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    Kaggle Inc meningioma mris
    Meningioma Mris, supplied by Kaggle 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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    86
    Thermo Fisher iomm meningioma cells
    (A) ADCC assay of <t>malignant</t> <t>meningioma</t> lines by healthy donor NK cells. Meningioma lines were incubated with avelumab alone, healthy donor NK cells and isotype antibody, or NK cells and avelumab. The ratio of NK to meningioma cells is indicated. Each sample was plated in triplicate. Data were analyzed with a 2-way ANOVA; *P < 0.05. Shown are representative data from 3 repeats using different healthy donors. (B) ADCC of <t>IOMM</t> incubated with avelumab or healthy donor NK cells with isotype, avelumab, or avelumab with α-CD16 (Fc-blocking) antibody. Data were analyzed with a 2-way ANOVA. (C) ADCC assay of 5 meningioma lines by NK cells from healthy donors with the F/F or V/V polymorphism of the CD16 receptor (effector/target [E/T] of 10:1). Data were analyzed with unpaired 1-tailed t test comparing NK and isotype with NK and avelumab conditions. (D) Lysis of IOMM meningioma by healthy donor NK cells versus haNK cells in the presence of avelumab. Samples were plated in triplicate. Data were analyzed with 1-way ANOVA.
    Iomm Meningioma Cells, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/iomm meningioma cells/product/Thermo Fisher
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    Thermo Fisher gse16581 meningioma
    (A) ADCC assay of <t>malignant</t> <t>meningioma</t> lines by healthy donor NK cells. Meningioma lines were incubated with avelumab alone, healthy donor NK cells and isotype antibody, or NK cells and avelumab. The ratio of NK to meningioma cells is indicated. Each sample was plated in triplicate. Data were analyzed with a 2-way ANOVA; *P < 0.05. Shown are representative data from 3 repeats using different healthy donors. (B) ADCC of <t>IOMM</t> incubated with avelumab or healthy donor NK cells with isotype, avelumab, or avelumab with α-CD16 (Fc-blocking) antibody. Data were analyzed with a 2-way ANOVA. (C) ADCC assay of 5 meningioma lines by NK cells from healthy donors with the F/F or V/V polymorphism of the CD16 receptor (effector/target [E/T] of 10:1). Data were analyzed with unpaired 1-tailed t test comparing NK and isotype with NK and avelumab conditions. (D) Lysis of IOMM meningioma by healthy donor NK cells versus haNK cells in the presence of avelumab. Samples were plated in triplicate. Data were analyzed with 1-way ANOVA.
    Gse16581 Meningioma, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/gse16581 meningioma/product/Thermo Fisher
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    DSMZ grade 1 meningioma cell line bm
    STAT1 and its phosphorylated forms are overexpressed in meningioma. (A) Representative WB analysis showing the expression of total and pSTAT1 in different grade meningiomas versus normal meningeal tissue (NMT). (B) Representative images showing the IHC staining of STAT1 and pSTAT1 in the 3 grades meningiomas compared to normal meninges (see black arrows) at 200× magnification. Mean scores are presented in the table below for the specimens and the normal controls examined (see also for the full list of specimens examined and the corresponding scores— n = 47). (C) STAT1 expression levels in WHO I ( n = 40), WHO II ( n = 25), and WHO III ( n = 10) meningioma tumors normalized versus NMT. Data are presented as mean ± SEM; * P ≤ .05. (D) WB showing pSTAT1 and STAT1 in normal brain (NB) and additional normal meninges (NMT-1 and NMT-2) compared to sample J6 (meningioma) as a positive control. (E) Representative WB analysis of STAT1 and pSTAT1 in <t>BM-1</t> and in WHO I MN cells (MNs) versus HMC. (F) STAT1 expression levels in BM-1 ( n = 4) and in MN cells ( n = 24) normalized versus HMC. Data are presented as mean ± SEM; ** P ≤ .01. (G) Confocal z-stack images showing the immunofluorescent staining of STAT1 (red) and pSTAT1 (Y701, green and S727, red) in MN cells versus HMC. Scale bar 50 μm. Nuclei were stained with DAPI (blue).
    Grade 1 Meningioma Cell Line Bm, supplied by DSMZ, 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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    Millipore meningioma enhancer landscapes trizol reagent
    STAT1 and its phosphorylated forms are overexpressed in meningioma. (A) Representative WB analysis showing the expression of total and pSTAT1 in different grade meningiomas versus normal meningeal tissue (NMT). (B) Representative images showing the IHC staining of STAT1 and pSTAT1 in the 3 grades meningiomas compared to normal meninges (see black arrows) at 200× magnification. Mean scores are presented in the table below for the specimens and the normal controls examined (see also for the full list of specimens examined and the corresponding scores— n = 47). (C) STAT1 expression levels in WHO I ( n = 40), WHO II ( n = 25), and WHO III ( n = 10) meningioma tumors normalized versus NMT. Data are presented as mean ± SEM; * P ≤ .05. (D) WB showing pSTAT1 and STAT1 in normal brain (NB) and additional normal meninges (NMT-1 and NMT-2) compared to sample J6 (meningioma) as a positive control. (E) Representative WB analysis of STAT1 and pSTAT1 in <t>BM-1</t> and in WHO I MN cells (MNs) versus HMC. (F) STAT1 expression levels in BM-1 ( n = 4) and in MN cells ( n = 24) normalized versus HMC. Data are presented as mean ± SEM; ** P ≤ .01. (G) Confocal z-stack images showing the immunofluorescent staining of STAT1 (red) and pSTAT1 (Y701, green and S727, red) in MN cells versus HMC. Scale bar 50 μm. Nuclei were stained with DAPI (blue).
    Meningioma Enhancer Landscapes Trizol Reagent, supplied by Millipore, 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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    Image Search Results


    (A) ADCC assay of malignant meningioma lines by healthy donor NK cells. Meningioma lines were incubated with avelumab alone, healthy donor NK cells and isotype antibody, or NK cells and avelumab. The ratio of NK to meningioma cells is indicated. Each sample was plated in triplicate. Data were analyzed with a 2-way ANOVA; *P < 0.05. Shown are representative data from 3 repeats using different healthy donors. (B) ADCC of IOMM incubated with avelumab or healthy donor NK cells with isotype, avelumab, or avelumab with α-CD16 (Fc-blocking) antibody. Data were analyzed with a 2-way ANOVA. (C) ADCC assay of 5 meningioma lines by NK cells from healthy donors with the F/F or V/V polymorphism of the CD16 receptor (effector/target [E/T] of 10:1). Data were analyzed with unpaired 1-tailed t test comparing NK and isotype with NK and avelumab conditions. (D) Lysis of IOMM meningioma by healthy donor NK cells versus haNK cells in the presence of avelumab. Samples were plated in triplicate. Data were analyzed with 1-way ANOVA.

    Journal: JCI Insight

    Article Title: Efficient ADCC killing of meningioma by avelumab and a high-affinity natural killer cell line, haNK

    doi: 10.1172/jci.insight.130688

    Figure Lengend Snippet: (A) ADCC assay of malignant meningioma lines by healthy donor NK cells. Meningioma lines were incubated with avelumab alone, healthy donor NK cells and isotype antibody, or NK cells and avelumab. The ratio of NK to meningioma cells is indicated. Each sample was plated in triplicate. Data were analyzed with a 2-way ANOVA; *P < 0.05. Shown are representative data from 3 repeats using different healthy donors. (B) ADCC of IOMM incubated with avelumab or healthy donor NK cells with isotype, avelumab, or avelumab with α-CD16 (Fc-blocking) antibody. Data were analyzed with a 2-way ANOVA. (C) ADCC assay of 5 meningioma lines by NK cells from healthy donors with the F/F or V/V polymorphism of the CD16 receptor (effector/target [E/T] of 10:1). Data were analyzed with unpaired 1-tailed t test comparing NK and isotype with NK and avelumab conditions. (D) Lysis of IOMM meningioma by healthy donor NK cells versus haNK cells in the presence of avelumab. Samples were plated in triplicate. Data were analyzed with 1-way ANOVA.

    Article Snippet: The sgRNA was designed according to the DNA sequence of CD274 exon 3 through http://crispr.mit.edu Targeting sequence TGAACTGACATGTC was subcloned into the PX459 plasmid (Addgene 62988) and transfected into IOMM meningioma cells using Lipofectamine 3000 (Thermo Fisher Scientific).

    Techniques: ADCC Assay, Incubation, Blocking Assay, Lysis

    (A) Total PD-L1 protein was detected by Western blotting in 5 meningioma cell lines cultured under 20%, 5%, or 1% oxygen. (B) Western analysis of PD-L1 protein from the indicated meningioma lines cultured with or without IFN-γ treatment. (C) Surface PD-L1 was measured by flow cytometry for the indicated cell lines. Cells were untreated (filled gray histogram) or treated with IFN-γ (dashed line). (D) ADCC assay of IOMM cells incubated with isotype or avelumab antibody and haNK cells under 20% or 1% oxygen (E/T of 25:1). (E) ADCC assay of IOMM cells cultured with vehicle or IFN-γ for 2 days before incubating with isotype or avelumab antibody and haNK cells (E/T of 25:1). Each condition was plated in triplicate, and data were analyzed with a 2-way ANOVA.

    Journal: JCI Insight

    Article Title: Efficient ADCC killing of meningioma by avelumab and a high-affinity natural killer cell line, haNK

    doi: 10.1172/jci.insight.130688

    Figure Lengend Snippet: (A) Total PD-L1 protein was detected by Western blotting in 5 meningioma cell lines cultured under 20%, 5%, or 1% oxygen. (B) Western analysis of PD-L1 protein from the indicated meningioma lines cultured with or without IFN-γ treatment. (C) Surface PD-L1 was measured by flow cytometry for the indicated cell lines. Cells were untreated (filled gray histogram) or treated with IFN-γ (dashed line). (D) ADCC assay of IOMM cells incubated with isotype or avelumab antibody and haNK cells under 20% or 1% oxygen (E/T of 25:1). (E) ADCC assay of IOMM cells cultured with vehicle or IFN-γ for 2 days before incubating with isotype or avelumab antibody and haNK cells (E/T of 25:1). Each condition was plated in triplicate, and data were analyzed with a 2-way ANOVA.

    Article Snippet: The sgRNA was designed according to the DNA sequence of CD274 exon 3 through http://crispr.mit.edu Targeting sequence TGAACTGACATGTC was subcloned into the PX459 plasmid (Addgene 62988) and transfected into IOMM meningioma cells using Lipofectamine 3000 (Thermo Fisher Scientific).

    Techniques: Western Blot, Cell Culture, Flow Cytometry, ADCC Assay, Incubation

    (A and B) Female athymic nude mice were implanted with IOMM meningioma cells in a skull base model. Mice were randomized to the indicated cohorts with 9–10 mice per group. Treatment commenced 4 days following tumor implantation. Mice received 7 treatments. (A) Luminescence from GFP-luciferase–expressing IOMM tumor cells was quantified weekly. Each line represents an individual mouse. Arrows indicate commencement of treatment. P/s/cm2, photons/s/cm2. (B) Kaplan-Meier survival analysis of tumor-bearing mice. (C–E) IOMM meningioma cells were implanted subcutaneously. Mice were randomized based on tumor volume and treated as in A and B. Treatment commenced 17 days following tumor implantation, and mice received 6 treatments. Each cohort contained 9–10 mice. (C) Mean tumor volume with SEM is shown for each cohort. (D) Tumor volume on day 32 following tumor implantation. Each symbol represents an individual mouse, and data are displayed with mean and SD. Data were analyzed using an unpaired 1-tailed t test with Welch’s correction. (E) Subcutaneous tumors on day 32 of tumor growth. (F) Granzyme B (GZMB) was detected by immunohistochemistry in subcutaneous meningioma tumors on day 24 of tumor growth. Vehicle-treated (left, n = 2) or combination-treated (right, n = 2) are shown at original magnification ×20. Scale bar: 200 μm. (G) Hematoxylin and eosin (H&E) stain of serial sections from tumor samples in F. Scale bar: 200 μm.

    Journal: JCI Insight

    Article Title: Efficient ADCC killing of meningioma by avelumab and a high-affinity natural killer cell line, haNK

    doi: 10.1172/jci.insight.130688

    Figure Lengend Snippet: (A and B) Female athymic nude mice were implanted with IOMM meningioma cells in a skull base model. Mice were randomized to the indicated cohorts with 9–10 mice per group. Treatment commenced 4 days following tumor implantation. Mice received 7 treatments. (A) Luminescence from GFP-luciferase–expressing IOMM tumor cells was quantified weekly. Each line represents an individual mouse. Arrows indicate commencement of treatment. P/s/cm2, photons/s/cm2. (B) Kaplan-Meier survival analysis of tumor-bearing mice. (C–E) IOMM meningioma cells were implanted subcutaneously. Mice were randomized based on tumor volume and treated as in A and B. Treatment commenced 17 days following tumor implantation, and mice received 6 treatments. Each cohort contained 9–10 mice. (C) Mean tumor volume with SEM is shown for each cohort. (D) Tumor volume on day 32 following tumor implantation. Each symbol represents an individual mouse, and data are displayed with mean and SD. Data were analyzed using an unpaired 1-tailed t test with Welch’s correction. (E) Subcutaneous tumors on day 32 of tumor growth. (F) Granzyme B (GZMB) was detected by immunohistochemistry in subcutaneous meningioma tumors on day 24 of tumor growth. Vehicle-treated (left, n = 2) or combination-treated (right, n = 2) are shown at original magnification ×20. Scale bar: 200 μm. (G) Hematoxylin and eosin (H&E) stain of serial sections from tumor samples in F. Scale bar: 200 μm.

    Article Snippet: The sgRNA was designed according to the DNA sequence of CD274 exon 3 through http://crispr.mit.edu Targeting sequence TGAACTGACATGTC was subcloned into the PX459 plasmid (Addgene 62988) and transfected into IOMM meningioma cells using Lipofectamine 3000 (Thermo Fisher Scientific).

    Techniques: Tumor Implantation, Luciferase, Expressing, Immunohistochemistry, Staining

    (A) Schematic illustration for CRISPR/Cas9–knockout strategy. Single-guide RNA (sgRNA, shown in green) was designed to target the genetic sequence of CD274 exon 3. The protospacer adjacent motif (PAM) is shown in orange. Genotypes of resultant clone variants 1–4 are shown. (B) Surveyor assay shows successful cleavage of CD274 exon 3. Arrows indicate DNA fragments resulting from CRISPR targeting. (C) Western blot of parental IOMM and CD274–/– IOMM meningioma cell lysates. GAPDH was used as a loading control. (D) Flow cytometry histogram of parental (WT) and CD274–/– (IOMM PD-L1–KO) IOMM cells stained with PD-L1 (blue histograms) or isotype control (red histograms). (E) ADCC assay of parental or CD274–/– IOMM cells exposed to the indicated conditions. Each condition was run in triplicate. Data were analyzed with an unpaired 1-tailed t test. (F–H) CD274–/– IOMM meningioma cells were implanted subcutaneously. Female athymic nude mice were randomized based on tumor volume into the indicated cohorts with n = 10 mice/group. Treatment commenced on day 16 following tumor implantation. Mice received 8 treatments. (F) Mean tumor volume with SEM is shown for each cohort. (G) Tumor volume on day 36 following tumor implantation. Each symbol represents an individual mouse, and data are displayed with mean and SD. Data were analyzed using a 1-way ANOVA with Welch’s correction. (H) Subcutaneous tumors on day 36 of tumor growth. (I) PD-L1 IHC of an IOMM-CD274–/– subcutaneous xenograft tumor (top) and normal human placenta (bottom; positive control). Images were taken with original magnification ×20 (left) or ×40 (right) magnification.

    Journal: JCI Insight

    Article Title: Efficient ADCC killing of meningioma by avelumab and a high-affinity natural killer cell line, haNK

    doi: 10.1172/jci.insight.130688

    Figure Lengend Snippet: (A) Schematic illustration for CRISPR/Cas9–knockout strategy. Single-guide RNA (sgRNA, shown in green) was designed to target the genetic sequence of CD274 exon 3. The protospacer adjacent motif (PAM) is shown in orange. Genotypes of resultant clone variants 1–4 are shown. (B) Surveyor assay shows successful cleavage of CD274 exon 3. Arrows indicate DNA fragments resulting from CRISPR targeting. (C) Western blot of parental IOMM and CD274–/– IOMM meningioma cell lysates. GAPDH was used as a loading control. (D) Flow cytometry histogram of parental (WT) and CD274–/– (IOMM PD-L1–KO) IOMM cells stained with PD-L1 (blue histograms) or isotype control (red histograms). (E) ADCC assay of parental or CD274–/– IOMM cells exposed to the indicated conditions. Each condition was run in triplicate. Data were analyzed with an unpaired 1-tailed t test. (F–H) CD274–/– IOMM meningioma cells were implanted subcutaneously. Female athymic nude mice were randomized based on tumor volume into the indicated cohorts with n = 10 mice/group. Treatment commenced on day 16 following tumor implantation. Mice received 8 treatments. (F) Mean tumor volume with SEM is shown for each cohort. (G) Tumor volume on day 36 following tumor implantation. Each symbol represents an individual mouse, and data are displayed with mean and SD. Data were analyzed using a 1-way ANOVA with Welch’s correction. (H) Subcutaneous tumors on day 36 of tumor growth. (I) PD-L1 IHC of an IOMM-CD274–/– subcutaneous xenograft tumor (top) and normal human placenta (bottom; positive control). Images were taken with original magnification ×20 (left) or ×40 (right) magnification.

    Article Snippet: The sgRNA was designed according to the DNA sequence of CD274 exon 3 through http://crispr.mit.edu Targeting sequence TGAACTGACATGTC was subcloned into the PX459 plasmid (Addgene 62988) and transfected into IOMM meningioma cells using Lipofectamine 3000 (Thermo Fisher Scientific).

    Techniques: CRISPR, Knock-Out, Sequencing, Western Blot, Flow Cytometry, Staining, ADCC Assay, Tumor Implantation, Positive Control

    STAT1 and its phosphorylated forms are overexpressed in meningioma. (A) Representative WB analysis showing the expression of total and pSTAT1 in different grade meningiomas versus normal meningeal tissue (NMT). (B) Representative images showing the IHC staining of STAT1 and pSTAT1 in the 3 grades meningiomas compared to normal meninges (see black arrows) at 200× magnification. Mean scores are presented in the table below for the specimens and the normal controls examined (see also for the full list of specimens examined and the corresponding scores— n = 47). (C) STAT1 expression levels in WHO I ( n = 40), WHO II ( n = 25), and WHO III ( n = 10) meningioma tumors normalized versus NMT. Data are presented as mean ± SEM; * P ≤ .05. (D) WB showing pSTAT1 and STAT1 in normal brain (NB) and additional normal meninges (NMT-1 and NMT-2) compared to sample J6 (meningioma) as a positive control. (E) Representative WB analysis of STAT1 and pSTAT1 in BM-1 and in WHO I MN cells (MNs) versus HMC. (F) STAT1 expression levels in BM-1 ( n = 4) and in MN cells ( n = 24) normalized versus HMC. Data are presented as mean ± SEM; ** P ≤ .01. (G) Confocal z-stack images showing the immunofluorescent staining of STAT1 (red) and pSTAT1 (Y701, green and S727, red) in MN cells versus HMC. Scale bar 50 μm. Nuclei were stained with DAPI (blue).

    Journal: Neuro-oncology Advances

    Article Title: Constitutive activation of the EGFR–STAT1 axis increases proliferation of meningioma tumor cells

    doi: 10.1093/noajnl/vdaa008

    Figure Lengend Snippet: STAT1 and its phosphorylated forms are overexpressed in meningioma. (A) Representative WB analysis showing the expression of total and pSTAT1 in different grade meningiomas versus normal meningeal tissue (NMT). (B) Representative images showing the IHC staining of STAT1 and pSTAT1 in the 3 grades meningiomas compared to normal meninges (see black arrows) at 200× magnification. Mean scores are presented in the table below for the specimens and the normal controls examined (see also for the full list of specimens examined and the corresponding scores— n = 47). (C) STAT1 expression levels in WHO I ( n = 40), WHO II ( n = 25), and WHO III ( n = 10) meningioma tumors normalized versus NMT. Data are presented as mean ± SEM; * P ≤ .05. (D) WB showing pSTAT1 and STAT1 in normal brain (NB) and additional normal meninges (NMT-1 and NMT-2) compared to sample J6 (meningioma) as a positive control. (E) Representative WB analysis of STAT1 and pSTAT1 in BM-1 and in WHO I MN cells (MNs) versus HMC. (F) STAT1 expression levels in BM-1 ( n = 4) and in MN cells ( n = 24) normalized versus HMC. Data are presented as mean ± SEM; ** P ≤ .01. (G) Confocal z-stack images showing the immunofluorescent staining of STAT1 (red) and pSTAT1 (Y701, green and S727, red) in MN cells versus HMC. Scale bar 50 μm. Nuclei were stained with DAPI (blue).

    Article Snippet: Normal HMCs were purchased from ScienCell (UK distributor: Caltag Medsystems; Catalog # 1400), U251 glioma cells were purchased from ECACC (Catalog # 09063001), an immortalized grade 1 meningioma cell line BM-1 was from DSMZ (Catalog # ACC 599) and authenticated via genomic fingerprinting (Eurofins Genomics Europe Applied Genomics GmbH).

    Techniques: Expressing, Immunohistochemistry, Positive Control, Staining

    STAT1 phosphorylation in meningioma cells is not dependent on the JAK–STAT pathway. (A) WB of WHO I meningioma tumor tissue lysates ( n = 8); the presence of gamma interferon (IFNγ) and macrophage infiltration (CD163) into the tumor were analyzed in relation to STAT1 and pSTAT1 levels. Phospho-JAK1 was used to detect activation of the JAK–STAT pathway (*positive control for pJAK1 antibody). (B) WB of total and pSTAT1 in BM-1 and HMC cells, grown in different culture condition. HMC, HMC cells media; MN, MN cells media; MN-SF, MN-serum free media; MN-SF+FBS, MN serum free for 24 h + FBS for 24 h; MN Cond, meningioma cells-conditioned media. (C) WB analysis of STAT1 and pSTAT1 protein levels in HMC and 2 primary MN cells after IFNγ treatment at the concentration of 50 ng/ml for the indicated amount of time. Phosho-JAK1 and pJAK2 are shown to confirm the activation of the JAK–STAT pathway. (D) Representative confocal images (z-stack) showing localization of pSTAT1-Y701 (green) and pSTAT1-S727 (red) in primary MN cells before and after IFNγ stimulation (50 ng/ml for 1 h). Scale bar 50 μm. Nuclei were stain with DAPI (blue). (E) WB analysis of SOCSs and PIASs protein levels in BM-1 and primary MNs compared to HMC.

    Journal: Neuro-oncology Advances

    Article Title: Constitutive activation of the EGFR–STAT1 axis increases proliferation of meningioma tumor cells

    doi: 10.1093/noajnl/vdaa008

    Figure Lengend Snippet: STAT1 phosphorylation in meningioma cells is not dependent on the JAK–STAT pathway. (A) WB of WHO I meningioma tumor tissue lysates ( n = 8); the presence of gamma interferon (IFNγ) and macrophage infiltration (CD163) into the tumor were analyzed in relation to STAT1 and pSTAT1 levels. Phospho-JAK1 was used to detect activation of the JAK–STAT pathway (*positive control for pJAK1 antibody). (B) WB of total and pSTAT1 in BM-1 and HMC cells, grown in different culture condition. HMC, HMC cells media; MN, MN cells media; MN-SF, MN-serum free media; MN-SF+FBS, MN serum free for 24 h + FBS for 24 h; MN Cond, meningioma cells-conditioned media. (C) WB analysis of STAT1 and pSTAT1 protein levels in HMC and 2 primary MN cells after IFNγ treatment at the concentration of 50 ng/ml for the indicated amount of time. Phosho-JAK1 and pJAK2 are shown to confirm the activation of the JAK–STAT pathway. (D) Representative confocal images (z-stack) showing localization of pSTAT1-Y701 (green) and pSTAT1-S727 (red) in primary MN cells before and after IFNγ stimulation (50 ng/ml for 1 h). Scale bar 50 μm. Nuclei were stain with DAPI (blue). (E) WB analysis of SOCSs and PIASs protein levels in BM-1 and primary MNs compared to HMC.

    Article Snippet: Normal HMCs were purchased from ScienCell (UK distributor: Caltag Medsystems; Catalog # 1400), U251 glioma cells were purchased from ECACC (Catalog # 09063001), an immortalized grade 1 meningioma cell line BM-1 was from DSMZ (Catalog # ACC 599) and authenticated via genomic fingerprinting (Eurofins Genomics Europe Applied Genomics GmbH).

    Techniques: Activation Assay, Positive Control, Concentration Assay, Staining

    STAT1 activating mutations induce phosphorylation of AKT, ERK1/2 and increased proliferation of U251-MG cells. (A) WB representing total and phosphorylated STAT1 levels in U251-MG compared to HMC and BM-1 cells. (B) WB showing overexpression of STAT1-WT and activating mutants in U251-MG cells and the related activation of pAKT and pERK1/2. (C) STAT1 expression levels in U251-MG cells normalized versus STAT1 expression levels in pcDNA transfected cells. Data are presented as mean ± SEM; *** P ≤ .001. (D) Histogram presenting the statistical increase in cell proliferation in U251-MG cells overexpressing the activating STAT1 mutants (STAT1-Y701F, STAT1-S727E, STAT1-Y701F/S727E). Data were normalized for STAT1-pcDNA-transfected cells and presented as FC of growth versus STAT1-WT; *** P ≤ .001.

    Journal: Neuro-oncology Advances

    Article Title: Constitutive activation of the EGFR–STAT1 axis increases proliferation of meningioma tumor cells

    doi: 10.1093/noajnl/vdaa008

    Figure Lengend Snippet: STAT1 activating mutations induce phosphorylation of AKT, ERK1/2 and increased proliferation of U251-MG cells. (A) WB representing total and phosphorylated STAT1 levels in U251-MG compared to HMC and BM-1 cells. (B) WB showing overexpression of STAT1-WT and activating mutants in U251-MG cells and the related activation of pAKT and pERK1/2. (C) STAT1 expression levels in U251-MG cells normalized versus STAT1 expression levels in pcDNA transfected cells. Data are presented as mean ± SEM; *** P ≤ .001. (D) Histogram presenting the statistical increase in cell proliferation in U251-MG cells overexpressing the activating STAT1 mutants (STAT1-Y701F, STAT1-S727E, STAT1-Y701F/S727E). Data were normalized for STAT1-pcDNA-transfected cells and presented as FC of growth versus STAT1-WT; *** P ≤ .001.

    Article Snippet: Normal HMCs were purchased from ScienCell (UK distributor: Caltag Medsystems; Catalog # 1400), U251 glioma cells were purchased from ECACC (Catalog # 09063001), an immortalized grade 1 meningioma cell line BM-1 was from DSMZ (Catalog # ACC 599) and authenticated via genomic fingerprinting (Eurofins Genomics Europe Applied Genomics GmbH).

    Techniques: Over Expression, Activation Assay, Expressing, Transfection

    The constitutive activation of the EGFR in meningioma induces STAT1 phosphorylation. (A) Representative WB analysis of total and pEGFR-Y1068 in meningioma, when compared to control. Upper panel: WHO I, II, and III meningioma tissues compared to NMT; lower panel: BM-1 and primary MN cells compared to HMC. (B) WB of STAT1 and pSTAT1 protein levels after treatment with 5 μM of canertinib, afatinib, and erlotinib in BM-1 cells. The reduced levels of pEGFR-Y1068 confirmed drug activity. (C) ATP-proliferation assay performed in BM-1 cells after treatment with different concentrations of canertinib, afatinib, and erlotinib for 24 h. (D) WB analysis of STAT1, pSTAT1, and other markers of proliferation in primary MN cells after treatment with 10 μM of canertinib. (E) Histograms representing WB quantification at 3 and 24 h for STAT1, pSTAT1, pAKT, pERK1/2, and cyclin D1 after canertinib treatment in 3 different primary MN cells (see ). Data are presented as mean ± SEM, * P < .05, ** P < .01, *** P < .001. (F) qPCR analysis showing the statistical reduction of STAT1 gene expression at 3, 6, and 24 h after treatment with 10 μM of canertinib ( n = 3). Data are presented as mean ± SEM; ** P < .01. (G) WB representing STAT1 and pSTAT1 in BM-1 cells, following treatment with EGF (50 ng/ml) for 5, 30, and 60 min.

    Journal: Neuro-oncology Advances

    Article Title: Constitutive activation of the EGFR–STAT1 axis increases proliferation of meningioma tumor cells

    doi: 10.1093/noajnl/vdaa008

    Figure Lengend Snippet: The constitutive activation of the EGFR in meningioma induces STAT1 phosphorylation. (A) Representative WB analysis of total and pEGFR-Y1068 in meningioma, when compared to control. Upper panel: WHO I, II, and III meningioma tissues compared to NMT; lower panel: BM-1 and primary MN cells compared to HMC. (B) WB of STAT1 and pSTAT1 protein levels after treatment with 5 μM of canertinib, afatinib, and erlotinib in BM-1 cells. The reduced levels of pEGFR-Y1068 confirmed drug activity. (C) ATP-proliferation assay performed in BM-1 cells after treatment with different concentrations of canertinib, afatinib, and erlotinib for 24 h. (D) WB analysis of STAT1, pSTAT1, and other markers of proliferation in primary MN cells after treatment with 10 μM of canertinib. (E) Histograms representing WB quantification at 3 and 24 h for STAT1, pSTAT1, pAKT, pERK1/2, and cyclin D1 after canertinib treatment in 3 different primary MN cells (see ). Data are presented as mean ± SEM, * P < .05, ** P < .01, *** P < .001. (F) qPCR analysis showing the statistical reduction of STAT1 gene expression at 3, 6, and 24 h after treatment with 10 μM of canertinib ( n = 3). Data are presented as mean ± SEM; ** P < .01. (G) WB representing STAT1 and pSTAT1 in BM-1 cells, following treatment with EGF (50 ng/ml) for 5, 30, and 60 min.

    Article Snippet: Normal HMCs were purchased from ScienCell (UK distributor: Caltag Medsystems; Catalog # 1400), U251 glioma cells were purchased from ECACC (Catalog # 09063001), an immortalized grade 1 meningioma cell line BM-1 was from DSMZ (Catalog # ACC 599) and authenticated via genomic fingerprinting (Eurofins Genomics Europe Applied Genomics GmbH).

    Techniques: Activation Assay, Activity Assay, ATP Proliferation Assay, Expressing