human tumor brain cell line u87 mg Search Results


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ATCC u87 glioma cell line
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 <t>U87</t> 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.
U87 Glioma Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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CLS Cell Lines Service GmbH u87 mg u87 cell lines
Effect of arginine deprivation on glioblastoma cells. a Cell growth of U251 ( upper panel ) and <t>U87</t> ( lower panel ) cells cultivated in control, -Arg, -Lys and conditions. b U251 cell viability assessed under deprivation and re-supplementation conditions, as indicated. Upper and lower panels , arginine and lysine re-supplementation, respectively. 100 %, the number of the viable cells at time 0. Data in a and b are means ± SD; *** and *Statistical relevance p < 0.001 and p < 0.05, respectively
U87 Mg U87 Cell Lines, supplied by CLS Cell Lines Service GmbH, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Procell Inc human glioma cell line u87 mg
Evaluation of GS Rg1 Effect on the Viability and Proliferation of Human <t>Glioblastoma</t> <t>U87-MG</t> 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).
Human Glioma Cell Line U87 Mg, supplied by Procell Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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96
ATCC human glioblastoma
Evaluation of GS Rg1 Effect on the Viability and Proliferation of Human <t>Glioblastoma</t> <t>U87-MG</t> 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).
Human Glioblastoma, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC human cancer cell lines
Evaluation of GS Rg1 Effect on the Viability and Proliferation of Human <t>Glioblastoma</t> <t>U87-MG</t> 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).
Human Cancer Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC human tumor cell lines
Evaluation of GS Rg1 Effect on the Viability and Proliferation of Human <t>Glioblastoma</t> <t>U87-MG</t> 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).
Human Tumor Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC human carcinoma cell lines
Evaluation of GS Rg1 Effect on the Viability and Proliferation of Human <t>Glioblastoma</t> <t>U87-MG</t> 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).
Human Carcinoma Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC human cervical cancer cell lines
Evaluation of GS Rg1 Effect on the Viability and Proliferation of Human <t>Glioblastoma</t> <t>U87-MG</t> 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).
Human Cervical Cancer Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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96
ATCC glioma cell lines
Evaluation of GS Rg1 Effect on the Viability and Proliferation of Human <t>Glioblastoma</t> <t>U87-MG</t> 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).
Glioma Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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99
ATCC human cell lines
Evaluation of GS Rg1 Effect on the Viability and Proliferation of Human <t>Glioblastoma</t> <t>U87-MG</t> 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).
Human Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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97
ATCC human glioblastoma cell line u87mg
Fig. 1. Analysis of COL16A1 knockdown efficiency. (A) The knockdown was translated to the protein level as shown for the full-length collagen XVI chain in cell lysates in comparison to the scr control and untreated <t>U87MG</t> cells. E-actin. protein expression is unaffected which indicates a specific knockdown of collagen XVI. N = 4 (B) Collagen XVI inhibited cells secreted less collagen XVI into the supernatant in comparison to scr controls. Ponceau Red stained blot membrane served as loading control. N=3 (C) Knockdown efficiency of COL16A1 was analyzed with qRT-PCR and shows an average of 60% lower COL16A1 gene expression in transfected U87MG cells (si1 and si2) compared to control cells transfected with scrambled RNA (scr). N = 19, si1= siRNA 1, si2 = siRNA 2, scr = scrambled RNA = controls.
Human Glioblastoma Cell Line U87mg, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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BioResource International Inc u87-mg human glioma cell line
Fig. 1. Analysis of COL16A1 knockdown efficiency. (A) The knockdown was translated to the protein level as shown for the full-length collagen XVI chain in cell lysates in comparison to the scr control and untreated <t>U87MG</t> cells. E-actin. protein expression is unaffected which indicates a specific knockdown of collagen XVI. N = 4 (B) Collagen XVI inhibited cells secreted less collagen XVI into the supernatant in comparison to scr controls. Ponceau Red stained blot membrane served as loading control. N=3 (C) Knockdown efficiency of COL16A1 was analyzed with qRT-PCR and shows an average of 60% lower COL16A1 gene expression in transfected U87MG cells (si1 and si2) compared to control cells transfected with scrambled RNA (scr). N = 19, si1= siRNA 1, si2 = siRNA 2, scr = scrambled RNA = controls.
U87 Mg Human Glioma Cell Line, supplied by BioResource International Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


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.

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 U87 glioma cell line and human telomerase reverse transcriptase (hTERT)‐immortalized normal human fibroblasts (NHF1) were obtained from the American Type Culture Collection and as previously described.

Techniques: Cell Culture, Control, Flow Cytometry, Migration, Generated, Modification

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.

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 U87 glioma cell line and human telomerase reverse transcriptase (hTERT)‐immortalized normal human fibroblasts (NHF1) were obtained from the American Type Culture Collection and as previously described.

Techniques: Transduction, Selection, Fluorescence, Imaging, Migration, Control, Transwell Migration Assay, Flow Cytometry, Co-Culture Assay, Activity Assay, Modification

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.

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 U87 glioma cell line and human telomerase reverse transcriptase (hTERT)‐immortalized normal human fibroblasts (NHF1) were obtained from the American Type Culture Collection and as previously described.

Techniques: Immunohistochemistry, Modification

Effect of arginine deprivation on glioblastoma cells. a Cell growth of U251 ( upper panel ) and U87 ( lower panel ) cells cultivated in control, -Arg, -Lys and conditions. b U251 cell viability assessed under deprivation and re-supplementation conditions, as indicated. Upper and lower panels , arginine and lysine re-supplementation, respectively. 100 %, the number of the viable cells at time 0. Data in a and b are means ± SD; *** and *Statistical relevance p < 0.001 and p < 0.05, respectively

Journal: Amino Acids

Article Title: Arginine deprivation affects glioblastoma cell adhesion, invasiveness and actin cytoskeleton organization by impairment of β-actin arginylation

doi: 10.1007/s00726-014-1857-1

Figure Lengend Snippet: Effect of arginine deprivation on glioblastoma cells. a Cell growth of U251 ( upper panel ) and U87 ( lower panel ) cells cultivated in control, -Arg, -Lys and conditions. b U251 cell viability assessed under deprivation and re-supplementation conditions, as indicated. Upper and lower panels , arginine and lysine re-supplementation, respectively. 100 %, the number of the viable cells at time 0. Data in a and b are means ± SD; *** and *Statistical relevance p < 0.001 and p < 0.05, respectively

Article Snippet: Human glioblastoma U251 MG (U251) and U87 MG (U87) cell lines were purchased from CLS Cell Lines Service (Germany) and monitored for correct genetic profile via microsatellite analyses according to a protocol described earlier (Peickert et al. ).

Techniques:

Arginine deprivation affects morphology of glioblastoma but not glia cells. a , b , d Rat glia, U251 and U87 cells stained with Alexa 488-phalloidin, respectively. c Micrographs of U251 cells attained with scanning electron microscope. Insets in a , b and d ~2–3× magnification of the marked areas . Bars , in a , b and d 50 μm, and in c 10 μm. e U251 cells stained with Alexa 488-phalloidin before and after re-supplementation with Arg or Lys up to 0.4 and 0.8 mM concentration, respectively. Arrows point to lamellipodia, arrowheads point to elongated cells

Journal: Amino Acids

Article Title: Arginine deprivation affects glioblastoma cell adhesion, invasiveness and actin cytoskeleton organization by impairment of β-actin arginylation

doi: 10.1007/s00726-014-1857-1

Figure Lengend Snippet: Arginine deprivation affects morphology of glioblastoma but not glia cells. a , b , d Rat glia, U251 and U87 cells stained with Alexa 488-phalloidin, respectively. c Micrographs of U251 cells attained with scanning electron microscope. Insets in a , b and d ~2–3× magnification of the marked areas . Bars , in a , b and d 50 μm, and in c 10 μm. e U251 cells stained with Alexa 488-phalloidin before and after re-supplementation with Arg or Lys up to 0.4 and 0.8 mM concentration, respectively. Arrows point to lamellipodia, arrowheads point to elongated cells

Article Snippet: Human glioblastoma U251 MG (U251) and U87 MG (U87) cell lines were purchased from CLS Cell Lines Service (Germany) and monitored for correct genetic profile via microsatellite analyses according to a protocol described earlier (Peickert et al. ).

Techniques: Staining, Microscopy, Concentration Assay

Arginine deprivation impairs cell motility. a , b Migration tracks of U251 and U87 cells, respectively. Upper panels in a and b tracks of 10 randomly chosen cells; center panels images of migrating cells, and lower panels values of migration rate and mean distance based on tracks shown in upper panels . Values are means ± SD. ***Statistical relevance p < 0.001

Journal: Amino Acids

Article Title: Arginine deprivation affects glioblastoma cell adhesion, invasiveness and actin cytoskeleton organization by impairment of β-actin arginylation

doi: 10.1007/s00726-014-1857-1

Figure Lengend Snippet: Arginine deprivation impairs cell motility. a , b Migration tracks of U251 and U87 cells, respectively. Upper panels in a and b tracks of 10 randomly chosen cells; center panels images of migrating cells, and lower panels values of migration rate and mean distance based on tracks shown in upper panels . Values are means ± SD. ***Statistical relevance p < 0.001

Article Snippet: Human glioblastoma U251 MG (U251) and U87 MG (U87) cell lines were purchased from CLS Cell Lines Service (Germany) and monitored for correct genetic profile via microsatellite analyses according to a protocol described earlier (Peickert et al. ).

Techniques: Migration

Arginine deprivation impairs cell migration and invasiveness. Transwell filters not covered ( a ), and covered with Matrigel ( b , c) were used for analyses. Upper and lower panels in a and b images of U251 and U87 stained cells, respectively, taken on the filter trans side. c Images of LN-229 cells, analyzed as in b . Analyses were performed for three independent experiments run in duplicates. d Images of GFP-expressing U251 cells found within the E13 organotypic brain slice. The images represent the confocal 12.3-μm z -section of the planar center of brain slices. Right panel the quantification of GFP-expressing U251 cells within the confocal center of the slice per view area. The quantitative data in a – d are presented as % of control. Values are means ± SD. ***Statistical relevance p < 0.001

Journal: Amino Acids

Article Title: Arginine deprivation affects glioblastoma cell adhesion, invasiveness and actin cytoskeleton organization by impairment of β-actin arginylation

doi: 10.1007/s00726-014-1857-1

Figure Lengend Snippet: Arginine deprivation impairs cell migration and invasiveness. Transwell filters not covered ( a ), and covered with Matrigel ( b , c) were used for analyses. Upper and lower panels in a and b images of U251 and U87 stained cells, respectively, taken on the filter trans side. c Images of LN-229 cells, analyzed as in b . Analyses were performed for three independent experiments run in duplicates. d Images of GFP-expressing U251 cells found within the E13 organotypic brain slice. The images represent the confocal 12.3-μm z -section of the planar center of brain slices. Right panel the quantification of GFP-expressing U251 cells within the confocal center of the slice per view area. The quantitative data in a – d are presented as % of control. Values are means ± SD. ***Statistical relevance p < 0.001

Article Snippet: Human glioblastoma U251 MG (U251) and U87 MG (U87) cell lines were purchased from CLS Cell Lines Service (Germany) and monitored for correct genetic profile via microsatellite analyses according to a protocol described earlier (Peickert et al. ).

Techniques: Migration, Staining, Expressing, Slice Preparation

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).

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 human glioma cell line U87-MG (U87 Malignant Glioma, #CL-0238; Wuhan, China) and U251-MG(U251 Malignant Glioma, #CL-0237; Wuhan, China) were obtained from Procell and cultured in Dulbecco's Modified Eagle's Medium (DMEM; Gibco, Grand Island, NY, USA) supplemented with 10% fetal bovine serum (Zhejiang Tianhang Biotechnology, Huzhou, China) and 1% antibiotics (Gibco), at 37 °C in a 5% CO 2 atmosphere.

Techniques: Concentration Assay

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).

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 human glioma cell line U87-MG (U87 Malignant Glioma, #CL-0238; Wuhan, China) and U251-MG(U251 Malignant Glioma, #CL-0237; Wuhan, China) were obtained from Procell and cultured in Dulbecco's Modified Eagle's Medium (DMEM; Gibco, Grand Island, NY, USA) supplemented with 10% fetal bovine serum (Zhejiang Tianhang Biotechnology, Huzhou, China) and 1% antibiotics (Gibco), at 37 °C in a 5% CO 2 atmosphere.

Techniques: Inhibition, Expressing, Activity Assay, Reverse Transcription, Real-time Polymerase Chain Reaction, Control

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).

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 human glioma cell line U87-MG (U87 Malignant Glioma, #CL-0238; Wuhan, China) and U251-MG(U251 Malignant Glioma, #CL-0237; Wuhan, China) were obtained from Procell and cultured in Dulbecco's Modified Eagle's Medium (DMEM; Gibco, Grand Island, NY, USA) supplemented with 10% fetal bovine serum (Zhejiang Tianhang Biotechnology, Huzhou, China) and 1% antibiotics (Gibco), at 37 °C in a 5% CO 2 atmosphere.

Techniques: Activity Assay, Concentration Assay, Control

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.

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 human glioma cell line U87-MG (U87 Malignant Glioma, #CL-0238; Wuhan, China) and U251-MG(U251 Malignant Glioma, #CL-0237; Wuhan, China) were obtained from Procell and cultured in Dulbecco's Modified Eagle's Medium (DMEM; Gibco, Grand Island, NY, USA) supplemented with 10% fetal bovine serum (Zhejiang Tianhang Biotechnology, Huzhou, China) and 1% antibiotics (Gibco), at 37 °C in a 5% CO 2 atmosphere.

Techniques: Expressing, Control

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.

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 human glioma cell line U87-MG (U87 Malignant Glioma, #CL-0238; Wuhan, China) and U251-MG(U251 Malignant Glioma, #CL-0237; Wuhan, China) were obtained from Procell and cultured in Dulbecco's Modified Eagle's Medium (DMEM; Gibco, Grand Island, NY, USA) supplemented with 10% fetal bovine serum (Zhejiang Tianhang Biotechnology, Huzhou, China) and 1% antibiotics (Gibco), at 37 °C in a 5% CO 2 atmosphere.

Techniques: Expressing, Control

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.

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 human glioma cell line U87-MG (U87 Malignant Glioma, #CL-0238; Wuhan, China) and U251-MG(U251 Malignant Glioma, #CL-0237; Wuhan, China) were obtained from Procell and cultured in Dulbecco's Modified Eagle's Medium (DMEM; Gibco, Grand Island, NY, USA) supplemented with 10% fetal bovine serum (Zhejiang Tianhang Biotechnology, Huzhou, China) and 1% antibiotics (Gibco), at 37 °C in a 5% CO 2 atmosphere.

Techniques: Expressing, Control

Fig. 1. Analysis of COL16A1 knockdown efficiency. (A) The knockdown was translated to the protein level as shown for the full-length collagen XVI chain in cell lysates in comparison to the scr control and untreated U87MG cells. E-actin. protein expression is unaffected which indicates a specific knockdown of collagen XVI. N = 4 (B) Collagen XVI inhibited cells secreted less collagen XVI into the supernatant in comparison to scr controls. Ponceau Red stained blot membrane served as loading control. N=3 (C) Knockdown efficiency of COL16A1 was analyzed with qRT-PCR and shows an average of 60% lower COL16A1 gene expression in transfected U87MG cells (si1 and si2) compared to control cells transfected with scrambled RNA (scr). N = 19, si1= siRNA 1, si2 = siRNA 2, scr = scrambled RNA = controls.

Journal: Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

Article Title: Inhibition of collagen XVI expression reduces glioma cell invasiveness.

doi: 10.1159/000327947

Figure Lengend Snippet: Fig. 1. Analysis of COL16A1 knockdown efficiency. (A) The knockdown was translated to the protein level as shown for the full-length collagen XVI chain in cell lysates in comparison to the scr control and untreated U87MG cells. E-actin. protein expression is unaffected which indicates a specific knockdown of collagen XVI. N = 4 (B) Collagen XVI inhibited cells secreted less collagen XVI into the supernatant in comparison to scr controls. Ponceau Red stained blot membrane served as loading control. N=3 (C) Knockdown efficiency of COL16A1 was analyzed with qRT-PCR and shows an average of 60% lower COL16A1 gene expression in transfected U87MG cells (si1 and si2) compared to control cells transfected with scrambled RNA (scr). N = 19, si1= siRNA 1, si2 = siRNA 2, scr = scrambled RNA = controls.

Article Snippet: Materials and Methods Cell Culture The human glioblastoma cell line U87MG (ATCC: HTB- 14) was cultured in high glucose Dulbecco’s modified Eagle’s medium (DMEM, Invitrogen, Paisley, UK) supplemented with 10% fetal calf serum (Sigma, St. Louis, USA) and 1% penicillin/ streptomycin (PAA, Coelbe, Germany) at 37°C in 5% CO2.

Techniques: Knockdown, Comparison, Control, Expressing, Staining, Membrane, Quantitative RT-PCR, Gene Expression, Transfection

Fig. 2. Cell morphology and number of focal adhesion contacts. (A) U87MG cells were stained using vinculin antibodies to visualize cell morphology and focal adhesion contacts. Representative images (magnification 200x and 400x) demonstrate that in collagen XVI-knockdown cells FACs were found more concentrated in the cellular periphery while in control cells FACs (white arrows) appeared to be more evenly distributed. N = 4. (B) The number of FACs per cell is significantly decreased in collagen XVI knockdown cells. The evaluation of the number of focal adhesion contacts yielded a significant decrease of 40-45% of FACs per cell after inhibition of collagen XVI. A similar reduction of focal adhesion contacts was observed for both siRNAs. N = 4; * = p < 0.05.

Journal: Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

Article Title: Inhibition of collagen XVI expression reduces glioma cell invasiveness.

doi: 10.1159/000327947

Figure Lengend Snippet: Fig. 2. Cell morphology and number of focal adhesion contacts. (A) U87MG cells were stained using vinculin antibodies to visualize cell morphology and focal adhesion contacts. Representative images (magnification 200x and 400x) demonstrate that in collagen XVI-knockdown cells FACs were found more concentrated in the cellular periphery while in control cells FACs (white arrows) appeared to be more evenly distributed. N = 4. (B) The number of FACs per cell is significantly decreased in collagen XVI knockdown cells. The evaluation of the number of focal adhesion contacts yielded a significant decrease of 40-45% of FACs per cell after inhibition of collagen XVI. A similar reduction of focal adhesion contacts was observed for both siRNAs. N = 4; * = p < 0.05.

Article Snippet: Materials and Methods Cell Culture The human glioblastoma cell line U87MG (ATCC: HTB- 14) was cultured in high glucose Dulbecco’s modified Eagle’s medium (DMEM, Invitrogen, Paisley, UK) supplemented with 10% fetal calf serum (Sigma, St. Louis, USA) and 1% penicillin/ streptomycin (PAA, Coelbe, Germany) at 37°C in 5% CO2.

Techniques: Staining, Knockdown, Control, Inhibition

Fig. 3. Invasive potential of collagen XVI inhibited cells. (A) Downregulation of collagen XVI expression resulted in a reduced invasion of U87MG cells in a Boyden Chamber assay compared to scr-control cells. The number of cells migrated to the lower compartment after 4 hours was significantly decreased in knockdown cells compared to the control. N = 4; * = p< 0.05; ** = p<0.01. (B, C) Adhesion capacity after 4 hours and 6 hours was not influenced by reduced collagen XVI expression. N = 6.

Journal: Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

Article Title: Inhibition of collagen XVI expression reduces glioma cell invasiveness.

doi: 10.1159/000327947

Figure Lengend Snippet: Fig. 3. Invasive potential of collagen XVI inhibited cells. (A) Downregulation of collagen XVI expression resulted in a reduced invasion of U87MG cells in a Boyden Chamber assay compared to scr-control cells. The number of cells migrated to the lower compartment after 4 hours was significantly decreased in knockdown cells compared to the control. N = 4; * = p< 0.05; ** = p<0.01. (B, C) Adhesion capacity after 4 hours and 6 hours was not influenced by reduced collagen XVI expression. N = 6.

Article Snippet: Materials and Methods Cell Culture The human glioblastoma cell line U87MG (ATCC: HTB- 14) was cultured in high glucose Dulbecco’s modified Eagle’s medium (DMEM, Invitrogen, Paisley, UK) supplemented with 10% fetal calf serum (Sigma, St. Louis, USA) and 1% penicillin/ streptomycin (PAA, Coelbe, Germany) at 37°C in 5% CO2.

Techniques: Expressing, Boyden Chamber Assay, Control, Knockdown

Fig. 4. Downstream gene expression analysis. (A) Gene expression of PCDH18, kindlin-1 and kindlin-2 was determined by qRT-PCR and evaluated using the ''Ct method with GAPDH as endogenous loading control set to 0 and U87MG cells transfected with scrambled RNA as calibrator. PCDH18 gene expression was profoundly upregulated whereas gene expression of kindlin-1 and kindlin-2 was clearly downregulated. N = 6. ***= p< 0.001. Protein expres- sion of PCDH 18 (B), Kindlin-1 (C) and Kindlin-2 (D) was determined with western blotting analysis of cell lysates. E-Actin was used as internal loading control. N=3. Control: cell lysate from mouse lung.

Journal: Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

Article Title: Inhibition of collagen XVI expression reduces glioma cell invasiveness.

doi: 10.1159/000327947

Figure Lengend Snippet: Fig. 4. Downstream gene expression analysis. (A) Gene expression of PCDH18, kindlin-1 and kindlin-2 was determined by qRT-PCR and evaluated using the ''Ct method with GAPDH as endogenous loading control set to 0 and U87MG cells transfected with scrambled RNA as calibrator. PCDH18 gene expression was profoundly upregulated whereas gene expression of kindlin-1 and kindlin-2 was clearly downregulated. N = 6. ***= p< 0.001. Protein expres- sion of PCDH 18 (B), Kindlin-1 (C) and Kindlin-2 (D) was determined with western blotting analysis of cell lysates. E-Actin was used as internal loading control. N=3. Control: cell lysate from mouse lung.

Article Snippet: Materials and Methods Cell Culture The human glioblastoma cell line U87MG (ATCC: HTB- 14) was cultured in high glucose Dulbecco’s modified Eagle’s medium (DMEM, Invitrogen, Paisley, UK) supplemented with 10% fetal calf serum (Sigma, St. Louis, USA) and 1% penicillin/ streptomycin (PAA, Coelbe, Germany) at 37°C in 5% CO2.

Techniques: Gene Expression, Quantitative RT-PCR, Control, Transfection, Western Blot

Fig. 6. Flow cytometric analysis of E1-integrin expression and activation status. FACS analysis was performed to determine E1-integrin expression and activation on collagen XVI-knock- down U87MG cells and scr controls 96 hours post transfection. (A) The antibody integrin beta1D (MAB2259Z) recognizes activated E1-integrin only. Compared to controls E1-integrin was about 50% less activated on collagen XVI-knockdown cells. (B) The antibody integrin beta1 (MAB1900) binds to to- tal E1-integrins (both activated and inactivated forms). There- fore, the result demonstrates that total expression of E1-integrin was not altered on collagen XVI-knockdown cells. black line: Isotype control which is the secondary antibody without first antibody. si1= siRNA 1, si2 = siRNA 2, scr = scrambled RNA.

Journal: Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

Article Title: Inhibition of collagen XVI expression reduces glioma cell invasiveness.

doi: 10.1159/000327947

Figure Lengend Snippet: Fig. 6. Flow cytometric analysis of E1-integrin expression and activation status. FACS analysis was performed to determine E1-integrin expression and activation on collagen XVI-knock- down U87MG cells and scr controls 96 hours post transfection. (A) The antibody integrin beta1D (MAB2259Z) recognizes activated E1-integrin only. Compared to controls E1-integrin was about 50% less activated on collagen XVI-knockdown cells. (B) The antibody integrin beta1 (MAB1900) binds to to- tal E1-integrins (both activated and inactivated forms). There- fore, the result demonstrates that total expression of E1-integrin was not altered on collagen XVI-knockdown cells. black line: Isotype control which is the secondary antibody without first antibody. si1= siRNA 1, si2 = siRNA 2, scr = scrambled RNA.

Article Snippet: Materials and Methods Cell Culture The human glioblastoma cell line U87MG (ATCC: HTB- 14) was cultured in high glucose Dulbecco’s modified Eagle’s medium (DMEM, Invitrogen, Paisley, UK) supplemented with 10% fetal calf serum (Sigma, St. Louis, USA) and 1% penicillin/ streptomycin (PAA, Coelbe, Germany) at 37°C in 5% CO2.

Techniques: Expressing, Activation Assay, Knockdown, Transfection, Control