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u118 human gbm cell lines  (ATCC)


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    ATCC u118 human gbm cell lines
    U118 Human Gbm 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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    Average 96 stars, based on 1 article reviews
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    ATCC u118 human gbm cell lines
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    Thermo Fisher human gbm cell lines u118
    (A) EdU proliferation assay of <t>U118</t> and U251 cells. Cells were labeled with Apollo 567 and the nuclei were counterstained with DAPI. Scale bar = 200 μm. (B) Colony formation of U118 and U251 cells after treatment with FGF21 or 3-MTyr. (C) Transwell assay of U118 and U251 cells. Data are presented as the mean ± SD (n=3). *p < 0.05. Abbreviations: EdU, 5-Ethynyl-2´-deoxyuridine; FGF21, fibroblast growth factor 21; 3-MTyr, 3-methoxytyrosine.
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    Procell Inc u118 mg human gbm cell line
    (A) EdU proliferation assay of <t>U118</t> and U251 cells. Cells were labeled with Apollo 567 and the nuclei were counterstained with DAPI. Scale bar = 200 μm. (B) Colony formation of U118 and U251 cells after treatment with FGF21 or 3-MTyr. (C) Transwell assay of U118 and U251 cells. Data are presented as the mean ± SD (n=3). *p < 0.05. Abbreviations: EdU, 5-Ethynyl-2´-deoxyuridine; FGF21, fibroblast growth factor 21; 3-MTyr, 3-methoxytyrosine.
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    ATCC human gbm cell line models
    Treatments with metformin and/or simvastatin significantly decrease proliferation rate in different glioblastoma <t>(GBM)</t> <t>cell</t> models and high grade (III) astrocytomas, but not the viability in non-tumour brain cells in vitro . (a) Metformin dose–response carried out in U-87 MG and U-118 MG cells (n = 4). (b) IC 50 of metformin in vitro in U-87 MG and U-118 MG cells. (c) Simvastatin dose–response carried out in U-87 MG and U-118 MG cells (n = 4). (d) IC 50 of simvastatin in vitro in U-87 MG and U-118 MG cells. Proliferation/viability rates of GBM cell lines [U-87 MG (e) and U-118 MG (f) ; n = 5], primary patient-derived cell cultures from AIII [grade III (g) , n = 4] and grade IV-GBM [ (h); n = 4], primary non-tumour brain cell cultures [ (i) ; n = 4] and mouse primary-astrocytes progenitor derived cells [ (j) ; n = 4] in response to metformin, simvastatin, and their combination compared to vehicle-treated controls. Four technical replicates (tr) were assessed in each condition. Data represent medians (interquartile range) or means ± SEM (error bars). ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001, were set as statistically significant differences vs. control conditions.
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    ATCC u 118 mg htb 15 human gbm cell lines
    In ( A ) LN-229 and ( B ) <t>U-118</t> MG human GBM cells, protein levels of PODX and soluble and total β-cat were determined with western blot analyses in normal control cells (NC, lane 1), cells stably transfected with the empty pcDNA3.1 vector (VC, lane 2), cells stably transfected with PODX (lane 3), cells stably transfected with PODX and treated with selective p38 mitogen-activated protein kinase (MAPK) inhibitor PD169316 (25 µM) for 30 hours (PODX+PD, lane 4), cells stably transfected with PODX and treated with selective β-cat signaling inhibitor CCT031374 (50 µM) for 30 hours (PODX+CCT, lane 5), cells stably transduced with scramble control shRNA (SC, lane 6), cells stably transduced with PODX-shRNA (lane 7), and cells stably transduced with PODX-shRNA and stably transfected with constitutively active (ΔN151) β-cat (PODX-shRNA+active-cat, lane 8). Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) blotting was used as a loading control. The total β-cat protein level was not significantly altered by PODX in both LN-229 and U-118 MG cells. Density of the PODX and the soluble β-cat blots was normalized against that of the GAPDH blot to obtain a relative blot density, which was expressed as fold changes to that of NC (designated as 1) to represent the relative protein content. Three independent experiments were performed for each Western blot analysis. Data values were expressed as Mean+SD. a p <0.05 vs. controls (NC, VC and SC); b p <0.05 vs. PODX; c p <0.05 vs. PODX+PD; d p <0.05 vs. PODX+CCT.
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    Procell Inc u 118 mg human gbm cell line
    Biological functional validation of MSH2 in GBM cell. (A) Silencing efficiency of MSH2. CCK8 assay (B) , EDU assay (C) , and colony formation assay (D) showing the effect of MSH2 knockdown on proliferation of <t>U-118</t> MG cells. (E) Transwell assay indicating that MSH2 depletion markedly weakens migration and invasion by U-118 MG cells (* p < 0.05, ** p < 0.01, and *** p < 0.001, n = 3).
    U 118 Mg Human Gbm Cell Line, 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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    ATCC u 118 gbm human cell line
    EGFR mRNA, miR-200c and ZEB1 mRNA expression in the cultures with different levels of EGFR amplification. Results were normalized to actin ( EGFR and ZEB1 ) or U66 (miR-200c) housekeeping genes. Changes in RNA expression are reported as the mean and standard error with respect to the nonamplified EGFR group using the 2-∆∆Ct method. Four independent experiments were performed. Statistical analyses were performed using one-way analysis of variance, followed by Dunnett’s t-test for multiple comparisons. Significant expression changes ( p ≤ 0.05 and p ≤ 0.01) with respect to <t>U-118</t> are marked with * and **, respectively.
    U 118 Gbm Human Cell Line, 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
    https://www.bioz.com/result/u 118 gbm human cell line/product/ATCC
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    ATCC human gbm cell line
    EGFR mRNA, miR-200c and ZEB1 mRNA expression in the cultures with different levels of EGFR amplification. Results were normalized to actin ( EGFR and ZEB1 ) or U66 (miR-200c) housekeeping genes. Changes in RNA expression are reported as the mean and standard error with respect to the nonamplified EGFR group using the 2-∆∆Ct method. Four independent experiments were performed. Statistical analyses were performed using one-way analysis of variance, followed by Dunnett’s t-test for multiple comparisons. Significant expression changes ( p ≤ 0.05 and p ≤ 0.01) with respect to <t>U-118</t> are marked with * and **, respectively.
    Human Gbm Cell Line, 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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    Image Search Results


    (A) EdU proliferation assay of U118 and U251 cells. Cells were labeled with Apollo 567 and the nuclei were counterstained with DAPI. Scale bar = 200 μm. (B) Colony formation of U118 and U251 cells after treatment with FGF21 or 3-MTyr. (C) Transwell assay of U118 and U251 cells. Data are presented as the mean ± SD (n=3). *p < 0.05. Abbreviations: EdU, 5-Ethynyl-2´-deoxyuridine; FGF21, fibroblast growth factor 21; 3-MTyr, 3-methoxytyrosine.

    Journal: Journal of Cancer

    Article Title: Genetically Predicted 3-Methoxytyrosine Mediates the Causal Association between Fibroblast Growth Factor 21 and Glioblastoma Multiforme

    doi: 10.7150/jca.98035

    Figure Lengend Snippet: (A) EdU proliferation assay of U118 and U251 cells. Cells were labeled with Apollo 567 and the nuclei were counterstained with DAPI. Scale bar = 200 μm. (B) Colony formation of U118 and U251 cells after treatment with FGF21 or 3-MTyr. (C) Transwell assay of U118 and U251 cells. Data are presented as the mean ± SD (n=3). *p < 0.05. Abbreviations: EdU, 5-Ethynyl-2´-deoxyuridine; FGF21, fibroblast growth factor 21; 3-MTyr, 3-methoxytyrosine.

    Article Snippet: The human GBM cell lines U118 and U251 were procured from the Chinese Academy of Sciences Cell Bank and maintained in DMEM supplemented with 10% fetal bovine serum (FBS) (Gibco, Waltham, MA, USA).

    Techniques: Proliferation Assay, Labeling, Transwell Assay

    Treatments with metformin and/or simvastatin significantly decrease proliferation rate in different glioblastoma (GBM) cell models and high grade (III) astrocytomas, but not the viability in non-tumour brain cells in vitro . (a) Metformin dose–response carried out in U-87 MG and U-118 MG cells (n = 4). (b) IC 50 of metformin in vitro in U-87 MG and U-118 MG cells. (c) Simvastatin dose–response carried out in U-87 MG and U-118 MG cells (n = 4). (d) IC 50 of simvastatin in vitro in U-87 MG and U-118 MG cells. Proliferation/viability rates of GBM cell lines [U-87 MG (e) and U-118 MG (f) ; n = 5], primary patient-derived cell cultures from AIII [grade III (g) , n = 4] and grade IV-GBM [ (h); n = 4], primary non-tumour brain cell cultures [ (i) ; n = 4] and mouse primary-astrocytes progenitor derived cells [ (j) ; n = 4] in response to metformin, simvastatin, and their combination compared to vehicle-treated controls. Four technical replicates (tr) were assessed in each condition. Data represent medians (interquartile range) or means ± SEM (error bars). ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001, were set as statistically significant differences vs. control conditions.

    Journal: eBioMedicine

    Article Title: Metformin and simvastatin exert additive antitumour effects in glioblastoma via senescence-state: clinical and translational evidence

    doi: 10.1016/j.ebiom.2023.104484

    Figure Lengend Snippet: Treatments with metformin and/or simvastatin significantly decrease proliferation rate in different glioblastoma (GBM) cell models and high grade (III) astrocytomas, but not the viability in non-tumour brain cells in vitro . (a) Metformin dose–response carried out in U-87 MG and U-118 MG cells (n = 4). (b) IC 50 of metformin in vitro in U-87 MG and U-118 MG cells. (c) Simvastatin dose–response carried out in U-87 MG and U-118 MG cells (n = 4). (d) IC 50 of simvastatin in vitro in U-87 MG and U-118 MG cells. Proliferation/viability rates of GBM cell lines [U-87 MG (e) and U-118 MG (f) ; n = 5], primary patient-derived cell cultures from AIII [grade III (g) , n = 4] and grade IV-GBM [ (h); n = 4], primary non-tumour brain cell cultures [ (i) ; n = 4] and mouse primary-astrocytes progenitor derived cells [ (j) ; n = 4] in response to metformin, simvastatin, and their combination compared to vehicle-treated controls. Four technical replicates (tr) were assessed in each condition. Data represent medians (interquartile range) or means ± SEM (error bars). ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001, were set as statistically significant differences vs. control conditions.

    Article Snippet: Two human GBM cell line models (U-87 MG and U-118 MG) were obtained from the American Type Culture Collection (ATCC, #HTB-14, RRID:CVCL_0022/#HTB-15, respectively; Manassas, VA, USA) and cultured according to the supplier's recommendations.

    Techniques: In Vitro, Derivative Assay, Control

    The combination of metformin and simvastatin altered the expression levels of key elements involved in the Senescence-Associated Secretory Phenotype (SASP), and in the splicing process in GBM cells. (a) Hierarchical heatmap generated using the expression levels of 32 SASP genes in all GBM experimental cell models treated with metformin, simvastatin, and the combination of both drugs (n = 3; tr = 2; mean value U-87 MG + U-118 MG + primary-derived cell cultures). Hierarchical heatmap showing the expression levels of 20 top altered genes (b) and Partial Least Squares Discriminant Analysis (PLS-DA) (c) of the expression of SASP genes in response to metformin, simvastatin, and their combination in GBM cells [cell lines (U-87 MG and U-118 MG) and primary patient-derived GBM cells (PPdC); data represent the mean value of 3 experiments (4 treatment conditions/experiment) in each GBM cell model]. d) Variable Importance in Projection (VIP) score of the expression levels of SASP key genes in GBM cells. e) Heatmap generated using the expression levels of 4 spliceosome components and (f) individual expression levels of these components in response to metformin, simvastatin, and their combination in GBM cells (n = 3; tr = 2; data represent mean value of U-87 MG + U-118 MG). Data represent medians (interquartile range) or means ± SEM (error bars). ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001, were set as statistically significant differences vs. control conditions.

    Journal: eBioMedicine

    Article Title: Metformin and simvastatin exert additive antitumour effects in glioblastoma via senescence-state: clinical and translational evidence

    doi: 10.1016/j.ebiom.2023.104484

    Figure Lengend Snippet: The combination of metformin and simvastatin altered the expression levels of key elements involved in the Senescence-Associated Secretory Phenotype (SASP), and in the splicing process in GBM cells. (a) Hierarchical heatmap generated using the expression levels of 32 SASP genes in all GBM experimental cell models treated with metformin, simvastatin, and the combination of both drugs (n = 3; tr = 2; mean value U-87 MG + U-118 MG + primary-derived cell cultures). Hierarchical heatmap showing the expression levels of 20 top altered genes (b) and Partial Least Squares Discriminant Analysis (PLS-DA) (c) of the expression of SASP genes in response to metformin, simvastatin, and their combination in GBM cells [cell lines (U-87 MG and U-118 MG) and primary patient-derived GBM cells (PPdC); data represent the mean value of 3 experiments (4 treatment conditions/experiment) in each GBM cell model]. d) Variable Importance in Projection (VIP) score of the expression levels of SASP key genes in GBM cells. e) Heatmap generated using the expression levels of 4 spliceosome components and (f) individual expression levels of these components in response to metformin, simvastatin, and their combination in GBM cells (n = 3; tr = 2; data represent mean value of U-87 MG + U-118 MG). Data represent medians (interquartile range) or means ± SEM (error bars). ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001, were set as statistically significant differences vs. control conditions.

    Article Snippet: Two human GBM cell line models (U-87 MG and U-118 MG) were obtained from the American Type Culture Collection (ATCC, #HTB-14, RRID:CVCL_0022/#HTB-15, respectively; Manassas, VA, USA) and cultured according to the supplier's recommendations.

    Techniques: Expressing, Generated, Derivative Assay, Control

    In ( A ) LN-229 and ( B ) U-118 MG human GBM cells, protein levels of PODX and soluble and total β-cat were determined with western blot analyses in normal control cells (NC, lane 1), cells stably transfected with the empty pcDNA3.1 vector (VC, lane 2), cells stably transfected with PODX (lane 3), cells stably transfected with PODX and treated with selective p38 mitogen-activated protein kinase (MAPK) inhibitor PD169316 (25 µM) for 30 hours (PODX+PD, lane 4), cells stably transfected with PODX and treated with selective β-cat signaling inhibitor CCT031374 (50 µM) for 30 hours (PODX+CCT, lane 5), cells stably transduced with scramble control shRNA (SC, lane 6), cells stably transduced with PODX-shRNA (lane 7), and cells stably transduced with PODX-shRNA and stably transfected with constitutively active (ΔN151) β-cat (PODX-shRNA+active-cat, lane 8). Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) blotting was used as a loading control. The total β-cat protein level was not significantly altered by PODX in both LN-229 and U-118 MG cells. Density of the PODX and the soluble β-cat blots was normalized against that of the GAPDH blot to obtain a relative blot density, which was expressed as fold changes to that of NC (designated as 1) to represent the relative protein content. Three independent experiments were performed for each Western blot analysis. Data values were expressed as Mean+SD. a p <0.05 vs. controls (NC, VC and SC); b p <0.05 vs. PODX; c p <0.05 vs. PODX+PD; d p <0.05 vs. PODX+CCT.

    Journal: PLoS ONE

    Article Title: Podocalyxin Promotes Glioblastoma Multiforme Cell Invasion and Proliferation via β-Catenin Signaling

    doi: 10.1371/journal.pone.0111343

    Figure Lengend Snippet: In ( A ) LN-229 and ( B ) U-118 MG human GBM cells, protein levels of PODX and soluble and total β-cat were determined with western blot analyses in normal control cells (NC, lane 1), cells stably transfected with the empty pcDNA3.1 vector (VC, lane 2), cells stably transfected with PODX (lane 3), cells stably transfected with PODX and treated with selective p38 mitogen-activated protein kinase (MAPK) inhibitor PD169316 (25 µM) for 30 hours (PODX+PD, lane 4), cells stably transfected with PODX and treated with selective β-cat signaling inhibitor CCT031374 (50 µM) for 30 hours (PODX+CCT, lane 5), cells stably transduced with scramble control shRNA (SC, lane 6), cells stably transduced with PODX-shRNA (lane 7), and cells stably transduced with PODX-shRNA and stably transfected with constitutively active (ΔN151) β-cat (PODX-shRNA+active-cat, lane 8). Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) blotting was used as a loading control. The total β-cat protein level was not significantly altered by PODX in both LN-229 and U-118 MG cells. Density of the PODX and the soluble β-cat blots was normalized against that of the GAPDH blot to obtain a relative blot density, which was expressed as fold changes to that of NC (designated as 1) to represent the relative protein content. Three independent experiments were performed for each Western blot analysis. Data values were expressed as Mean+SD. a p <0.05 vs. controls (NC, VC and SC); b p <0.05 vs. PODX; c p <0.05 vs. PODX+PD; d p <0.05 vs. PODX+CCT.

    Article Snippet: LN-229 (CRL-2611) and U-118 MG (HTB-15) human GBM cell lines were purchased from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Western Blot, Stable Transfection, Transfection, Plasmid Preparation, Transduction, shRNA

    ( A ) LN-229 and ( B ) U-118 MG GBM cells were transfected with TOPflash, a synthetic β-catenin luciferase reporter, or FOPflash, a negative control reporter for TOPflash. Thirty hours later, the luciferase activity was determined in normal control cells (NC), cells stably transfected with the empty pcDNA3.1 vector (VC), cells stably transfected with PODX, cells stably transfected with PODX and treated with selective p38 mitogen-activated protein kinase (MAPK) inhibitor PD169316 (25 µM) for 30 hours (PODX+PD), cells stably transfected with PODX and treated with selective β-cat signaling inhibitor CCT031374 (50 µM) for 30 hours (PODX+CCT), cells stably transduced with scramble control shRNA (SC), cells stably transduced with PODX-shRNA, and cells stably transduced with PODX-shRNA and stably transfected with constitutively active (ΔN151) β-cat (PODX-shRNA+active-cat). The luciferase activity was expressed as fold changes to that of NC (designated as 1). a p <0.05 vs. controls (NC, VC and SC); b p <0.05 vs. PODX; c p <0.05 vs. PODX+PD; d p <0.05 vs. PODX+CCT; e p <0.05 vs. PODX-shRNA.

    Journal: PLoS ONE

    Article Title: Podocalyxin Promotes Glioblastoma Multiforme Cell Invasion and Proliferation via β-Catenin Signaling

    doi: 10.1371/journal.pone.0111343

    Figure Lengend Snippet: ( A ) LN-229 and ( B ) U-118 MG GBM cells were transfected with TOPflash, a synthetic β-catenin luciferase reporter, or FOPflash, a negative control reporter for TOPflash. Thirty hours later, the luciferase activity was determined in normal control cells (NC), cells stably transfected with the empty pcDNA3.1 vector (VC), cells stably transfected with PODX, cells stably transfected with PODX and treated with selective p38 mitogen-activated protein kinase (MAPK) inhibitor PD169316 (25 µM) for 30 hours (PODX+PD), cells stably transfected with PODX and treated with selective β-cat signaling inhibitor CCT031374 (50 µM) for 30 hours (PODX+CCT), cells stably transduced with scramble control shRNA (SC), cells stably transduced with PODX-shRNA, and cells stably transduced with PODX-shRNA and stably transfected with constitutively active (ΔN151) β-cat (PODX-shRNA+active-cat). The luciferase activity was expressed as fold changes to that of NC (designated as 1). a p <0.05 vs. controls (NC, VC and SC); b p <0.05 vs. PODX; c p <0.05 vs. PODX+PD; d p <0.05 vs. PODX+CCT; e p <0.05 vs. PODX-shRNA.

    Article Snippet: LN-229 (CRL-2611) and U-118 MG (HTB-15) human GBM cell lines were purchased from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Transfection, Luciferase, Negative Control, Activity Assay, Stable Transfection, Plasmid Preparation, Transduction, shRNA

    The mRNA levels of β-cat and β-cat signaling target genes C-Myc and C-Jun were determined in ( A ) LN-229 and ( B ) U-118 MG GBM cells. Real-time RT-PCR was performed with normal control cells (NC), cells stably transfected with the empty pcDNA3.1 vector (VC), cells stably transfected with PODX, cells stably transfected with PODX and treated with selective p38 mitogen-activated protein kinase (MAPK) inhibitor PD169316 (25 µM) for 30 hours (PODX+PD), cells stably transfected with PODX and treated with selective β-cat signaling inhibitor CCT031374 (50 µM) for 30 hours (PODX+CCT), cells stably transduced with scramble control shRNA (SC), cells stably transduced with PODX-shRNA, and cells stably transduced with PODX-shRNA and stably transfected with constitutively active (ΔN151) β-cat (PODX-shRNA+active-cat). The mRNA level was expressed as fold changes to that of NC (designated as 1). * p <0.05 vs. controls (NC, VC and SC).

    Journal: PLoS ONE

    Article Title: Podocalyxin Promotes Glioblastoma Multiforme Cell Invasion and Proliferation via β-Catenin Signaling

    doi: 10.1371/journal.pone.0111343

    Figure Lengend Snippet: The mRNA levels of β-cat and β-cat signaling target genes C-Myc and C-Jun were determined in ( A ) LN-229 and ( B ) U-118 MG GBM cells. Real-time RT-PCR was performed with normal control cells (NC), cells stably transfected with the empty pcDNA3.1 vector (VC), cells stably transfected with PODX, cells stably transfected with PODX and treated with selective p38 mitogen-activated protein kinase (MAPK) inhibitor PD169316 (25 µM) for 30 hours (PODX+PD), cells stably transfected with PODX and treated with selective β-cat signaling inhibitor CCT031374 (50 µM) for 30 hours (PODX+CCT), cells stably transduced with scramble control shRNA (SC), cells stably transduced with PODX-shRNA, and cells stably transduced with PODX-shRNA and stably transfected with constitutively active (ΔN151) β-cat (PODX-shRNA+active-cat). The mRNA level was expressed as fold changes to that of NC (designated as 1). * p <0.05 vs. controls (NC, VC and SC).

    Article Snippet: LN-229 (CRL-2611) and U-118 MG (HTB-15) human GBM cell lines were purchased from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Quantitative RT-PCR, Stable Transfection, Transfection, Plasmid Preparation, Transduction, shRNA

    In vitro cell invasion assays were performed in ( A ) LN-229 and ( B ) U-118 MG GBM cells. Invading cells were fixed and counted in normal control cells (NC), cells stably transfected with the empty pcDNA3.1 vector (VC), cells stably transfected with PODX, cells stably transfected with PODX and treated with selective p38 mitogen-activated protein kinase (MAPK) inhibitor PD169316 (25 µM) for 30 hours (PODX+PD), cells stably transfected with PODX and treated with selective β-cat signaling inhibitor CCT031374 (50 µM) for 30 hours (PODX+CCT), cells stably transduced with scramble control shRNA (SC), cells stably transduced with PODX-shRNA, and cells stably transduced with PODX-shRNA and stably transfected with constitutively active (ΔN151) β-cat (PODX-shRNA+active-cat). Representative cell invasion images are shown. a p <0.05 vs. controls (NC, VC and SC); b p <0.05 vs. PODX; c p <0.05 vs. PODX+PD; d p <0.05 vs. PODX+CCT; e p <0.05 vs. PODX-shRNA.

    Journal: PLoS ONE

    Article Title: Podocalyxin Promotes Glioblastoma Multiforme Cell Invasion and Proliferation via β-Catenin Signaling

    doi: 10.1371/journal.pone.0111343

    Figure Lengend Snippet: In vitro cell invasion assays were performed in ( A ) LN-229 and ( B ) U-118 MG GBM cells. Invading cells were fixed and counted in normal control cells (NC), cells stably transfected with the empty pcDNA3.1 vector (VC), cells stably transfected with PODX, cells stably transfected with PODX and treated with selective p38 mitogen-activated protein kinase (MAPK) inhibitor PD169316 (25 µM) for 30 hours (PODX+PD), cells stably transfected with PODX and treated with selective β-cat signaling inhibitor CCT031374 (50 µM) for 30 hours (PODX+CCT), cells stably transduced with scramble control shRNA (SC), cells stably transduced with PODX-shRNA, and cells stably transduced with PODX-shRNA and stably transfected with constitutively active (ΔN151) β-cat (PODX-shRNA+active-cat). Representative cell invasion images are shown. a p <0.05 vs. controls (NC, VC and SC); b p <0.05 vs. PODX; c p <0.05 vs. PODX+PD; d p <0.05 vs. PODX+CCT; e p <0.05 vs. PODX-shRNA.

    Article Snippet: LN-229 (CRL-2611) and U-118 MG (HTB-15) human GBM cell lines were purchased from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: In Vitro, Stable Transfection, Transfection, Plasmid Preparation, Transduction, shRNA

    The ( A ) mRNA and the ( B ) protein levels of MMP9 in LN-229 ( left panel ) and U-118 MG ( right panel ) GBM cells were respectively determined by real-time RT-PCR and Western blot analyses in normal control cells (NC, lane 1), cells stably transfected with the empty pcDNA3.1 vector (VC, lane 2), cells stably transfected with PODX (lane 3), cells stably transfected with PODX and treated with selective p38 mitogen-activated protein kinase (MAPK) inhibitor PD169316 (25 µM) for 30 hours (PODX+PD, lane 4), cells stably transfected with PODX and treated with selective β-cat signaling inhibitor CCT031374 (50 µM) for 30 hours (PODX+CCT, lane 5), cells stably transduced with scramble control shRNA (SC, lane 6), cells stably transduced with PODX-shRNA (lane 7), and cells stably transduced with PODX-shRNA and stably transfected with constitutively active (ΔN151) β-cat (PODX-shRNA+active-cat, lane 8). The mRNA and the protein levels of MMP9 were expressed as fold changes to those of NC (designated as 1), respectively. Three independent experiments were performed for each Western blot analysis. Data values were expressed as Mean+SD. a p <0.05 vs. controls (NC, VC and SC); b p <0.05 vs. PODX; c p <0.05 vs. PODX+PD; d p <0.05 vs. PODX+CCT; e p <0.05 vs. PODX-shRNA.

    Journal: PLoS ONE

    Article Title: Podocalyxin Promotes Glioblastoma Multiforme Cell Invasion and Proliferation via β-Catenin Signaling

    doi: 10.1371/journal.pone.0111343

    Figure Lengend Snippet: The ( A ) mRNA and the ( B ) protein levels of MMP9 in LN-229 ( left panel ) and U-118 MG ( right panel ) GBM cells were respectively determined by real-time RT-PCR and Western blot analyses in normal control cells (NC, lane 1), cells stably transfected with the empty pcDNA3.1 vector (VC, lane 2), cells stably transfected with PODX (lane 3), cells stably transfected with PODX and treated with selective p38 mitogen-activated protein kinase (MAPK) inhibitor PD169316 (25 µM) for 30 hours (PODX+PD, lane 4), cells stably transfected with PODX and treated with selective β-cat signaling inhibitor CCT031374 (50 µM) for 30 hours (PODX+CCT, lane 5), cells stably transduced with scramble control shRNA (SC, lane 6), cells stably transduced with PODX-shRNA (lane 7), and cells stably transduced with PODX-shRNA and stably transfected with constitutively active (ΔN151) β-cat (PODX-shRNA+active-cat, lane 8). The mRNA and the protein levels of MMP9 were expressed as fold changes to those of NC (designated as 1), respectively. Three independent experiments were performed for each Western blot analysis. Data values were expressed as Mean+SD. a p <0.05 vs. controls (NC, VC and SC); b p <0.05 vs. PODX; c p <0.05 vs. PODX+PD; d p <0.05 vs. PODX+CCT; e p <0.05 vs. PODX-shRNA.

    Article Snippet: LN-229 (CRL-2611) and U-118 MG (HTB-15) human GBM cell lines were purchased from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Quantitative RT-PCR, Western Blot, Stable Transfection, Transfection, Plasmid Preparation, Transduction, shRNA

    In ( A ) LN-229 and ( B ) U-118 MG GBM cells, MMP9 activities were determined with a SensoLyte 520 MMP9 Assay Kit (AnaSpec) in normal control cells (NC), cells stably transfected with the empty pcDNA3.1 vector (VC), cells stably transfected with PODX, cells stably transfected with PODX and treated with selective p38 mitogen-activated protein kinase (MAPK) inhibitor PD169316 (25 µM) for 30 hours (PODX+PD), cells stably transfected with PODX and treated with selective β-cat signaling inhibitor CCT031374 (50 µM) for 30 hours (PODX+CCT), cells stably transduced with scramble control shRNA (SC), cells stably transduced with PODX-shRNA, and cells stably transduced with PODX-shRNA and stably transfected with constitutively active (ΔN151) β-cat (PODX-shRNA+active-cat). The MMP9 activity was shown as fold changes to that of NC (designated as 1). a p <0.05 vs. controls (NC, VC and SC); b p <0.05 vs. PODX; c p <0.05 vs. PODX+PD; d p <0.05 vs. PODX+CCT; e p <0.05 vs. PODX-shRNA.

    Journal: PLoS ONE

    Article Title: Podocalyxin Promotes Glioblastoma Multiforme Cell Invasion and Proliferation via β-Catenin Signaling

    doi: 10.1371/journal.pone.0111343

    Figure Lengend Snippet: In ( A ) LN-229 and ( B ) U-118 MG GBM cells, MMP9 activities were determined with a SensoLyte 520 MMP9 Assay Kit (AnaSpec) in normal control cells (NC), cells stably transfected with the empty pcDNA3.1 vector (VC), cells stably transfected with PODX, cells stably transfected with PODX and treated with selective p38 mitogen-activated protein kinase (MAPK) inhibitor PD169316 (25 µM) for 30 hours (PODX+PD), cells stably transfected with PODX and treated with selective β-cat signaling inhibitor CCT031374 (50 µM) for 30 hours (PODX+CCT), cells stably transduced with scramble control shRNA (SC), cells stably transduced with PODX-shRNA, and cells stably transduced with PODX-shRNA and stably transfected with constitutively active (ΔN151) β-cat (PODX-shRNA+active-cat). The MMP9 activity was shown as fold changes to that of NC (designated as 1). a p <0.05 vs. controls (NC, VC and SC); b p <0.05 vs. PODX; c p <0.05 vs. PODX+PD; d p <0.05 vs. PODX+CCT; e p <0.05 vs. PODX-shRNA.

    Article Snippet: LN-229 (CRL-2611) and U-118 MG (HTB-15) human GBM cell lines were purchased from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Stable Transfection, Transfection, Plasmid Preparation, Transduction, shRNA, Activity Assay

    In ( A ) LN-229 and ( B ) U-118 MG GBM cells, methlythiazoletetrazolium (MTT) cell proliferation assays were performed for 15 or 30 hours in normal control cells (NC), cells stably transfected with the empty pcDNA3.1 vector (VC), cells stably transfected with PODX, cells stably transfected with PODX and treated with selective p38 mitogen-activated protein kinase (MAPK) inhibitor PD169316 (25 µM) for 30 hours (PODX+PD), cells stably transfected with PODX and treated with selective β-cat signaling inhibitor CCT031374 (50 µM) for 15 or 30 hours (PODX+CCT), cells stably transduced with scramble control shRNA (SC), cells stably transduced with PODX-shRNA, and cells stably transduced with PODX-shRNA and stably transfected with constitutively active (ΔN151) β-cat (PODX-shRNA+active-cat). Cell proliferation at 15 and 30 hours was expressed as fold changes to that of NC (designated as 1). * p <0.05 vs. controls (NC, VC and SC) at 30 hours.

    Journal: PLoS ONE

    Article Title: Podocalyxin Promotes Glioblastoma Multiforme Cell Invasion and Proliferation via β-Catenin Signaling

    doi: 10.1371/journal.pone.0111343

    Figure Lengend Snippet: In ( A ) LN-229 and ( B ) U-118 MG GBM cells, methlythiazoletetrazolium (MTT) cell proliferation assays were performed for 15 or 30 hours in normal control cells (NC), cells stably transfected with the empty pcDNA3.1 vector (VC), cells stably transfected with PODX, cells stably transfected with PODX and treated with selective p38 mitogen-activated protein kinase (MAPK) inhibitor PD169316 (25 µM) for 30 hours (PODX+PD), cells stably transfected with PODX and treated with selective β-cat signaling inhibitor CCT031374 (50 µM) for 15 or 30 hours (PODX+CCT), cells stably transduced with scramble control shRNA (SC), cells stably transduced with PODX-shRNA, and cells stably transduced with PODX-shRNA and stably transfected with constitutively active (ΔN151) β-cat (PODX-shRNA+active-cat). Cell proliferation at 15 and 30 hours was expressed as fold changes to that of NC (designated as 1). * p <0.05 vs. controls (NC, VC and SC) at 30 hours.

    Article Snippet: LN-229 (CRL-2611) and U-118 MG (HTB-15) human GBM cell lines were purchased from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: MTT Cell Proliferation, Stable Transfection, Transfection, Plasmid Preparation, Transduction, shRNA

    In ( A ) LN-229 and ( B ) U-118 MG GBM cells, the p38 MAPK activity was determined with a p38 MAPK Assay kit (Cell Signaling Technology) by measuring phosphorylation of ATF2, a substrate of activated p38 MAPK. The levels of phosphorylated ATF2 (p-ATF2) were determined with western blot in normal control cells (NC, lane 1), cells stably transfected with the empty pcDNA3.1 vector (VC, lane 2), cells stably transfected with PODX (lane 3), cells stably transfected with PODX and treated with selective p38 mitogen-activated protein kinase (MAPK) inhibitor PD169316 (25 µM) for 30 hours (PODX+PD, lane 4), cells stably transfected with PODX and treated with selective β-cat signaling inhibitor CCT031374 (50 µM) for 30 hours (PODX+CCT, lane 5), cells stably transduced with scramble control shRNA (SC, lane 6), cells stably transduced with PODX-shRNA (lane 7), and cells stably transduced with PODX-shRNA and stably transfected with constitutively active (ΔN151) β-cat (PODX-shRNA+active-cat, lane 8). The p-ATF2 content/p38 MAPK activity was shown as fold changes to that of NC (designated as 1). Each experiment was repeated for three times in duplicates. Data values were expressed as Mean+SD. a p <0.05 vs. controls (NC, VC and SC); b p <0.05 vs. PODX; c p <0.05 vs. PODX+PD; d p <0.05 vs. PODX+CCT.

    Journal: PLoS ONE

    Article Title: Podocalyxin Promotes Glioblastoma Multiforme Cell Invasion and Proliferation via β-Catenin Signaling

    doi: 10.1371/journal.pone.0111343

    Figure Lengend Snippet: In ( A ) LN-229 and ( B ) U-118 MG GBM cells, the p38 MAPK activity was determined with a p38 MAPK Assay kit (Cell Signaling Technology) by measuring phosphorylation of ATF2, a substrate of activated p38 MAPK. The levels of phosphorylated ATF2 (p-ATF2) were determined with western blot in normal control cells (NC, lane 1), cells stably transfected with the empty pcDNA3.1 vector (VC, lane 2), cells stably transfected with PODX (lane 3), cells stably transfected with PODX and treated with selective p38 mitogen-activated protein kinase (MAPK) inhibitor PD169316 (25 µM) for 30 hours (PODX+PD, lane 4), cells stably transfected with PODX and treated with selective β-cat signaling inhibitor CCT031374 (50 µM) for 30 hours (PODX+CCT, lane 5), cells stably transduced with scramble control shRNA (SC, lane 6), cells stably transduced with PODX-shRNA (lane 7), and cells stably transduced with PODX-shRNA and stably transfected with constitutively active (ΔN151) β-cat (PODX-shRNA+active-cat, lane 8). The p-ATF2 content/p38 MAPK activity was shown as fold changes to that of NC (designated as 1). Each experiment was repeated for three times in duplicates. Data values were expressed as Mean+SD. a p <0.05 vs. controls (NC, VC and SC); b p <0.05 vs. PODX; c p <0.05 vs. PODX+PD; d p <0.05 vs. PODX+CCT.

    Article Snippet: LN-229 (CRL-2611) and U-118 MG (HTB-15) human GBM cell lines were purchased from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Activity Assay, Western Blot, Stable Transfection, Transfection, Plasmid Preparation, Transduction, shRNA

    In ( A ) LN-229 and ( B ) U-118 MG GBM cells, the levels of p-GSK-3β at serine 389 and total GSK-3β were determined with Western blot analyses in normal control cells (NC, lane 1), cells stably transfected with the empty pcDNA3.1 vector (VC, lane 2), cells stably transfected with PODX (lane 3), cells stably transfected with PODX and treated with selective p38 mitogen-activated protein kinase (MAPK) inhibitor PD169316 (25 µM) for 30 hours (PODX+PD, lane 4), cells stably transfected with PODX and treated with selective β-cat signaling inhibitor CCT031374 (50 µM) for 30 hours (PODX+CCT, lane 5), cells stably transduced with scramble control shRNA (SC, lane 6), cells stably transduced with PODX-shRNA (lane 7), and cells stably transduced with PODX-shRNA and stably transfected with constitutively active (ΔN151) β-cat (PODX-shRNA+active-cat, lane 8). The total GSK-3β protein level was not significantly altered by PODX in both LN-229 and U-118 MG cells. Density of the p-GSK-3β (serine 389) blot was normalized against that of the total GSK-3β blot to obtain a relative blot density, which was expressed as fold changes to that of NC (designated as 1). Three independent experiments were performed for each Western blot analysis. Data values were expressed as Mean+SD. a p <0.05 vs. controls (NC, VC and SC); b p <0.05 vs. PODX; c p <0.05 vs. PODX+PD; d p <0.05 vs. PODX+CCT.

    Journal: PLoS ONE

    Article Title: Podocalyxin Promotes Glioblastoma Multiforme Cell Invasion and Proliferation via β-Catenin Signaling

    doi: 10.1371/journal.pone.0111343

    Figure Lengend Snippet: In ( A ) LN-229 and ( B ) U-118 MG GBM cells, the levels of p-GSK-3β at serine 389 and total GSK-3β were determined with Western blot analyses in normal control cells (NC, lane 1), cells stably transfected with the empty pcDNA3.1 vector (VC, lane 2), cells stably transfected with PODX (lane 3), cells stably transfected with PODX and treated with selective p38 mitogen-activated protein kinase (MAPK) inhibitor PD169316 (25 µM) for 30 hours (PODX+PD, lane 4), cells stably transfected with PODX and treated with selective β-cat signaling inhibitor CCT031374 (50 µM) for 30 hours (PODX+CCT, lane 5), cells stably transduced with scramble control shRNA (SC, lane 6), cells stably transduced with PODX-shRNA (lane 7), and cells stably transduced with PODX-shRNA and stably transfected with constitutively active (ΔN151) β-cat (PODX-shRNA+active-cat, lane 8). The total GSK-3β protein level was not significantly altered by PODX in both LN-229 and U-118 MG cells. Density of the p-GSK-3β (serine 389) blot was normalized against that of the total GSK-3β blot to obtain a relative blot density, which was expressed as fold changes to that of NC (designated as 1). Three independent experiments were performed for each Western blot analysis. Data values were expressed as Mean+SD. a p <0.05 vs. controls (NC, VC and SC); b p <0.05 vs. PODX; c p <0.05 vs. PODX+PD; d p <0.05 vs. PODX+CCT.

    Article Snippet: LN-229 (CRL-2611) and U-118 MG (HTB-15) human GBM cell lines were purchased from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Western Blot, Stable Transfection, Transfection, Plasmid Preparation, Transduction, shRNA

    Biological functional validation of MSH2 in GBM cell. (A) Silencing efficiency of MSH2. CCK8 assay (B) , EDU assay (C) , and colony formation assay (D) showing the effect of MSH2 knockdown on proliferation of U-118 MG cells. (E) Transwell assay indicating that MSH2 depletion markedly weakens migration and invasion by U-118 MG cells (* p < 0.05, ** p < 0.01, and *** p < 0.001, n = 3).

    Journal: Frontiers in Genetics

    Article Title: Comprehensive development and validation of gene signature for predicting survival in patients with glioblastoma

    doi: 10.3389/fgene.2022.900911

    Figure Lengend Snippet: Biological functional validation of MSH2 in GBM cell. (A) Silencing efficiency of MSH2. CCK8 assay (B) , EDU assay (C) , and colony formation assay (D) showing the effect of MSH2 knockdown on proliferation of U-118 MG cells. (E) Transwell assay indicating that MSH2 depletion markedly weakens migration and invasion by U-118 MG cells (* p < 0.05, ** p < 0.01, and *** p < 0.001, n = 3).

    Article Snippet: The U-118 MG human GBM cell line was purchased from the Procell Life Science and Technology Company (Wuhan, China).

    Techniques: Functional Assay, CCK-8 Assay, EdU Assay, Colony Assay, Transwell Assay, Migration

    EGFR mRNA, miR-200c and ZEB1 mRNA expression in the cultures with different levels of EGFR amplification. Results were normalized to actin ( EGFR and ZEB1 ) or U66 (miR-200c) housekeeping genes. Changes in RNA expression are reported as the mean and standard error with respect to the nonamplified EGFR group using the 2-∆∆Ct method. Four independent experiments were performed. Statistical analyses were performed using one-way analysis of variance, followed by Dunnett’s t-test for multiple comparisons. Significant expression changes ( p ≤ 0.05 and p ≤ 0.01) with respect to U-118 are marked with * and **, respectively.

    Journal: International Journal of Molecular Sciences

    Article Title: The Status of EGFR Modulates the Effect of miRNA-200c on ZEB1 Expression and Cell Migration in Glioblastoma Cells

    doi: 10.3390/ijms22010368

    Figure Lengend Snippet: EGFR mRNA, miR-200c and ZEB1 mRNA expression in the cultures with different levels of EGFR amplification. Results were normalized to actin ( EGFR and ZEB1 ) or U66 (miR-200c) housekeeping genes. Changes in RNA expression are reported as the mean and standard error with respect to the nonamplified EGFR group using the 2-∆∆Ct method. Four independent experiments were performed. Statistical analyses were performed using one-way analysis of variance, followed by Dunnett’s t-test for multiple comparisons. Significant expression changes ( p ≤ 0.05 and p ≤ 0.01) with respect to U-118 are marked with * and **, respectively.

    Article Snippet: We also used the U-118 GBM human cell line from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Expressing, Amplification, RNA Expression

    Cell viability. Cell viability study by luminescence in the four transfected cell cultures (U-118, HC-444, HC-534 and HC-466) with miR-200c mimic, miR-200c inhibitor and EGFR silencer conditions, with respect to control (h: hours). The points for each curve represent the mean values ± SDs of three independent experiments. Statistical analyses were performed using one-way analysis of variance, followed by Dunnett’s t-test for multiple comparisons.

    Journal: International Journal of Molecular Sciences

    Article Title: The Status of EGFR Modulates the Effect of miRNA-200c on ZEB1 Expression and Cell Migration in Glioblastoma Cells

    doi: 10.3390/ijms22010368

    Figure Lengend Snippet: Cell viability. Cell viability study by luminescence in the four transfected cell cultures (U-118, HC-444, HC-534 and HC-466) with miR-200c mimic, miR-200c inhibitor and EGFR silencer conditions, with respect to control (h: hours). The points for each curve represent the mean values ± SDs of three independent experiments. Statistical analyses were performed using one-way analysis of variance, followed by Dunnett’s t-test for multiple comparisons.

    Article Snippet: We also used the U-118 GBM human cell line from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Transfection