glia cell line NHA was used as the negative control. ( C ) U87 and U251 cells were transfected with siRNA targeting MALAT1, QRT-PCR assay was employed to detect the endogenous expression of MALAT1 to confirm the knockdown efficiency. The glioma cells transfected with Scramble was used as the negative control. * P < 0.05 vs. the control; † P < 0.01 vs. the control.
Article Snippet: Normal glia cell line NHA and the human
Techniques: Quantitative RT-PCR, Expressing, Negative Control, Cell Culture, Transfection, Knockdown, Control
Journal: Journal of Korean Medical Science
Article Title: Silencing of Long Non-Coding RNA MALAT1 Promotes Apoptosis of Glioma Cells
doi: 10.3346/jkms.2016.31.5.688
Figure Lengend Snippet: Knockdown of MALAT1 decreased the growth of glioma cells. ( A, B ) U87 and U251 cells were seeded into 96-well plates and cultured for 0 hours, 24 hours, 48 hours, 72 hours and 96 hours respectively, MTT assay was employed to detect the effect of MALAT1 knockdown on cell growth at different time points in both cells. The glioma cells transfected with Scramble was used as the negative control. * P < 0.05 vs. the control. ( C, D ) U87 and U251 cells in serum-free medium were placed into the upper transwell chamber, the invasion assays in vitro were carried out to detect the effect of MALAT1 knockdown on cell invasion after 24 hours of incubation. The glioma cells transfected with Scramble was used as the negative control. * P < 0.05 vs. the control.
Article Snippet: Normal glia cell line NHA and the human
Techniques: Knockdown, Cell Culture, MTT Assay, Transfection, Negative Control, Control, In Vitro, Incubation
Journal: Journal of Korean Medical Science
Article Title: Silencing of Long Non-Coding RNA MALAT1 Promotes Apoptosis of Glioma Cells
doi: 10.3346/jkms.2016.31.5.688
Figure Lengend Snippet: Knockdown of MALAT1 increased the apoptosis rate of glioma cells. ( A, B ) U87 and U251 cells were seeded in 6 well plates and grow to a confluency of 70%, then both cells were transfected with si-MALAT1 or Scramble respectively. Annexin V-FITC/PI double staining assay was employed to detect the effect of MALAT1 knockdown on the apoptosis rate in U87 ( A ) and U251 ( B ) cells. The glioma cells transfected with Scramble was used as the negative control. FL2-H, FL2-Height.
Article Snippet: Normal glia cell line NHA and the human
Techniques: Knockdown, Transfection, Double Staining, Negative Control
Journal: Journal of Korean Medical Science
Article Title: Silencing of Long Non-Coding RNA MALAT1 Promotes Apoptosis of Glioma Cells
doi: 10.3346/jkms.2016.31.5.688
Figure Lengend Snippet: CCND1 and MYC was down-regulated with MALAT1 knockdown. U87 and U251 cells were seeded in 60 mm plates and grow to a confluency of 70%, then both cells were transfected with si-MALAT1 or Scramble respectively. QRT-PCR and western blot analysis were employed to verify the change of expression levels of CCND1 and MYC in response to MALAT1 knockdown in U87 cells ( A, B ) and U251 cells ( C, D ). The cells transfected with Scramble was used as the negative control. * P < 0.05 vs. the control; † P < 0.01 vs. the control.
Article Snippet: Normal glia cell line NHA and the human
Techniques: Knockdown, Transfection, Quantitative RT-PCR, Western Blot, Expressing, Negative Control, Control