cd147 antibody  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc cd147 antibody
    Expressions of CyPA and <t>CD147</t> are associated with glioma grade, histological type, and prognosis. The expression of CyPA (a) and CD147 (b) in GBM and LGG compared with normal tissue and correlation with prognosis in TCGA and CGGA databases. The expression of CyPA (c) and CD147 (d) in different WHO grades and histological types of glioma in TCGA and CGGA database. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗∗ P < 0.0001, ns stands for no significance.
    Cd147 Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cd147 antibody/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    cd147 antibody - by Bioz Stars, 2023-03
    94/100 stars

    Images

    1) Product Images from "Downregulation of CyclophilinA/CD147 Axis Induces Cell Apoptosis and Inhibits Glioma Aggressiveness"

    Article Title: Downregulation of CyclophilinA/CD147 Axis Induces Cell Apoptosis and Inhibits Glioma Aggressiveness

    Journal: BioMed Research International

    doi: 10.1155/2020/7035847

    Expressions of CyPA and CD147 are associated with glioma grade, histological type, and prognosis. The expression of CyPA (a) and CD147 (b) in GBM and LGG compared with normal tissue and correlation with prognosis in TCGA and CGGA databases. The expression of CyPA (c) and CD147 (d) in different WHO grades and histological types of glioma in TCGA and CGGA database. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗∗ P < 0.0001, ns stands for no significance.
    Figure Legend Snippet: Expressions of CyPA and CD147 are associated with glioma grade, histological type, and prognosis. The expression of CyPA (a) and CD147 (b) in GBM and LGG compared with normal tissue and correlation with prognosis in TCGA and CGGA databases. The expression of CyPA (c) and CD147 (d) in different WHO grades and histological types of glioma in TCGA and CGGA database. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗∗ P < 0.0001, ns stands for no significance.

    Techniques Used: Expressing

    Expression and knockdown of CyPA and CD147 in glioma cell lines. The expressions of CyPA (a) and CD147 (b) in glioma cell lines are detected by RT-qPCR and western blot.(c) Specific si-RNA could inhibit CyPA and CD147 expression in U251 cell line. ∗ P < 0.05, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001.
    Figure Legend Snippet: Expression and knockdown of CyPA and CD147 in glioma cell lines. The expressions of CyPA (a) and CD147 (b) in glioma cell lines are detected by RT-qPCR and western blot.(c) Specific si-RNA could inhibit CyPA and CD147 expression in U251 cell line. ∗ P < 0.05, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001.

    Techniques Used: Expressing, Quantitative RT-PCR, Western Blot

    Knockdown of CyPA and CD147 reduces glioma proliferation. (a). EdU assay shows that inhibition of CyPA and CD147 significantly decreases glioma cell proliferation. U251 wild type cell is taken as the control group. (b). Flow cytometry analysis reveals the effect of CyPA and CD147 inhibition on glioma cell proliferation.
    Figure Legend Snippet: Knockdown of CyPA and CD147 reduces glioma proliferation. (a). EdU assay shows that inhibition of CyPA and CD147 significantly decreases glioma cell proliferation. U251 wild type cell is taken as the control group. (b). Flow cytometry analysis reveals the effect of CyPA and CD147 inhibition on glioma cell proliferation.

    Techniques Used: EdU Assay, Inhibition, Flow Cytometry

    Predictive value of CyPA and CD147 in different grades of glioma. CyPA and CD147 expression pattern in different grades of glioma in TCGA database (a) and CGGA database (b) analyzed by ROC curve analysis.
    Figure Legend Snippet: Predictive value of CyPA and CD147 in different grades of glioma. CyPA and CD147 expression pattern in different grades of glioma in TCGA database (a) and CGGA database (b) analyzed by ROC curve analysis.

    Techniques Used: Expressing

    cd147  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc cd147
    Expression levels of key gastric cancer stem cell (GCSC) markers, CypA, and <t>CD147</t> in MKN45 adherent and tumorsphere cells. Protein levels were detected via Western blot analysis using specific antibodies and were further quantified using densitometry. β-actin levels were used as an internal control. The ratio of each target protein to β-actin for adherent cells was normalized to onefold. * p < 0.05 vs. the adherent cells.
    Cd147, supplied by Cell Signaling Technology Inc, 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/cd147/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    cd147 - by Bioz Stars, 2023-03
    86/100 stars

    Images

    1) Product Images from "Cyclophilin A Inhibitors Suppress Proliferation and Induce Apoptosis of MKN45 Gastric Cancer Stem-like Cells by Regulating CypA/CD147-Mediated Signaling Pathway"

    Article Title: Cyclophilin A Inhibitors Suppress Proliferation and Induce Apoptosis of MKN45 Gastric Cancer Stem-like Cells by Regulating CypA/CD147-Mediated Signaling Pathway

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms24054734

    Expression levels of key gastric cancer stem cell (GCSC) markers, CypA, and CD147 in MKN45 adherent and tumorsphere cells. Protein levels were detected via Western blot analysis using specific antibodies and were further quantified using densitometry. β-actin levels were used as an internal control. The ratio of each target protein to β-actin for adherent cells was normalized to onefold. * p < 0.05 vs. the adherent cells.
    Figure Legend Snippet: Expression levels of key gastric cancer stem cell (GCSC) markers, CypA, and CD147 in MKN45 adherent and tumorsphere cells. Protein levels were detected via Western blot analysis using specific antibodies and were further quantified using densitometry. β-actin levels were used as an internal control. The ratio of each target protein to β-actin for adherent cells was normalized to onefold. * p < 0.05 vs. the adherent cells.

    Techniques Used: Expressing, Western Blot

    Effects of C9 and CsA on the CypA/CD147-mediated signaling pathways in MKN45 GCSCs. ( A , B ) MKN45-derived GCSCs were treated with the indicated concentrations of each compound for 72 h. Protein levels were detected via Western blot analysis using specific antibodies and were further quantified using densitometry. β-actin levels were used as an internal control. The ratio of each target protein to β-actin for untreated control was normalized to onefold. * p < 0.05 vs. the control.
    Figure Legend Snippet: Effects of C9 and CsA on the CypA/CD147-mediated signaling pathways in MKN45 GCSCs. ( A , B ) MKN45-derived GCSCs were treated with the indicated concentrations of each compound for 72 h. Protein levels were detected via Western blot analysis using specific antibodies and were further quantified using densitometry. β-actin levels were used as an internal control. The ratio of each target protein to β-actin for untreated control was normalized to onefold. * p < 0.05 vs. the control.

    Techniques Used: Derivative Assay, Western Blot

    cd147  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc cd147
    Sequences of specific primers used in RT-qPCR.
    Cd147, supplied by Cell Signaling Technology Inc, 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/cd147/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    cd147 - by Bioz Stars, 2023-03
    86/100 stars

    Images

    1) Product Images from "CypB-CD147 Signaling Is Involved in Crosstalk between Cartilage and FLS in Collagen-Induced Arthritis"

    Article Title: CypB-CD147 Signaling Is Involved in Crosstalk between Cartilage and FLS in Collagen-Induced Arthritis

    Journal: Mediators of Inflammation

    doi: 10.1155/2020/6473858

    Sequences of specific primers used in RT-qPCR.
    Figure Legend Snippet: Sequences of specific primers used in RT-qPCR.

    Techniques Used:

    Gene expressions of MMPs, CypB, CD147, and inflammation-related genes in normal and CIA cartilage. Normal cartilage explants were treated with vehicle and 10 ng/mL IL-1 α , and CIA cartilages were treated with vehicle, 10 ng/mL IL-1 α , and 10 ng/mL IL-1 α plus 10 μ M dexamethasone, respectively, before collected for total mRNA extraction. All data were presented as a value relative to those in the first group. Values are represented as the mean ± S.E.M. △ P < 0.05, △△ P < 0.01, △△△ P < 0.001, and △△△△ P < 0.0001 as compared with the indicated group.
    Figure Legend Snippet: Gene expressions of MMPs, CypB, CD147, and inflammation-related genes in normal and CIA cartilage. Normal cartilage explants were treated with vehicle and 10 ng/mL IL-1 α , and CIA cartilages were treated with vehicle, 10 ng/mL IL-1 α , and 10 ng/mL IL-1 α plus 10 μ M dexamethasone, respectively, before collected for total mRNA extraction. All data were presented as a value relative to those in the first group. Values are represented as the mean ± S.E.M. △ P < 0.05, △△ P < 0.01, △△△ P < 0.001, and △△△△ P < 0.0001 as compared with the indicated group.

    Techniques Used:

    Western blot analysis of the NF- κ B pathway and CD147 and gene expression of CD147 from cocultured FLS. (a) Grey value of NF- κ B p65, I- κ B α , and IKK- β . (b) A graphic figure of protein expression in the NF- κ B pathway. (c) Gene expression of CD147 in three groups of cocultured FLS. (d, e) Western blot analysis of CD147 in all groups of cocultured FLS. Relative expressions of each protein in the Ctrl group were defined as 1. Values are represented as the mean ± S.E.M. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001 as compared with the Ctrl group; # P < 0.05, ## P < 0.01, ### P < 0.001, and #### P < 0.0001 as compared with the IL-1 α group (see for other definitions).
    Figure Legend Snippet: Western blot analysis of the NF- κ B pathway and CD147 and gene expression of CD147 from cocultured FLS. (a) Grey value of NF- κ B p65, I- κ B α , and IKK- β . (b) A graphic figure of protein expression in the NF- κ B pathway. (c) Gene expression of CD147 in three groups of cocultured FLS. (d, e) Western blot analysis of CD147 in all groups of cocultured FLS. Relative expressions of each protein in the Ctrl group were defined as 1. Values are represented as the mean ± S.E.M. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001 as compared with the Ctrl group; # P < 0.05, ## P < 0.01, ### P < 0.001, and #### P < 0.0001 as compared with the IL-1 α group (see for other definitions).

    Techniques Used: Western Blot, Expressing

    Immunofluorescence staining of p65 nuclear translocation in cocultured FLS from four groups. FLS in the anti-CD147 group were pretreated with 10 μ g/mL anti-CD147 monoantibody for 4 hours before coculture with IL-1 α -induced cartilage, and continually given anti-CD147 treatment in two days of coculture setting. Results are representative images of experiments from at least three independent experiments with similar findings. Values are represented as the mean ± S.E.M; scale bar, 50 μ m (see for other definitions).
    Figure Legend Snippet: Immunofluorescence staining of p65 nuclear translocation in cocultured FLS from four groups. FLS in the anti-CD147 group were pretreated with 10 μ g/mL anti-CD147 monoantibody for 4 hours before coculture with IL-1 α -induced cartilage, and continually given anti-CD147 treatment in two days of coculture setting. Results are representative images of experiments from at least three independent experiments with similar findings. Values are represented as the mean ± S.E.M; scale bar, 50 μ m (see for other definitions).

    Techniques Used: Immunofluorescence, Staining, Translocation Assay

    Graphical summary of the crosstalk between cartilage and FLS involving CypB-CD147 signaling in CIA cartilage-synovioctyes coculture system. Upon being challenged by IL-1, CIA cartilage rapidly produces MMPs (e.g., MMP-3, MMP-9, and MMP-13) and releases CypB. As a paracrine proinflammatory cytokine, CypB interacts with CD147 which expresses on the membrane of CIA FLS. Activated by CD147, translocation of NF- κ B into the nucleus occurs, followed by a subsequent secretion of inflammatory cytokines, which in turns aggravates the inflammation of cocultured cartilage. Consequently, a vicious circle loop starts.
    Figure Legend Snippet: Graphical summary of the crosstalk between cartilage and FLS involving CypB-CD147 signaling in CIA cartilage-synovioctyes coculture system. Upon being challenged by IL-1, CIA cartilage rapidly produces MMPs (e.g., MMP-3, MMP-9, and MMP-13) and releases CypB. As a paracrine proinflammatory cytokine, CypB interacts with CD147 which expresses on the membrane of CIA FLS. Activated by CD147, translocation of NF- κ B into the nucleus occurs, followed by a subsequent secretion of inflammatory cytokines, which in turns aggravates the inflammation of cocultured cartilage. Consequently, a vicious circle loop starts.

    Techniques Used: Translocation Assay

    cd147 antibody  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc cd147 antibody
    Expressions of CyPA and <t>CD147</t> are associated with glioma grade, histological type, and prognosis. The expression of CyPA (a) and CD147 (b) in GBM and LGG compared with normal tissue and correlation with prognosis in TCGA and CGGA databases. The expression of CyPA (c) and CD147 (d) in different WHO grades and histological types of glioma in TCGA and CGGA database. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗∗ P < 0.0001, ns stands for no significance.
    Cd147 Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cd147 antibody/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    cd147 antibody - by Bioz Stars, 2023-03
    94/100 stars

    Images

    1) Product Images from "Downregulation of CyclophilinA/CD147 Axis Induces Cell Apoptosis and Inhibits Glioma Aggressiveness"

    Article Title: Downregulation of CyclophilinA/CD147 Axis Induces Cell Apoptosis and Inhibits Glioma Aggressiveness

    Journal: BioMed Research International

    doi: 10.1155/2020/7035847

    Expressions of CyPA and CD147 are associated with glioma grade, histological type, and prognosis. The expression of CyPA (a) and CD147 (b) in GBM and LGG compared with normal tissue and correlation with prognosis in TCGA and CGGA databases. The expression of CyPA (c) and CD147 (d) in different WHO grades and histological types of glioma in TCGA and CGGA database. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗∗ P < 0.0001, ns stands for no significance.
    Figure Legend Snippet: Expressions of CyPA and CD147 are associated with glioma grade, histological type, and prognosis. The expression of CyPA (a) and CD147 (b) in GBM and LGG compared with normal tissue and correlation with prognosis in TCGA and CGGA databases. The expression of CyPA (c) and CD147 (d) in different WHO grades and histological types of glioma in TCGA and CGGA database. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗∗ P < 0.0001, ns stands for no significance.

    Techniques Used: Expressing

    Expression and knockdown of CyPA and CD147 in glioma cell lines. The expressions of CyPA (a) and CD147 (b) in glioma cell lines are detected by RT-qPCR and western blot.(c) Specific si-RNA could inhibit CyPA and CD147 expression in U251 cell line. ∗ P < 0.05, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001.
    Figure Legend Snippet: Expression and knockdown of CyPA and CD147 in glioma cell lines. The expressions of CyPA (a) and CD147 (b) in glioma cell lines are detected by RT-qPCR and western blot.(c) Specific si-RNA could inhibit CyPA and CD147 expression in U251 cell line. ∗ P < 0.05, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001.

    Techniques Used: Expressing, Quantitative RT-PCR, Western Blot

    Knockdown of CyPA and CD147 reduces glioma proliferation. (a). EdU assay shows that inhibition of CyPA and CD147 significantly decreases glioma cell proliferation. U251 wild type cell is taken as the control group. (b). Flow cytometry analysis reveals the effect of CyPA and CD147 inhibition on glioma cell proliferation.
    Figure Legend Snippet: Knockdown of CyPA and CD147 reduces glioma proliferation. (a). EdU assay shows that inhibition of CyPA and CD147 significantly decreases glioma cell proliferation. U251 wild type cell is taken as the control group. (b). Flow cytometry analysis reveals the effect of CyPA and CD147 inhibition on glioma cell proliferation.

    Techniques Used: EdU Assay, Inhibition, Flow Cytometry

    Predictive value of CyPA and CD147 in different grades of glioma. CyPA and CD147 expression pattern in different grades of glioma in TCGA database (a) and CGGA database (b) analyzed by ROC curve analysis.
    Figure Legend Snippet: Predictive value of CyPA and CD147 in different grades of glioma. CyPA and CD147 expression pattern in different grades of glioma in TCGA database (a) and CGGA database (b) analyzed by ROC curve analysis.

    Techniques Used: Expressing

    cd147  (Cell Signaling Technology Inc)


    Bioz Verified Symbol Cell Signaling Technology Inc is a verified supplier
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    Structured Review

    Cell Signaling Technology Inc cd147
    Expressions of CyPA and <t>CD147</t> are associated with glioma grade, histological type, and prognosis. The expression of CyPA (a) and CD147 (b) in GBM and LGG compared with normal tissue and correlation with prognosis in TCGA and CGGA databases. The expression of CyPA (c) and CD147 (d) in different WHO grades and histological types of glioma in TCGA and CGGA database. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗∗ P < 0.0001, ns stands for no significance.
    Cd147, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cd147/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    cd147 - by Bioz Stars, 2023-03
    94/100 stars

    Images

    1) Product Images from "Downregulation of CyclophilinA/CD147 Axis Induces Cell Apoptosis and Inhibits Glioma Aggressiveness"

    Article Title: Downregulation of CyclophilinA/CD147 Axis Induces Cell Apoptosis and Inhibits Glioma Aggressiveness

    Journal: BioMed Research International

    doi: 10.1155/2020/7035847

    Expressions of CyPA and CD147 are associated with glioma grade, histological type, and prognosis. The expression of CyPA (a) and CD147 (b) in GBM and LGG compared with normal tissue and correlation with prognosis in TCGA and CGGA databases. The expression of CyPA (c) and CD147 (d) in different WHO grades and histological types of glioma in TCGA and CGGA database. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗∗ P < 0.0001, ns stands for no significance.
    Figure Legend Snippet: Expressions of CyPA and CD147 are associated with glioma grade, histological type, and prognosis. The expression of CyPA (a) and CD147 (b) in GBM and LGG compared with normal tissue and correlation with prognosis in TCGA and CGGA databases. The expression of CyPA (c) and CD147 (d) in different WHO grades and histological types of glioma in TCGA and CGGA database. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗∗ P < 0.0001, ns stands for no significance.

    Techniques Used: Expressing

    Expression and knockdown of CyPA and CD147 in glioma cell lines. The expressions of CyPA (a) and CD147 (b) in glioma cell lines are detected by RT-qPCR and western blot.(c) Specific si-RNA could inhibit CyPA and CD147 expression in U251 cell line. ∗ P < 0.05, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001.
    Figure Legend Snippet: Expression and knockdown of CyPA and CD147 in glioma cell lines. The expressions of CyPA (a) and CD147 (b) in glioma cell lines are detected by RT-qPCR and western blot.(c) Specific si-RNA could inhibit CyPA and CD147 expression in U251 cell line. ∗ P < 0.05, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001.

    Techniques Used: Expressing, Quantitative RT-PCR, Western Blot

    Knockdown of CyPA and CD147 reduces glioma proliferation. (a). EdU assay shows that inhibition of CyPA and CD147 significantly decreases glioma cell proliferation. U251 wild type cell is taken as the control group. (b). Flow cytometry analysis reveals the effect of CyPA and CD147 inhibition on glioma cell proliferation.
    Figure Legend Snippet: Knockdown of CyPA and CD147 reduces glioma proliferation. (a). EdU assay shows that inhibition of CyPA and CD147 significantly decreases glioma cell proliferation. U251 wild type cell is taken as the control group. (b). Flow cytometry analysis reveals the effect of CyPA and CD147 inhibition on glioma cell proliferation.

    Techniques Used: EdU Assay, Inhibition, Flow Cytometry

    Predictive value of CyPA and CD147 in different grades of glioma. CyPA and CD147 expression pattern in different grades of glioma in TCGA database (a) and CGGA database (b) analyzed by ROC curve analysis.
    Figure Legend Snippet: Predictive value of CyPA and CD147 in different grades of glioma. CyPA and CD147 expression pattern in different grades of glioma in TCGA database (a) and CGGA database (b) analyzed by ROC curve analysis.

    Techniques Used: Expressing

    anti cd147  (Cell Signaling Technology Inc)


    Bioz Verified Symbol Cell Signaling Technology Inc is a verified supplier
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    Cell Signaling Technology Inc anti cd147
    <t>CD147</t> is highly expressed in glioma tissues and associated with tumor malignancy (A-B) Silico analysis of glioma tissues of the multidimensional data set from The Cancer Genome Atlas (TCGA) PROTEINATLAS data set. CD147 protein expression and copy numbers were determined in various types of tumor sections respectively. (C-D) Immunohistochemistry staining of CD147 in human normal and glioma tissues with different grade (C) and the statistical analysis (D). (E) The methylation status of the CD147 promoter was analyzed by methylation-specific PCR in each of the 20 normal and glioma tissues. The white and black colors represent hypomethylation and hypermethylation, respectively. (F) The correlation between the TCGA expression and methylation data for CD147 in glioma tissues. (G-H) Clinical outcomes for the gene expression patterns given at the top of each panel by UALCAN analysis.
    Anti Cd147, supplied by Cell Signaling Technology Inc, 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/anti cd147/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti cd147 - by Bioz Stars, 2023-03
    86/100 stars

    Images

    1) Product Images from "CD147 confers temozolomide resistance of glioma cells via the regulation of β-TrCP/Nrf2 pathway"

    Article Title: CD147 confers temozolomide resistance of glioma cells via the regulation of β-TrCP/Nrf2 pathway

    Journal: International Journal of Biological Sciences

    doi: 10.7150/ijbs.60894

    CD147 is highly expressed in glioma tissues and associated with tumor malignancy (A-B) Silico analysis of glioma tissues of the multidimensional data set from The Cancer Genome Atlas (TCGA) PROTEINATLAS data set. CD147 protein expression and copy numbers were determined in various types of tumor sections respectively. (C-D) Immunohistochemistry staining of CD147 in human normal and glioma tissues with different grade (C) and the statistical analysis (D). (E) The methylation status of the CD147 promoter was analyzed by methylation-specific PCR in each of the 20 normal and glioma tissues. The white and black colors represent hypomethylation and hypermethylation, respectively. (F) The correlation between the TCGA expression and methylation data for CD147 in glioma tissues. (G-H) Clinical outcomes for the gene expression patterns given at the top of each panel by UALCAN analysis.
    Figure Legend Snippet: CD147 is highly expressed in glioma tissues and associated with tumor malignancy (A-B) Silico analysis of glioma tissues of the multidimensional data set from The Cancer Genome Atlas (TCGA) PROTEINATLAS data set. CD147 protein expression and copy numbers were determined in various types of tumor sections respectively. (C-D) Immunohistochemistry staining of CD147 in human normal and glioma tissues with different grade (C) and the statistical analysis (D). (E) The methylation status of the CD147 promoter was analyzed by methylation-specific PCR in each of the 20 normal and glioma tissues. The white and black colors represent hypomethylation and hypermethylation, respectively. (F) The correlation between the TCGA expression and methylation data for CD147 in glioma tissues. (G-H) Clinical outcomes for the gene expression patterns given at the top of each panel by UALCAN analysis.

    Techniques Used: Expressing, Immunohistochemistry, Staining, Methylation

    CD147 contributes to the resistance to TMZ treatment via the elimination of intracellular ROS (A-F) We reduced CD147 levels in U251 and T98G cells using lentivirus expressing CD147 shRNA, and then treated with 50 μM TMZ as indicated. (A) Identification of CD147 protein levels. (B-D) Cell viabilities were determined by Edu incorporation (B) and CCK8 assay (C-D) in indicated cells. (E) TUNEL staining was performed to determine cell apoptosis. (F) Relative ROS production was determined by Flow cytometry. (G-K) CD147 was overexpressed in U251 and T98G cells with CD147 overexpressing lentivirus, and then treated with TMZ as indicated. (G) Identification of CD147 protein levels. (H-K) cell viabilities (H-I), apoptosis (J) and ROS production (K) were determined, respectively.
    Figure Legend Snippet: CD147 contributes to the resistance to TMZ treatment via the elimination of intracellular ROS (A-F) We reduced CD147 levels in U251 and T98G cells using lentivirus expressing CD147 shRNA, and then treated with 50 μM TMZ as indicated. (A) Identification of CD147 protein levels. (B-D) Cell viabilities were determined by Edu incorporation (B) and CCK8 assay (C-D) in indicated cells. (E) TUNEL staining was performed to determine cell apoptosis. (F) Relative ROS production was determined by Flow cytometry. (G-K) CD147 was overexpressed in U251 and T98G cells with CD147 overexpressing lentivirus, and then treated with TMZ as indicated. (G) Identification of CD147 protein levels. (H-K) cell viabilities (H-I), apoptosis (J) and ROS production (K) were determined, respectively.

    Techniques Used: Expressing, shRNA, CCK-8 Assay, TUNEL Assay, Staining, Flow Cytometry

    CD147 promotes Nrf2 expression through blocking its protein degradation (A) Nrf2 protein levels were determined in U251 or T98G cells after CD147 knockdown. (B) The indicated protein levels were determined in cells with or without CD147 knockdown. (C-E) NQO-1 (C), HO-1(D) and GCLC-1 (E) mRNA levels were determined by qCPR respectively. (F-G) Luciferase reporter gene assay was performed to determine CD147 knockdown could suppress the ARE activity. (H-I) Nrf2 protein stability were determined by western blotting in cells treated with CHX (10 μg/ml) for indicated time or MG-132 (10 μM) for 4 h, respectively.
    Figure Legend Snippet: CD147 promotes Nrf2 expression through blocking its protein degradation (A) Nrf2 protein levels were determined in U251 or T98G cells after CD147 knockdown. (B) The indicated protein levels were determined in cells with or without CD147 knockdown. (C-E) NQO-1 (C), HO-1(D) and GCLC-1 (E) mRNA levels were determined by qCPR respectively. (F-G) Luciferase reporter gene assay was performed to determine CD147 knockdown could suppress the ARE activity. (H-I) Nrf2 protein stability were determined by western blotting in cells treated with CHX (10 μg/ml) for indicated time or MG-132 (10 μM) for 4 h, respectively.

    Techniques Used: Expressing, Blocking Assay, Luciferase, Reporter Gene Assay, Activity Assay, Western Blot

    CD147 dictates Nrf2 stability through the suppression of GSK3β/β-TrCP dependent protein degradation (A-B) The indicated proteins were determined in U251 cells with CD147 knockdown (A) or overexpression (B). (C) Nrf2 and GSK3β protein levels were determined in U251 cells following Capivasertib (10nM) treatment. (D-E) Immunoprecipitation was performed to determine the interaction between β-TrCP and Nrf2 in indicated U251 cells. After the β-TrCP protein was immunoprecipitated with an anti-β-TrCP antibody, indicated proteins were detected by western blotting. (F) Suppresion of CD147 decreased the total and nuclear Nrf2 expression. β-Actin and Lamin B served as internal controls. WCL, whole cell lysate; N, nuclear; C, cytoplasmic.
    Figure Legend Snippet: CD147 dictates Nrf2 stability through the suppression of GSK3β/β-TrCP dependent protein degradation (A-B) The indicated proteins were determined in U251 cells with CD147 knockdown (A) or overexpression (B). (C) Nrf2 and GSK3β protein levels were determined in U251 cells following Capivasertib (10nM) treatment. (D-E) Immunoprecipitation was performed to determine the interaction between β-TrCP and Nrf2 in indicated U251 cells. After the β-TrCP protein was immunoprecipitated with an anti-β-TrCP antibody, indicated proteins were detected by western blotting. (F) Suppresion of CD147 decreased the total and nuclear Nrf2 expression. β-Actin and Lamin B served as internal controls. WCL, whole cell lysate; N, nuclear; C, cytoplasmic.

    Techniques Used: Over Expression, Immunoprecipitation, Western Blot, Expressing

    CD147-dependent Nrf2 expression is required for glioma cells survival and drug resistance (A) Suppression of CD147 increased anti-tumor effect of TMZ in nude mice. Mice were injected into the groin with 1 × 10 6 U251 cells. The mice were given intraperitoneal injections of 50 mg/kg TMZ or DMSO once every day from days 1 to 5. The Tumor size was measured and tumor volume was calculated. (B) Immunohistochemistry staining of CD147 and Nrf2 in the sections of tumor graft. (C-F) Nrf2 levels were increased with lentivirus overexpressing Nrf2 in U251 cells with CD147 knockdown. (C-D) Nrf2 overexpression blocked TMZ mediated inhibitions of tumor growth in vivo (C) and in vitro (D). (E-F) Nrf2 overexpression blocked TMZ induced apoptosis (E) and ROS production (F).
    Figure Legend Snippet: CD147-dependent Nrf2 expression is required for glioma cells survival and drug resistance (A) Suppression of CD147 increased anti-tumor effect of TMZ in nude mice. Mice were injected into the groin with 1 × 10 6 U251 cells. The mice were given intraperitoneal injections of 50 mg/kg TMZ or DMSO once every day from days 1 to 5. The Tumor size was measured and tumor volume was calculated. (B) Immunohistochemistry staining of CD147 and Nrf2 in the sections of tumor graft. (C-F) Nrf2 levels were increased with lentivirus overexpressing Nrf2 in U251 cells with CD147 knockdown. (C-D) Nrf2 overexpression blocked TMZ mediated inhibitions of tumor growth in vivo (C) and in vitro (D). (E-F) Nrf2 overexpression blocked TMZ induced apoptosis (E) and ROS production (F).

    Techniques Used: Expressing, Injection, Immunohistochemistry, Staining, Over Expression, In Vivo, In Vitro

    CD147 and Nrf2 are positively correlated in glioma tissues and associated with patient outcome (A-B) Immunohistochemistry staining of CD147 and Nrf2 in human adjacent normal and gioma tissues from patients (A) and the statistical analysis (B). (C) Positive correlation between CD147 and Nr2 expression levels with linear regression and Pearson's correlation significance (P < 0.0001, ANOVA test). (D-G) Positive association of CD147 with NQO-1 (D), HO-1 (E), GSTK-1 (F) and GSS (G) mRNA expression patterns in glioma tissues from TCGA data set by GEPIA with linear regression and Pearson's correlation significance. (H-J) Silico analysis of 509 cases of glioma tissues of the multidimensional data set from TCGA portal data set. KaplaneMeier plots indicate the clinical outcomes for Nrf2 (H), or CD147/Nrf2 levels (I and J) in glioma tissues. C, CD147; N, Nrf2; n, indicates the number of patient samples evaluated in each analysis. p-values were calculated using the ManteleCox log-rank test.
    Figure Legend Snippet: CD147 and Nrf2 are positively correlated in glioma tissues and associated with patient outcome (A-B) Immunohistochemistry staining of CD147 and Nrf2 in human adjacent normal and gioma tissues from patients (A) and the statistical analysis (B). (C) Positive correlation between CD147 and Nr2 expression levels with linear regression and Pearson's correlation significance (P < 0.0001, ANOVA test). (D-G) Positive association of CD147 with NQO-1 (D), HO-1 (E), GSTK-1 (F) and GSS (G) mRNA expression patterns in glioma tissues from TCGA data set by GEPIA with linear regression and Pearson's correlation significance. (H-J) Silico analysis of 509 cases of glioma tissues of the multidimensional data set from TCGA portal data set. KaplaneMeier plots indicate the clinical outcomes for Nrf2 (H), or CD147/Nrf2 levels (I and J) in glioma tissues. C, CD147; N, Nrf2; n, indicates the number of patient samples evaluated in each analysis. p-values were calculated using the ManteleCox log-rank test.

    Techniques Used: Immunohistochemistry, Staining, Expressing

    cd147  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc cd147
    Epigenetic inactivation of CSC surface markers ( CD24 , CD44 , CD133 , and <t>CD147</t> ) in OSCC cell lines. Quantitative real-time RT-PCR analysis was carried out to assess the transcriptional expression level of ( A ) CD24 , ( B ) CD44 , ( C ) CD133 , and ( D ) CD147 genes in OSCC cell lines before and after treatment with 5-aza-dC (5 μM) for 72 h and TSA (0.3 μM) for 18 h. The expression levels of the genes were internally normalized to the expression levels of GAPDH , and the normalized expression for each gene before 5-aza-dC treatments was set to one. The asterisks indicate significant increases in gene expression after 5-aza-dC treatment ( p < 0.05). All data were statistically analyzed using the Student’s t -test. * p < 0.05; ** p < 0.01; *** p < 0.001; no asterisk, not significant. A two-tailed Student’s t -test was used to compare data between the two groups.
    Cd147, supplied by Cell Signaling Technology 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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    1) Product Images from "Promoter Methylation of Cancer Stem Cell Surface Markers as an Epigenetic Biomarker for Prognosis of Oral Squamous Cell Carcinoma"

    Article Title: Promoter Methylation of Cancer Stem Cell Surface Markers as an Epigenetic Biomarker for Prognosis of Oral Squamous Cell Carcinoma

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms232314624

    Epigenetic inactivation of CSC surface markers ( CD24 , CD44 , CD133 , and CD147 ) in OSCC cell lines. Quantitative real-time RT-PCR analysis was carried out to assess the transcriptional expression level of ( A ) CD24 , ( B ) CD44 , ( C ) CD133 , and ( D ) CD147 genes in OSCC cell lines before and after treatment with 5-aza-dC (5 μM) for 72 h and TSA (0.3 μM) for 18 h. The expression levels of the genes were internally normalized to the expression levels of GAPDH , and the normalized expression for each gene before 5-aza-dC treatments was set to one. The asterisks indicate significant increases in gene expression after 5-aza-dC treatment ( p < 0.05). All data were statistically analyzed using the Student’s t -test. * p < 0.05; ** p < 0.01; *** p < 0.001; no asterisk, not significant. A two-tailed Student’s t -test was used to compare data between the two groups.
    Figure Legend Snippet: Epigenetic inactivation of CSC surface markers ( CD24 , CD44 , CD133 , and CD147 ) in OSCC cell lines. Quantitative real-time RT-PCR analysis was carried out to assess the transcriptional expression level of ( A ) CD24 , ( B ) CD44 , ( C ) CD133 , and ( D ) CD147 genes in OSCC cell lines before and after treatment with 5-aza-dC (5 μM) for 72 h and TSA (0.3 μM) for 18 h. The expression levels of the genes were internally normalized to the expression levels of GAPDH , and the normalized expression for each gene before 5-aza-dC treatments was set to one. The asterisks indicate significant increases in gene expression after 5-aza-dC treatment ( p < 0.05). All data were statistically analyzed using the Student’s t -test. * p < 0.05; ** p < 0.01; *** p < 0.001; no asterisk, not significant. A two-tailed Student’s t -test was used to compare data between the two groups.

    Techniques Used: Quantitative RT-PCR, Expressing, Two Tailed Test

    Promoter DNA methylation analysis of the CD24 , CD44 , CD133 , and CD147 genes in OSCC cell lines, primary OSCC tumor tissues, and normal oral mucosal tissues. ( A ) Schematic structure of the CpG islands at the promoter regions for CD24 , CD44 , CD133 , and CD147. ( A ) The primer locations for MSP were indicated as an orange bar for each gene. ( B ) MSP results in OSCC cell lines. Gel pictures describe the methylation analysis by MSP. DNA methyltransferase 1 and 3b knockout HCT116 cells (DKO) were included as positive controls. The PCR products recognized the unmethylated (U) and methylated (M) genes. DKO cells were used for the unmethylated control. IVD = in vitro methylated control; ddH 2 O = water control containing no DNA. ( C ) Methylation frequency of the CD24 , CD133 , and CD147 genes between the samples from patients with OSCC ( n = 102) and the normal oral mucosal tissue samples ( n = 45).
    Figure Legend Snippet: Promoter DNA methylation analysis of the CD24 , CD44 , CD133 , and CD147 genes in OSCC cell lines, primary OSCC tumor tissues, and normal oral mucosal tissues. ( A ) Schematic structure of the CpG islands at the promoter regions for CD24 , CD44 , CD133 , and CD147. ( A ) The primer locations for MSP were indicated as an orange bar for each gene. ( B ) MSP results in OSCC cell lines. Gel pictures describe the methylation analysis by MSP. DNA methyltransferase 1 and 3b knockout HCT116 cells (DKO) were included as positive controls. The PCR products recognized the unmethylated (U) and methylated (M) genes. DKO cells were used for the unmethylated control. IVD = in vitro methylated control; ddH 2 O = water control containing no DNA. ( C ) Methylation frequency of the CD24 , CD133 , and CD147 genes between the samples from patients with OSCC ( n = 102) and the normal oral mucosal tissue samples ( n = 45).

    Techniques Used: DNA Methylation Assay, Methylation, Knock-Out, In Vitro

    Representative bisulfite sequencing results of the CpG islands in the CD24 , CD133 , and CD147 gene promoter regions in OSCC cell lines, primary OSCC tumors ( n = 3), and normal oral mucosal tissues ( n = 3). The locations of the CpG sites ( CD24 : upstream region from −903 to −770; CD133: exon 1 region from −230 to +90 ; and CD147: upstream region from −552 to −291) relative to the transcription start sites (TSSs) of exon 1 are shown. Each box represents a CpG dinucleotide. The black boxes represent methylated cytosines, and the white boxes represent unmethylated cytosines.
    Figure Legend Snippet: Representative bisulfite sequencing results of the CpG islands in the CD24 , CD133 , and CD147 gene promoter regions in OSCC cell lines, primary OSCC tumors ( n = 3), and normal oral mucosal tissues ( n = 3). The locations of the CpG sites ( CD24 : upstream region from −903 to −770; CD133: exon 1 region from −230 to +90 ; and CD147: upstream region from −552 to −291) relative to the transcription start sites (TSSs) of exon 1 are shown. Each box represents a CpG dinucleotide. The black boxes represent methylated cytosines, and the white boxes represent unmethylated cytosines.

    Techniques Used: Methylation Sequencing, Methylation

    Correlation analysis between gene expression level and promoter methylation level from the TCGA database. ( A , D ) The expression levels of CD133 (PROM1) and CD147 (BSG) in tumor tissues were inversely correlated with the promoter DNA methylation rates. Expression levels of ( A ) CD133 and ( D ) CD147 in primary OSCC tumors ( n = 328) compared to normal oral mucosa ( n = 32), extracted from the TCGA HNSCC database. ( B , E ) The methylation levels of the CpG sites of ( B ) CD133 and ( E ) CD147 in primary OSCC tumors ( n = 338) compared to normal oral mucosa ( n = 34), extracted from the HNSCC TCGA database. ( C , F ) Negative correlation between the gene expression and promoter methylation of ( C , F ). Spearman’s correlation analysis was performed between the methylation (vertical axis) and gene expression (horizontal axis) of the CD133 ( R = −0.20, p = 0.002686) and CD147 genes ( R = −0.17, p = 0.0002601). The Spearman’s correlation coefficients and p -values are shown in each plot.
    Figure Legend Snippet: Correlation analysis between gene expression level and promoter methylation level from the TCGA database. ( A , D ) The expression levels of CD133 (PROM1) and CD147 (BSG) in tumor tissues were inversely correlated with the promoter DNA methylation rates. Expression levels of ( A ) CD133 and ( D ) CD147 in primary OSCC tumors ( n = 328) compared to normal oral mucosa ( n = 32), extracted from the TCGA HNSCC database. ( B , E ) The methylation levels of the CpG sites of ( B ) CD133 and ( E ) CD147 in primary OSCC tumors ( n = 338) compared to normal oral mucosa ( n = 34), extracted from the HNSCC TCGA database. ( C , F ) Negative correlation between the gene expression and promoter methylation of ( C , F ). Spearman’s correlation analysis was performed between the methylation (vertical axis) and gene expression (horizontal axis) of the CD133 ( R = −0.20, p = 0.002686) and CD147 genes ( R = −0.17, p = 0.0002601). The Spearman’s correlation coefficients and p -values are shown in each plot.

    Techniques Used: Expressing, Methylation, DNA Methylation Assay

    Protein expression levels of CD133 and CD147 in primary OSCC tumors and normal oral mucosal tissue samples. The representative immunohistochemical analysis results show ( A ) CD133 and ( B ) CD147 expression in primary OSCC tissues and normal oral mucosal tissues (left images: × 40, scale bar, 50 µm; right images: × 20, scale bar, 100 µm).
    Figure Legend Snippet: Protein expression levels of CD133 and CD147 in primary OSCC tumors and normal oral mucosal tissue samples. The representative immunohistochemical analysis results show ( A ) CD133 and ( B ) CD147 expression in primary OSCC tissues and normal oral mucosal tissues (left images: × 40, scale bar, 50 µm; right images: × 20, scale bar, 100 µm).

    Techniques Used: Expressing, Immunohistochemical staining

    Kaplan-Meier curves showing the effect of CD133 and CD147 DNA methylation on overall survival among patients with OSCC ( n = 338) from the HNSCC TCGA dataset. The overall survival for ( A ) CD133 ( p = 0.018) and ( B ) CD147 ( p = 0.0054), respectively, is shown. A probability of <0.05 was considered to represent a statistically significant difference. ( C ) Combination of CD133 and CD147 gene methylation ( p = 0.025). The clinical information of patients with OSCC ( n = 338) was divided into two groups according to their methylation status (β-values) on CD133 (methylation high (red line), n = 209 and methylation low (blue line), n = 129), CD147 (methylation high (red line), n = 113 and methylation low (blue line), n = 55), and a combination of CD133 and CD147 (methylation high (red line), n = 143 and methylation low (blue line), n = 195).
    Figure Legend Snippet: Kaplan-Meier curves showing the effect of CD133 and CD147 DNA methylation on overall survival among patients with OSCC ( n = 338) from the HNSCC TCGA dataset. The overall survival for ( A ) CD133 ( p = 0.018) and ( B ) CD147 ( p = 0.0054), respectively, is shown. A probability of <0.05 was considered to represent a statistically significant difference. ( C ) Combination of CD133 and CD147 gene methylation ( p = 0.025). The clinical information of patients with OSCC ( n = 338) was divided into two groups according to their methylation status (β-values) on CD133 (methylation high (red line), n = 209 and methylation low (blue line), n = 129), CD147 (methylation high (red line), n = 113 and methylation low (blue line), n = 55), and a combination of CD133 and CD147 (methylation high (red line), n = 143 and methylation low (blue line), n = 195).

    Techniques Used: DNA Methylation Assay, Methylation

    cd147 antibody  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc cd147 antibody
    The proteome profiler with antibodies arrays reveals induction of cytokines in primary human umbilical vein endothelial cells (HUVEC). The cells were treated either with sterile phosphate buffered saline (PBS/saline) alone or SP; or with 10 mg of Poly I:C, or both SP and Poly I:C. The quantitation and comparison of SP induced <t>CD147,</t> IL-6 and IL-8, MIG, and uPAR are shown in comparison with respective controls. Depicted are the fluorescence intensity of different proteins measured, n = 3–5 petri dish/group
    Cd147 Antibody, supplied by Cell Signaling Technology Inc, 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/cd147 antibody/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
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    1) Product Images from "Simulation of COVID-19 symptoms in a genetically engineered mouse model: implications for the long haulers"

    Article Title: Simulation of COVID-19 symptoms in a genetically engineered mouse model: implications for the long haulers

    Journal: Molecular and Cellular Biochemistry

    doi: 10.1007/s11010-022-04487-0

    The proteome profiler with antibodies arrays reveals induction of cytokines in primary human umbilical vein endothelial cells (HUVEC). The cells were treated either with sterile phosphate buffered saline (PBS/saline) alone or SP; or with 10 mg of Poly I:C, or both SP and Poly I:C. The quantitation and comparison of SP induced CD147, IL-6 and IL-8, MIG, and uPAR are shown in comparison with respective controls. Depicted are the fluorescence intensity of different proteins measured, n = 3–5 petri dish/group
    Figure Legend Snippet: The proteome profiler with antibodies arrays reveals induction of cytokines in primary human umbilical vein endothelial cells (HUVEC). The cells were treated either with sterile phosphate buffered saline (PBS/saline) alone or SP; or with 10 mg of Poly I:C, or both SP and Poly I:C. The quantitation and comparison of SP induced CD147, IL-6 and IL-8, MIG, and uPAR are shown in comparison with respective controls. Depicted are the fluorescence intensity of different proteins measured, n = 3–5 petri dish/group

    Techniques Used: Quantitation Assay, Fluorescence

    Western blot analyses of the key target proteins. Supernatants from human primary umbilical vein endothelial cells (HUVEC) at 6- and 24-h post treatment using the control (CTL), SP (spike protein), SP-Poly (spike protein and poly I:C), and Poly (poly I:C). The primary antibodies used were Interleukin-6 (IL-6), CD147 (EMPERIN), and uPAR and protein bands were normalized with GAPDH. The expression levels of each protein were also quantified as shown by the bar charts, n = 3–5 petri dish/group, ns not significant, * p < 0.01, **** p < 0.0001. Similarly, supernatants from human primary coronary artery endothelial cells (HCAEC) at 6- and 24-h post treatment were performed using the control (CTL), SP (spike protein), SP-Poly (spike protein and poly I:C), and Poly (poly I:C). The primary antibodies used were Interleukin-6 (IL-6), CD147 (EMPERIN), and uPAR, and the protein bands were normalized with GAPDH. The expression levels of each protein were also quantified as shown by the bar charts. n = 3–5 petri dish/group, ns not significant, * p < 0.01, **** p < 0.0001
    Figure Legend Snippet: Western blot analyses of the key target proteins. Supernatants from human primary umbilical vein endothelial cells (HUVEC) at 6- and 24-h post treatment using the control (CTL), SP (spike protein), SP-Poly (spike protein and poly I:C), and Poly (poly I:C). The primary antibodies used were Interleukin-6 (IL-6), CD147 (EMPERIN), and uPAR and protein bands were normalized with GAPDH. The expression levels of each protein were also quantified as shown by the bar charts, n = 3–5 petri dish/group, ns not significant, * p < 0.01, **** p < 0.0001. Similarly, supernatants from human primary coronary artery endothelial cells (HCAEC) at 6- and 24-h post treatment were performed using the control (CTL), SP (spike protein), SP-Poly (spike protein and poly I:C), and Poly (poly I:C). The primary antibodies used were Interleukin-6 (IL-6), CD147 (EMPERIN), and uPAR, and the protein bands were normalized with GAPDH. The expression levels of each protein were also quantified as shown by the bar charts. n = 3–5 petri dish/group, ns not significant, * p < 0.01, **** p < 0.0001

    Techniques Used: Western Blot, Expressing

    Schematics of plausible hypothesis regarding SARS-CoV-2 induced visceral organ damage. The binding of SARS-CoV-2 spike protein (SP) with ACE-2 receptor mimics SARS-CoV-2 infection, and causes the accumulation of Ang1-8, activation of inflammasome, and M1Q macrophages via the “TLR4/NLRP3/CD147/Nox4/iNOS/neopterin” axis in the heart. This cascade of events leads to endothelial blood-heart barrier (BHB) leakage; however, the iNOSKO/Nox4KO and iNOS antagonists may help mitigate the inflammasome/NLRP3/M1Q mediated endothelial BHB leakage ( A ), as reported earlier by Tyagi and Singh, Multi-organ damage by COVID-19: Congestive (cardio-pulmonary) heart failure, and blood-heart barrier leakage, Mol Cell Biochem. 2021;476 (4):1891–1895). Similarly, biding of the SARS-CoV-2 spike protein (SP) to ACE-2/CD147 on macrophages can cause M1Q activation by IFN-γ toward generating the neopterin, and thus stimulating the iNOS, Nox4, and NLRP3 inflammasome pathway in the kidney that in turn can trigger apoptosis which may lead to CD4+ and CD8+ cell lymphopenia. These alterations might inflict the proximal tubular epithelial cell/podocyte damage, and the resultant parenchymal leakage. In that case, the iNOSKO/Nox4KO, and Fas/FasL antagonists (Kp7-6)/IFN-λ treatment could help mitigate the cytokine storm, and T cell lymphopenia thus protecting the proximal tubular epithelial/podocyte function ( B ). M1; inflammatory macrophage (M1Q), iNOS; inducible of nitric oxide synthase, BH4; tetrahydrobiopterin, FH4; tetrahydrofolate
    Figure Legend Snippet: Schematics of plausible hypothesis regarding SARS-CoV-2 induced visceral organ damage. The binding of SARS-CoV-2 spike protein (SP) with ACE-2 receptor mimics SARS-CoV-2 infection, and causes the accumulation of Ang1-8, activation of inflammasome, and M1Q macrophages via the “TLR4/NLRP3/CD147/Nox4/iNOS/neopterin” axis in the heart. This cascade of events leads to endothelial blood-heart barrier (BHB) leakage; however, the iNOSKO/Nox4KO and iNOS antagonists may help mitigate the inflammasome/NLRP3/M1Q mediated endothelial BHB leakage ( A ), as reported earlier by Tyagi and Singh, Multi-organ damage by COVID-19: Congestive (cardio-pulmonary) heart failure, and blood-heart barrier leakage, Mol Cell Biochem. 2021;476 (4):1891–1895). Similarly, biding of the SARS-CoV-2 spike protein (SP) to ACE-2/CD147 on macrophages can cause M1Q activation by IFN-γ toward generating the neopterin, and thus stimulating the iNOS, Nox4, and NLRP3 inflammasome pathway in the kidney that in turn can trigger apoptosis which may lead to CD4+ and CD8+ cell lymphopenia. These alterations might inflict the proximal tubular epithelial cell/podocyte damage, and the resultant parenchymal leakage. In that case, the iNOSKO/Nox4KO, and Fas/FasL antagonists (Kp7-6)/IFN-λ treatment could help mitigate the cytokine storm, and T cell lymphopenia thus protecting the proximal tubular epithelial/podocyte function ( B ). M1; inflammatory macrophage (M1Q), iNOS; inducible of nitric oxide synthase, BH4; tetrahydrobiopterin, FH4; tetrahydrofolate

    Techniques Used: Binding Assay, Infection, Activation Assay

    cd147  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc cd147
    Cd147, supplied by Cell Signaling Technology 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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    anti cd147  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti cd147
    Anti Cd147, supplied by Cell Signaling Technology 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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    rabbit anti cd147 antibody  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti cd147 antibody
    Oligonucleotide sequence of polymerase chain reaction (PCR) primers.
    Rabbit Anti Cd147 Antibody, supplied by Cell Signaling Technology Inc, 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/rabbit anti cd147 antibody/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
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    rabbit anti cd147 antibody - by Bioz Stars, 2023-03
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    1) Product Images from "Psychological Stress Up-Regulates CD147 Expression Through Beta-Arrestin1/ERK to Promote Proliferation and Invasiveness of Glioma Cells"

    Article Title: Psychological Stress Up-Regulates CD147 Expression Through Beta-Arrestin1/ERK to Promote Proliferation and Invasiveness of Glioma Cells

    Journal: Frontiers in Oncology

    doi: 10.3389/fonc.2020.571181

    Oligonucleotide sequence of polymerase chain reaction (PCR) primers.
    Figure Legend Snippet: Oligonucleotide sequence of polymerase chain reaction (PCR) primers.

    Techniques Used: Sequencing, Polymerase Chain Reaction

    CD147 Silencing Inhibited the Proliferation of Xenograft Tumors Induced by Chronic Psychological Stress in Nude Mice. (A) The growth of transplanted tumors in nude mice (n=5). (B) epinephrine (EPI) and norepinephrine (NE) concentrations in the serum of nude mice with transplanted tumors were detected by ELISA, and the stress hormone levels were not affected after CD147 silencing. (C) Determination of lactic acid in the tumor tissues of nude mice. The expression of CD147, MMP-2, and MMP-9 in tumor tissues of nude mice were detected by western blotting. (D) Evaluated by Western blots and (E) Quantified. (left to right). CD147, MMP-2, and MMP-9 expression levels were increased in nude mice with glioma and psychological stress treatment. Data are expressed as the mean ± sd. *P < 0.05. **P < 0.01 vs Con. # P < 0.05. ## P < 0.01 vs Stress.
    Figure Legend Snippet: CD147 Silencing Inhibited the Proliferation of Xenograft Tumors Induced by Chronic Psychological Stress in Nude Mice. (A) The growth of transplanted tumors in nude mice (n=5). (B) epinephrine (EPI) and norepinephrine (NE) concentrations in the serum of nude mice with transplanted tumors were detected by ELISA, and the stress hormone levels were not affected after CD147 silencing. (C) Determination of lactic acid in the tumor tissues of nude mice. The expression of CD147, MMP-2, and MMP-9 in tumor tissues of nude mice were detected by western blotting. (D) Evaluated by Western blots and (E) Quantified. (left to right). CD147, MMP-2, and MMP-9 expression levels were increased in nude mice with glioma and psychological stress treatment. Data are expressed as the mean ± sd. *P < 0.05. **P < 0.01 vs Con. # P < 0.05. ## P < 0.01 vs Stress.

    Techniques Used: Enzyme-linked Immunosorbent Assay, Expressing, Western Blot

    CD147 Knockdown Reduced the Expression and Secretion of MMP-2 and MMP-9 Induced by norepinephrine (NE) in glioma Cells. (A) Detect the relative expression of CD147 in human glioma cell lines including HEB, U251, LN229, U87, and SHG44 by PCR. (B) Two glioma cells were incubated with different concentrations of NE for 1, 2, 3, 4, and 5 day. CCK-8 assay demonstrated that NE promoted the proliferation of glioma cells in a concentration-dependent and time-dependent manner. (C) NE increased expression of CD147 in a concentration-dependent manner. (D) The expression of CD147, MMP-2, and MMP-9 proteins was detected by western blotting. NE promoted the expression of CD147, MMP-2, and MMP-9. (E, F) qPCR confirmed that NE promoted the expression of MMP-2 and MMP-9, which were inhibited by CD147 knockdown. (G, H) Western blotting analysis showed that the expression of MMP-2 and MMP-9 protein in LN229 cells and U87 cells were decreased after transfection with shRNA-CD147. (I, J) Gelatinase assay showed that NE promoted matrix metalloproteinases (MMPs) secretion in two glioma cells, which was inhibited by CD147 knockdown. shRNA-Con was the negative control; data are expressed as the mean ± SD. *P < 0.05. **P < 0.01 vs Con (0 μmol/L NE). # P < 0.05. ## P < 0.01 vs 10 μmol/L NE.
    Figure Legend Snippet: CD147 Knockdown Reduced the Expression and Secretion of MMP-2 and MMP-9 Induced by norepinephrine (NE) in glioma Cells. (A) Detect the relative expression of CD147 in human glioma cell lines including HEB, U251, LN229, U87, and SHG44 by PCR. (B) Two glioma cells were incubated with different concentrations of NE for 1, 2, 3, 4, and 5 day. CCK-8 assay demonstrated that NE promoted the proliferation of glioma cells in a concentration-dependent and time-dependent manner. (C) NE increased expression of CD147 in a concentration-dependent manner. (D) The expression of CD147, MMP-2, and MMP-9 proteins was detected by western blotting. NE promoted the expression of CD147, MMP-2, and MMP-9. (E, F) qPCR confirmed that NE promoted the expression of MMP-2 and MMP-9, which were inhibited by CD147 knockdown. (G, H) Western blotting analysis showed that the expression of MMP-2 and MMP-9 protein in LN229 cells and U87 cells were decreased after transfection with shRNA-CD147. (I, J) Gelatinase assay showed that NE promoted matrix metalloproteinases (MMPs) secretion in two glioma cells, which was inhibited by CD147 knockdown. shRNA-Con was the negative control; data are expressed as the mean ± SD. *P < 0.05. **P < 0.01 vs Con (0 μmol/L NE). # P < 0.05. ## P < 0.01 vs 10 μmol/L NE.

    Techniques Used: Expressing, Incubation, CCK-8 Assay, Concentration Assay, Western Blot, Transfection, shRNA, Negative Control

    CD147 Knockout Inhibited the Proliferation, Invasiveness, and Migration of LN229 and U87 Cells. (A) Migration ability of LN229 and U87 cells were detected by scratch assay. (B) Representative images of the invasion ability of and U87 cells [control group, norepinephrine (NE) group, shRNACD147 group, shRNA CD147 + NE group and shRNA Con] in the Matrigel invasion assays ( × 200). Quantification of invaded cells showed that interference with CD147 expression significantly inhibited the invasion of Matrigel in NE -induced LN229 and U87 cells. (C) Colony formation assay. Interference with CD147 expression significantly inhibited the formation of LN229 and U87 cell clones induced by NE (10 μmol/L). (D) CCK-8 assay (at 0, 24, 48, 72, and 96 h) in two glioma cells induced by NE(10μmol/L). CD147-interference significantly inhibited the proliferation of two glioma cells induced by NE. (E) Detection of CD147 silencing effect by Western blot and quantified. Data are expressed as the mean ± sd. *P < 0.05. **P < 0.01 vs Con (0 μmol/L NE); # P < 0.05. ## P < 0.01 vs 10 μmol/L NE.
    Figure Legend Snippet: CD147 Knockout Inhibited the Proliferation, Invasiveness, and Migration of LN229 and U87 Cells. (A) Migration ability of LN229 and U87 cells were detected by scratch assay. (B) Representative images of the invasion ability of and U87 cells [control group, norepinephrine (NE) group, shRNACD147 group, shRNA CD147 + NE group and shRNA Con] in the Matrigel invasion assays ( × 200). Quantification of invaded cells showed that interference with CD147 expression significantly inhibited the invasion of Matrigel in NE -induced LN229 and U87 cells. (C) Colony formation assay. Interference with CD147 expression significantly inhibited the formation of LN229 and U87 cell clones induced by NE (10 μmol/L). (D) CCK-8 assay (at 0, 24, 48, 72, and 96 h) in two glioma cells induced by NE(10μmol/L). CD147-interference significantly inhibited the proliferation of two glioma cells induced by NE. (E) Detection of CD147 silencing effect by Western blot and quantified. Data are expressed as the mean ± sd. *P < 0.05. **P < 0.01 vs Con (0 μmol/L NE); # P < 0.05. ## P < 0.01 vs 10 μmol/L NE.

    Techniques Used: Knock-Out, Migration, Wound Healing Assay, shRNA, Expressing, Colony Assay, Clone Assay, CCK-8 Assay, Western Blot

    The β-adrenergic Receptors/β-arrestin1/ERK Signaling Pathway Regulated CD147 Expression. (A) Propranolol and U0126 reduced tumor size in vivo . (B) U0126 and Propranolol blocked the expression of CD147 induced by stress. (C) U0126 and Propranolol blocked norepinephrine (NE)-induced CD147 expression. (D) ERK1/2 signaling regulated CD147 expression in LN229 and (E) U87 cells downstream of β-AR. Cells were treated with NE (10 μmol/L) for 16 h. The effect of U0126 (10 μmol/L) on NE-induced CD147 expression was monitored by western blotting and quantified. (F) The production of lactic acid in extracellular and intracellular compartments of glioma cells under the effect of NE. The ERK1/2 inhibitor U0126 (10 μmol/L) inhibited NE-induced lactate release in LN229 cells (G) and U87 cells (H) , which was also inhibited by propranolol, shRNACD147, and si-β-arrestin1. Data are expressed as the mean ± SD. *P < 0.05. **P < 0.01 vs NE (0 μmol/L); # P < 0.05. ## P < 0.01 vs NE (10 μmol/L) or stress.
    Figure Legend Snippet: The β-adrenergic Receptors/β-arrestin1/ERK Signaling Pathway Regulated CD147 Expression. (A) Propranolol and U0126 reduced tumor size in vivo . (B) U0126 and Propranolol blocked the expression of CD147 induced by stress. (C) U0126 and Propranolol blocked norepinephrine (NE)-induced CD147 expression. (D) ERK1/2 signaling regulated CD147 expression in LN229 and (E) U87 cells downstream of β-AR. Cells were treated with NE (10 μmol/L) for 16 h. The effect of U0126 (10 μmol/L) on NE-induced CD147 expression was monitored by western blotting and quantified. (F) The production of lactic acid in extracellular and intracellular compartments of glioma cells under the effect of NE. The ERK1/2 inhibitor U0126 (10 μmol/L) inhibited NE-induced lactate release in LN229 cells (G) and U87 cells (H) , which was also inhibited by propranolol, shRNACD147, and si-β-arrestin1. Data are expressed as the mean ± SD. *P < 0.05. **P < 0.01 vs NE (0 μmol/L); # P < 0.05. ## P < 0.01 vs NE (10 μmol/L) or stress.

    Techniques Used: Expressing, In Vivo, Western Blot

    The Transcription Factor Sp1 Mediated the norepinephrine (NE)-Induced High Expression of CD147. (A) Schematic diagram of luciferase assay for different lengths of CD147 promoter activity, *P<0.05, **p<0.01 compared with the empty PGL4.16 vector. (B) Luciferase activity of different truncated human CD147 promoters after stimulation with 10 μmol/L NE. (C) Schematic diagram of the mutation in the node of Sp1 in the CD147 promoter. (D) Detection of 10 μmol/L NE-induced luciferase activity of CD147-P, CD147-M1, CD147-M2, CD147-M3, and CD147-M4 co-transfected with Sp1. (E) The effect of the β-adrenergic receptor inhibitor propranolol (10 μmol/L), the PKA inhibitor H89 (10 μmol/L), the ERK inhibitor U0126 (10 μmol/L), si-β-arrestin1, and si-β-arrestin2 on Sp1- mediated CD147-P (-245/+51) luciferase activity. Luciferase activity was normalized to that of renilla luciferase, *P < 0.05, **P < 0.01, compared with 0μmol/L NE; # P < 0.05, ## P < 0.01 compared with Sp1-CD147-P (-245/+51)+10 μmol/L NE.
    Figure Legend Snippet: The Transcription Factor Sp1 Mediated the norepinephrine (NE)-Induced High Expression of CD147. (A) Schematic diagram of luciferase assay for different lengths of CD147 promoter activity, *P<0.05, **p<0.01 compared with the empty PGL4.16 vector. (B) Luciferase activity of different truncated human CD147 promoters after stimulation with 10 μmol/L NE. (C) Schematic diagram of the mutation in the node of Sp1 in the CD147 promoter. (D) Detection of 10 μmol/L NE-induced luciferase activity of CD147-P, CD147-M1, CD147-M2, CD147-M3, and CD147-M4 co-transfected with Sp1. (E) The effect of the β-adrenergic receptor inhibitor propranolol (10 μmol/L), the PKA inhibitor H89 (10 μmol/L), the ERK inhibitor U0126 (10 μmol/L), si-β-arrestin1, and si-β-arrestin2 on Sp1- mediated CD147-P (-245/+51) luciferase activity. Luciferase activity was normalized to that of renilla luciferase, *P < 0.05, **P < 0.01, compared with 0μmol/L NE; # P < 0.05, ## P < 0.01 compared with Sp1-CD147-P (-245/+51)+10 μmol/L NE.

    Techniques Used: Expressing, Luciferase, Activity Assay, Plasmid Preparation, Mutagenesis, Transfection

    Norepinephrine (NE) Regulated CD147 Expression by Activating the β-AR/β-Arrestin1/ERK/Sp1 Pathway. (A) Expression of CD147 and Sp1 protein and statistical analysis (B) and mRNA in LN229 and U87 cells after transfection with Sp1 siRNA. (C) Effects of U0126, si-β-arrestin1 or Propranolol on NE-induced Sp1 expression in LN229 and U87 cells. (D) Schematic diagram of how NE regulates the expression of CD147 through the β- adrenergic receptor-β-arrestin1-ERK-Sp1 pathway. *P < 0.05, **P < 0.01, compared with 0 μmol/L NE; # P < 0.05, ## P < 0.01 compared with 10 μmol/L NE.
    Figure Legend Snippet: Norepinephrine (NE) Regulated CD147 Expression by Activating the β-AR/β-Arrestin1/ERK/Sp1 Pathway. (A) Expression of CD147 and Sp1 protein and statistical analysis (B) and mRNA in LN229 and U87 cells after transfection with Sp1 siRNA. (C) Effects of U0126, si-β-arrestin1 or Propranolol on NE-induced Sp1 expression in LN229 and U87 cells. (D) Schematic diagram of how NE regulates the expression of CD147 through the β- adrenergic receptor-β-arrestin1-ERK-Sp1 pathway. *P < 0.05, **P < 0.01, compared with 0 μmol/L NE; # P < 0.05, ## P < 0.01 compared with 10 μmol/L NE.

    Techniques Used: Expressing, Transfection

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    Cell Signaling Technology Inc cd147 antibody
    Expressions of CyPA and <t>CD147</t> are associated with glioma grade, histological type, and prognosis. The expression of CyPA (a) and CD147 (b) in GBM and LGG compared with normal tissue and correlation with prognosis in TCGA and CGGA databases. The expression of CyPA (c) and CD147 (d) in different WHO grades and histological types of glioma in TCGA and CGGA database. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗∗ P < 0.0001, ns stands for no significance.
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    Expression levels of key gastric cancer stem cell (GCSC) markers, CypA, and <t>CD147</t> in MKN45 adherent and tumorsphere cells. Protein levels were detected via Western blot analysis using specific antibodies and were further quantified using densitometry. β-actin levels were used as an internal control. The ratio of each target protein to β-actin for adherent cells was normalized to onefold. * p < 0.05 vs. the adherent cells.
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    Cell Signaling Technology Inc anti cd147
    <t>CD147</t> is highly expressed in glioma tissues and associated with tumor malignancy (A-B) Silico analysis of glioma tissues of the multidimensional data set from The Cancer Genome Atlas (TCGA) PROTEINATLAS data set. CD147 protein expression and copy numbers were determined in various types of tumor sections respectively. (C-D) Immunohistochemistry staining of CD147 in human normal and glioma tissues with different grade (C) and the statistical analysis (D). (E) The methylation status of the CD147 promoter was analyzed by methylation-specific PCR in each of the 20 normal and glioma tissues. The white and black colors represent hypomethylation and hypermethylation, respectively. (F) The correlation between the TCGA expression and methylation data for CD147 in glioma tissues. (G-H) Clinical outcomes for the gene expression patterns given at the top of each panel by UALCAN analysis.
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    Cell Signaling Technology Inc rabbit anti cd147 antibody
    Oligonucleotide sequence of polymerase chain reaction (PCR) primers.
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    Expressions of CyPA and CD147 are associated with glioma grade, histological type, and prognosis. The expression of CyPA (a) and CD147 (b) in GBM and LGG compared with normal tissue and correlation with prognosis in TCGA and CGGA databases. The expression of CyPA (c) and CD147 (d) in different WHO grades and histological types of glioma in TCGA and CGGA database. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗∗ P < 0.0001, ns stands for no significance.

    Journal: BioMed Research International

    Article Title: Downregulation of CyclophilinA/CD147 Axis Induces Cell Apoptosis and Inhibits Glioma Aggressiveness

    doi: 10.1155/2020/7035847

    Figure Lengend Snippet: Expressions of CyPA and CD147 are associated with glioma grade, histological type, and prognosis. The expression of CyPA (a) and CD147 (b) in GBM and LGG compared with normal tissue and correlation with prognosis in TCGA and CGGA databases. The expression of CyPA (c) and CD147 (d) in different WHO grades and histological types of glioma in TCGA and CGGA database. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗∗ P < 0.0001, ns stands for no significance.

    Article Snippet: After the blockade of nonspecific binding, tissue sections were incubated with the Cyclophilin A antibody (cat. no. 5360s; 1 : 150 dilution; Santa Cruz Biotechnology, Inc.) and CD147 antibody (cat. no. 13287; 1 : 400 dilution; Cell Signaling Technology, Inc.) for overnight at 4 centigrade.

    Techniques: Expressing

    Expression and knockdown of CyPA and CD147 in glioma cell lines. The expressions of CyPA (a) and CD147 (b) in glioma cell lines are detected by RT-qPCR and western blot.(c) Specific si-RNA could inhibit CyPA and CD147 expression in U251 cell line. ∗ P < 0.05, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001.

    Journal: BioMed Research International

    Article Title: Downregulation of CyclophilinA/CD147 Axis Induces Cell Apoptosis and Inhibits Glioma Aggressiveness

    doi: 10.1155/2020/7035847

    Figure Lengend Snippet: Expression and knockdown of CyPA and CD147 in glioma cell lines. The expressions of CyPA (a) and CD147 (b) in glioma cell lines are detected by RT-qPCR and western blot.(c) Specific si-RNA could inhibit CyPA and CD147 expression in U251 cell line. ∗ P < 0.05, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001.

    Article Snippet: After the blockade of nonspecific binding, tissue sections were incubated with the Cyclophilin A antibody (cat. no. 5360s; 1 : 150 dilution; Santa Cruz Biotechnology, Inc.) and CD147 antibody (cat. no. 13287; 1 : 400 dilution; Cell Signaling Technology, Inc.) for overnight at 4 centigrade.

    Techniques: Expressing, Quantitative RT-PCR, Western Blot

    Knockdown of CyPA and CD147 reduces glioma proliferation. (a). EdU assay shows that inhibition of CyPA and CD147 significantly decreases glioma cell proliferation. U251 wild type cell is taken as the control group. (b). Flow cytometry analysis reveals the effect of CyPA and CD147 inhibition on glioma cell proliferation.

    Journal: BioMed Research International

    Article Title: Downregulation of CyclophilinA/CD147 Axis Induces Cell Apoptosis and Inhibits Glioma Aggressiveness

    doi: 10.1155/2020/7035847

    Figure Lengend Snippet: Knockdown of CyPA and CD147 reduces glioma proliferation. (a). EdU assay shows that inhibition of CyPA and CD147 significantly decreases glioma cell proliferation. U251 wild type cell is taken as the control group. (b). Flow cytometry analysis reveals the effect of CyPA and CD147 inhibition on glioma cell proliferation.

    Article Snippet: After the blockade of nonspecific binding, tissue sections were incubated with the Cyclophilin A antibody (cat. no. 5360s; 1 : 150 dilution; Santa Cruz Biotechnology, Inc.) and CD147 antibody (cat. no. 13287; 1 : 400 dilution; Cell Signaling Technology, Inc.) for overnight at 4 centigrade.

    Techniques: EdU Assay, Inhibition, Flow Cytometry

    Predictive value of CyPA and CD147 in different grades of glioma. CyPA and CD147 expression pattern in different grades of glioma in TCGA database (a) and CGGA database (b) analyzed by ROC curve analysis.

    Journal: BioMed Research International

    Article Title: Downregulation of CyclophilinA/CD147 Axis Induces Cell Apoptosis and Inhibits Glioma Aggressiveness

    doi: 10.1155/2020/7035847

    Figure Lengend Snippet: Predictive value of CyPA and CD147 in different grades of glioma. CyPA and CD147 expression pattern in different grades of glioma in TCGA database (a) and CGGA database (b) analyzed by ROC curve analysis.

    Article Snippet: After the blockade of nonspecific binding, tissue sections were incubated with the Cyclophilin A antibody (cat. no. 5360s; 1 : 150 dilution; Santa Cruz Biotechnology, Inc.) and CD147 antibody (cat. no. 13287; 1 : 400 dilution; Cell Signaling Technology, Inc.) for overnight at 4 centigrade.

    Techniques: Expressing

    Expression levels of key gastric cancer stem cell (GCSC) markers, CypA, and CD147 in MKN45 adherent and tumorsphere cells. Protein levels were detected via Western blot analysis using specific antibodies and were further quantified using densitometry. β-actin levels were used as an internal control. The ratio of each target protein to β-actin for adherent cells was normalized to onefold. * p < 0.05 vs. the adherent cells.

    Journal: International Journal of Molecular Sciences

    Article Title: Cyclophilin A Inhibitors Suppress Proliferation and Induce Apoptosis of MKN45 Gastric Cancer Stem-like Cells by Regulating CypA/CD147-Mediated Signaling Pathway

    doi: 10.3390/ijms24054734

    Figure Lengend Snippet: Expression levels of key gastric cancer stem cell (GCSC) markers, CypA, and CD147 in MKN45 adherent and tumorsphere cells. Protein levels were detected via Western blot analysis using specific antibodies and were further quantified using densitometry. β-actin levels were used as an internal control. The ratio of each target protein to β-actin for adherent cells was normalized to onefold. * p < 0.05 vs. the adherent cells.

    Article Snippet: Antibodies against CypA (#2175), CD147 (#13287), CD44 (#37259), CD133 (#64326), integrin α6 (#3750), Sox2 (#3579), Nanog (#3580), Oct4 (#2750), ALDH1A1 (#12035), p53 (#2524), p21 Waf1/Cip1 (#2947), cleaved caspase-9 (#9501), cleaved caspase-3 (#9661), cleaved PARP (#9542), phospho-AKT (#4060), AKT (#9272), phospho-ERK1/2 (#9101), ERK1/2 (#9102), phospho-p38 (#4511), p38 (#8690), rabbit IgG (#7074), and mouse IgG (#7076) were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Expressing, Western Blot

    Effects of C9 and CsA on the CypA/CD147-mediated signaling pathways in MKN45 GCSCs. ( A , B ) MKN45-derived GCSCs were treated with the indicated concentrations of each compound for 72 h. Protein levels were detected via Western blot analysis using specific antibodies and were further quantified using densitometry. β-actin levels were used as an internal control. The ratio of each target protein to β-actin for untreated control was normalized to onefold. * p < 0.05 vs. the control.

    Journal: International Journal of Molecular Sciences

    Article Title: Cyclophilin A Inhibitors Suppress Proliferation and Induce Apoptosis of MKN45 Gastric Cancer Stem-like Cells by Regulating CypA/CD147-Mediated Signaling Pathway

    doi: 10.3390/ijms24054734

    Figure Lengend Snippet: Effects of C9 and CsA on the CypA/CD147-mediated signaling pathways in MKN45 GCSCs. ( A , B ) MKN45-derived GCSCs were treated with the indicated concentrations of each compound for 72 h. Protein levels were detected via Western blot analysis using specific antibodies and were further quantified using densitometry. β-actin levels were used as an internal control. The ratio of each target protein to β-actin for untreated control was normalized to onefold. * p < 0.05 vs. the control.

    Article Snippet: Antibodies against CypA (#2175), CD147 (#13287), CD44 (#37259), CD133 (#64326), integrin α6 (#3750), Sox2 (#3579), Nanog (#3580), Oct4 (#2750), ALDH1A1 (#12035), p53 (#2524), p21 Waf1/Cip1 (#2947), cleaved caspase-9 (#9501), cleaved caspase-3 (#9661), cleaved PARP (#9542), phospho-AKT (#4060), AKT (#9272), phospho-ERK1/2 (#9101), ERK1/2 (#9102), phospho-p38 (#4511), p38 (#8690), rabbit IgG (#7074), and mouse IgG (#7076) were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Derivative Assay, Western Blot

    CD147 is highly expressed in glioma tissues and associated with tumor malignancy (A-B) Silico analysis of glioma tissues of the multidimensional data set from The Cancer Genome Atlas (TCGA) PROTEINATLAS data set. CD147 protein expression and copy numbers were determined in various types of tumor sections respectively. (C-D) Immunohistochemistry staining of CD147 in human normal and glioma tissues with different grade (C) and the statistical analysis (D). (E) The methylation status of the CD147 promoter was analyzed by methylation-specific PCR in each of the 20 normal and glioma tissues. The white and black colors represent hypomethylation and hypermethylation, respectively. (F) The correlation between the TCGA expression and methylation data for CD147 in glioma tissues. (G-H) Clinical outcomes for the gene expression patterns given at the top of each panel by UALCAN analysis.

    Journal: International Journal of Biological Sciences

    Article Title: CD147 confers temozolomide resistance of glioma cells via the regulation of β-TrCP/Nrf2 pathway

    doi: 10.7150/ijbs.60894

    Figure Lengend Snippet: CD147 is highly expressed in glioma tissues and associated with tumor malignancy (A-B) Silico analysis of glioma tissues of the multidimensional data set from The Cancer Genome Atlas (TCGA) PROTEINATLAS data set. CD147 protein expression and copy numbers were determined in various types of tumor sections respectively. (C-D) Immunohistochemistry staining of CD147 in human normal and glioma tissues with different grade (C) and the statistical analysis (D). (E) The methylation status of the CD147 promoter was analyzed by methylation-specific PCR in each of the 20 normal and glioma tissues. The white and black colors represent hypomethylation and hypermethylation, respectively. (F) The correlation between the TCGA expression and methylation data for CD147 in glioma tissues. (G-H) Clinical outcomes for the gene expression patterns given at the top of each panel by UALCAN analysis.

    Article Snippet: Primary antibodies were used at dilutions of 1:1000 for anti-CD147 (ab108308, Abcam), anti-Nrf2 (ab180845, Abcam), anti-NQO-1 (ab28947, Abcam), anti-HO-1 (ab13248, Abcam), anti-GCLC-1 (ab190685, Abcam), anti-β-TrCP (#4394, Cell signaling Technology), anti-Phospho-GSK-3-beta (Ser9) (#9322, Cell Signaling Technology), anti-GSK-3-beta (#12456, Cell Signaling Technology), anti-Phospho-Akt (Ser473) (#4051, Cell Signaling Technology), anti-Akt (#9272, Cell Signaling Technology), and anti-β-actin (#A5441, Sigma) antibody, anti-Lamin B(#13435, Cell Signaling Technology), respectively.

    Techniques: Expressing, Immunohistochemistry, Staining, Methylation

    CD147 contributes to the resistance to TMZ treatment via the elimination of intracellular ROS (A-F) We reduced CD147 levels in U251 and T98G cells using lentivirus expressing CD147 shRNA, and then treated with 50 μM TMZ as indicated. (A) Identification of CD147 protein levels. (B-D) Cell viabilities were determined by Edu incorporation (B) and CCK8 assay (C-D) in indicated cells. (E) TUNEL staining was performed to determine cell apoptosis. (F) Relative ROS production was determined by Flow cytometry. (G-K) CD147 was overexpressed in U251 and T98G cells with CD147 overexpressing lentivirus, and then treated with TMZ as indicated. (G) Identification of CD147 protein levels. (H-K) cell viabilities (H-I), apoptosis (J) and ROS production (K) were determined, respectively.

    Journal: International Journal of Biological Sciences

    Article Title: CD147 confers temozolomide resistance of glioma cells via the regulation of β-TrCP/Nrf2 pathway

    doi: 10.7150/ijbs.60894

    Figure Lengend Snippet: CD147 contributes to the resistance to TMZ treatment via the elimination of intracellular ROS (A-F) We reduced CD147 levels in U251 and T98G cells using lentivirus expressing CD147 shRNA, and then treated with 50 μM TMZ as indicated. (A) Identification of CD147 protein levels. (B-D) Cell viabilities were determined by Edu incorporation (B) and CCK8 assay (C-D) in indicated cells. (E) TUNEL staining was performed to determine cell apoptosis. (F) Relative ROS production was determined by Flow cytometry. (G-K) CD147 was overexpressed in U251 and T98G cells with CD147 overexpressing lentivirus, and then treated with TMZ as indicated. (G) Identification of CD147 protein levels. (H-K) cell viabilities (H-I), apoptosis (J) and ROS production (K) were determined, respectively.

    Article Snippet: Primary antibodies were used at dilutions of 1:1000 for anti-CD147 (ab108308, Abcam), anti-Nrf2 (ab180845, Abcam), anti-NQO-1 (ab28947, Abcam), anti-HO-1 (ab13248, Abcam), anti-GCLC-1 (ab190685, Abcam), anti-β-TrCP (#4394, Cell signaling Technology), anti-Phospho-GSK-3-beta (Ser9) (#9322, Cell Signaling Technology), anti-GSK-3-beta (#12456, Cell Signaling Technology), anti-Phospho-Akt (Ser473) (#4051, Cell Signaling Technology), anti-Akt (#9272, Cell Signaling Technology), and anti-β-actin (#A5441, Sigma) antibody, anti-Lamin B(#13435, Cell Signaling Technology), respectively.

    Techniques: Expressing, shRNA, CCK-8 Assay, TUNEL Assay, Staining, Flow Cytometry

    CD147 promotes Nrf2 expression through blocking its protein degradation (A) Nrf2 protein levels were determined in U251 or T98G cells after CD147 knockdown. (B) The indicated protein levels were determined in cells with or without CD147 knockdown. (C-E) NQO-1 (C), HO-1(D) and GCLC-1 (E) mRNA levels were determined by qCPR respectively. (F-G) Luciferase reporter gene assay was performed to determine CD147 knockdown could suppress the ARE activity. (H-I) Nrf2 protein stability were determined by western blotting in cells treated with CHX (10 μg/ml) for indicated time or MG-132 (10 μM) for 4 h, respectively.

    Journal: International Journal of Biological Sciences

    Article Title: CD147 confers temozolomide resistance of glioma cells via the regulation of β-TrCP/Nrf2 pathway

    doi: 10.7150/ijbs.60894

    Figure Lengend Snippet: CD147 promotes Nrf2 expression through blocking its protein degradation (A) Nrf2 protein levels were determined in U251 or T98G cells after CD147 knockdown. (B) The indicated protein levels were determined in cells with or without CD147 knockdown. (C-E) NQO-1 (C), HO-1(D) and GCLC-1 (E) mRNA levels were determined by qCPR respectively. (F-G) Luciferase reporter gene assay was performed to determine CD147 knockdown could suppress the ARE activity. (H-I) Nrf2 protein stability were determined by western blotting in cells treated with CHX (10 μg/ml) for indicated time or MG-132 (10 μM) for 4 h, respectively.

    Article Snippet: Primary antibodies were used at dilutions of 1:1000 for anti-CD147 (ab108308, Abcam), anti-Nrf2 (ab180845, Abcam), anti-NQO-1 (ab28947, Abcam), anti-HO-1 (ab13248, Abcam), anti-GCLC-1 (ab190685, Abcam), anti-β-TrCP (#4394, Cell signaling Technology), anti-Phospho-GSK-3-beta (Ser9) (#9322, Cell Signaling Technology), anti-GSK-3-beta (#12456, Cell Signaling Technology), anti-Phospho-Akt (Ser473) (#4051, Cell Signaling Technology), anti-Akt (#9272, Cell Signaling Technology), and anti-β-actin (#A5441, Sigma) antibody, anti-Lamin B(#13435, Cell Signaling Technology), respectively.

    Techniques: Expressing, Blocking Assay, Luciferase, Reporter Gene Assay, Activity Assay, Western Blot

    CD147 dictates Nrf2 stability through the suppression of GSK3β/β-TrCP dependent protein degradation (A-B) The indicated proteins were determined in U251 cells with CD147 knockdown (A) or overexpression (B). (C) Nrf2 and GSK3β protein levels were determined in U251 cells following Capivasertib (10nM) treatment. (D-E) Immunoprecipitation was performed to determine the interaction between β-TrCP and Nrf2 in indicated U251 cells. After the β-TrCP protein was immunoprecipitated with an anti-β-TrCP antibody, indicated proteins were detected by western blotting. (F) Suppresion of CD147 decreased the total and nuclear Nrf2 expression. β-Actin and Lamin B served as internal controls. WCL, whole cell lysate; N, nuclear; C, cytoplasmic.

    Journal: International Journal of Biological Sciences

    Article Title: CD147 confers temozolomide resistance of glioma cells via the regulation of β-TrCP/Nrf2 pathway

    doi: 10.7150/ijbs.60894

    Figure Lengend Snippet: CD147 dictates Nrf2 stability through the suppression of GSK3β/β-TrCP dependent protein degradation (A-B) The indicated proteins were determined in U251 cells with CD147 knockdown (A) or overexpression (B). (C) Nrf2 and GSK3β protein levels were determined in U251 cells following Capivasertib (10nM) treatment. (D-E) Immunoprecipitation was performed to determine the interaction between β-TrCP and Nrf2 in indicated U251 cells. After the β-TrCP protein was immunoprecipitated with an anti-β-TrCP antibody, indicated proteins were detected by western blotting. (F) Suppresion of CD147 decreased the total and nuclear Nrf2 expression. β-Actin and Lamin B served as internal controls. WCL, whole cell lysate; N, nuclear; C, cytoplasmic.

    Article Snippet: Primary antibodies were used at dilutions of 1:1000 for anti-CD147 (ab108308, Abcam), anti-Nrf2 (ab180845, Abcam), anti-NQO-1 (ab28947, Abcam), anti-HO-1 (ab13248, Abcam), anti-GCLC-1 (ab190685, Abcam), anti-β-TrCP (#4394, Cell signaling Technology), anti-Phospho-GSK-3-beta (Ser9) (#9322, Cell Signaling Technology), anti-GSK-3-beta (#12456, Cell Signaling Technology), anti-Phospho-Akt (Ser473) (#4051, Cell Signaling Technology), anti-Akt (#9272, Cell Signaling Technology), and anti-β-actin (#A5441, Sigma) antibody, anti-Lamin B(#13435, Cell Signaling Technology), respectively.

    Techniques: Over Expression, Immunoprecipitation, Western Blot, Expressing

    CD147-dependent Nrf2 expression is required for glioma cells survival and drug resistance (A) Suppression of CD147 increased anti-tumor effect of TMZ in nude mice. Mice were injected into the groin with 1 × 10 6 U251 cells. The mice were given intraperitoneal injections of 50 mg/kg TMZ or DMSO once every day from days 1 to 5. The Tumor size was measured and tumor volume was calculated. (B) Immunohistochemistry staining of CD147 and Nrf2 in the sections of tumor graft. (C-F) Nrf2 levels were increased with lentivirus overexpressing Nrf2 in U251 cells with CD147 knockdown. (C-D) Nrf2 overexpression blocked TMZ mediated inhibitions of tumor growth in vivo (C) and in vitro (D). (E-F) Nrf2 overexpression blocked TMZ induced apoptosis (E) and ROS production (F).

    Journal: International Journal of Biological Sciences

    Article Title: CD147 confers temozolomide resistance of glioma cells via the regulation of β-TrCP/Nrf2 pathway

    doi: 10.7150/ijbs.60894

    Figure Lengend Snippet: CD147-dependent Nrf2 expression is required for glioma cells survival and drug resistance (A) Suppression of CD147 increased anti-tumor effect of TMZ in nude mice. Mice were injected into the groin with 1 × 10 6 U251 cells. The mice were given intraperitoneal injections of 50 mg/kg TMZ or DMSO once every day from days 1 to 5. The Tumor size was measured and tumor volume was calculated. (B) Immunohistochemistry staining of CD147 and Nrf2 in the sections of tumor graft. (C-F) Nrf2 levels were increased with lentivirus overexpressing Nrf2 in U251 cells with CD147 knockdown. (C-D) Nrf2 overexpression blocked TMZ mediated inhibitions of tumor growth in vivo (C) and in vitro (D). (E-F) Nrf2 overexpression blocked TMZ induced apoptosis (E) and ROS production (F).

    Article Snippet: Primary antibodies were used at dilutions of 1:1000 for anti-CD147 (ab108308, Abcam), anti-Nrf2 (ab180845, Abcam), anti-NQO-1 (ab28947, Abcam), anti-HO-1 (ab13248, Abcam), anti-GCLC-1 (ab190685, Abcam), anti-β-TrCP (#4394, Cell signaling Technology), anti-Phospho-GSK-3-beta (Ser9) (#9322, Cell Signaling Technology), anti-GSK-3-beta (#12456, Cell Signaling Technology), anti-Phospho-Akt (Ser473) (#4051, Cell Signaling Technology), anti-Akt (#9272, Cell Signaling Technology), and anti-β-actin (#A5441, Sigma) antibody, anti-Lamin B(#13435, Cell Signaling Technology), respectively.

    Techniques: Expressing, Injection, Immunohistochemistry, Staining, Over Expression, In Vivo, In Vitro

    CD147 and Nrf2 are positively correlated in glioma tissues and associated with patient outcome (A-B) Immunohistochemistry staining of CD147 and Nrf2 in human adjacent normal and gioma tissues from patients (A) and the statistical analysis (B). (C) Positive correlation between CD147 and Nr2 expression levels with linear regression and Pearson's correlation significance (P < 0.0001, ANOVA test). (D-G) Positive association of CD147 with NQO-1 (D), HO-1 (E), GSTK-1 (F) and GSS (G) mRNA expression patterns in glioma tissues from TCGA data set by GEPIA with linear regression and Pearson's correlation significance. (H-J) Silico analysis of 509 cases of glioma tissues of the multidimensional data set from TCGA portal data set. KaplaneMeier plots indicate the clinical outcomes for Nrf2 (H), or CD147/Nrf2 levels (I and J) in glioma tissues. C, CD147; N, Nrf2; n, indicates the number of patient samples evaluated in each analysis. p-values were calculated using the ManteleCox log-rank test.

    Journal: International Journal of Biological Sciences

    Article Title: CD147 confers temozolomide resistance of glioma cells via the regulation of β-TrCP/Nrf2 pathway

    doi: 10.7150/ijbs.60894

    Figure Lengend Snippet: CD147 and Nrf2 are positively correlated in glioma tissues and associated with patient outcome (A-B) Immunohistochemistry staining of CD147 and Nrf2 in human adjacent normal and gioma tissues from patients (A) and the statistical analysis (B). (C) Positive correlation between CD147 and Nr2 expression levels with linear regression and Pearson's correlation significance (P < 0.0001, ANOVA test). (D-G) Positive association of CD147 with NQO-1 (D), HO-1 (E), GSTK-1 (F) and GSS (G) mRNA expression patterns in glioma tissues from TCGA data set by GEPIA with linear regression and Pearson's correlation significance. (H-J) Silico analysis of 509 cases of glioma tissues of the multidimensional data set from TCGA portal data set. KaplaneMeier plots indicate the clinical outcomes for Nrf2 (H), or CD147/Nrf2 levels (I and J) in glioma tissues. C, CD147; N, Nrf2; n, indicates the number of patient samples evaluated in each analysis. p-values were calculated using the ManteleCox log-rank test.

    Article Snippet: Primary antibodies were used at dilutions of 1:1000 for anti-CD147 (ab108308, Abcam), anti-Nrf2 (ab180845, Abcam), anti-NQO-1 (ab28947, Abcam), anti-HO-1 (ab13248, Abcam), anti-GCLC-1 (ab190685, Abcam), anti-β-TrCP (#4394, Cell signaling Technology), anti-Phospho-GSK-3-beta (Ser9) (#9322, Cell Signaling Technology), anti-GSK-3-beta (#12456, Cell Signaling Technology), anti-Phospho-Akt (Ser473) (#4051, Cell Signaling Technology), anti-Akt (#9272, Cell Signaling Technology), and anti-β-actin (#A5441, Sigma) antibody, anti-Lamin B(#13435, Cell Signaling Technology), respectively.

    Techniques: Immunohistochemistry, Staining, Expressing

    Oligonucleotide sequence of polymerase chain reaction (PCR) primers.

    Journal: Frontiers in Oncology

    Article Title: Psychological Stress Up-Regulates CD147 Expression Through Beta-Arrestin1/ERK to Promote Proliferation and Invasiveness of Glioma Cells

    doi: 10.3389/fonc.2020.571181

    Figure Lengend Snippet: Oligonucleotide sequence of polymerase chain reaction (PCR) primers.

    Article Snippet: The same amount of protein was loaded onto an SDS-PAGE gel, transferred to a nitrocellulose (NC) membrane, and blocked with 50 g/L non-fat milk for 1 h. The membrane was then incubated with the following antibodies at 4°C: rabbit anti-CD147 antibody (MAB972-100, R@D, 1:3,000) and rabbit anti-ERK1/2 antibody (Cell Signaling Technology, 1:5,000), rabbit anti-phospho-ERK1/2 antibody (Cell Signaling Technology, 1:5,000), rabbit anti-Sp1 antibody (sc-14027, Santa Cruz Biotechnology, 1:2,000), rabbit anti-MMP2 antibody (ab86607, abcam, 1:3,000) rabbit anti-MMP9 antibody (ab236494, abcam, 1:2,000), and mouse anti-β-Actin (sc-8432; Santa Cruz Biotechnology,1:5,000).

    Techniques: Sequencing, Polymerase Chain Reaction

    CD147 Silencing Inhibited the Proliferation of Xenograft Tumors Induced by Chronic Psychological Stress in Nude Mice. (A) The growth of transplanted tumors in nude mice (n=5). (B) epinephrine (EPI) and norepinephrine (NE) concentrations in the serum of nude mice with transplanted tumors were detected by ELISA, and the stress hormone levels were not affected after CD147 silencing. (C) Determination of lactic acid in the tumor tissues of nude mice. The expression of CD147, MMP-2, and MMP-9 in tumor tissues of nude mice were detected by western blotting. (D) Evaluated by Western blots and (E) Quantified. (left to right). CD147, MMP-2, and MMP-9 expression levels were increased in nude mice with glioma and psychological stress treatment. Data are expressed as the mean ± sd. *P < 0.05. **P < 0.01 vs Con. # P < 0.05. ## P < 0.01 vs Stress.

    Journal: Frontiers in Oncology

    Article Title: Psychological Stress Up-Regulates CD147 Expression Through Beta-Arrestin1/ERK to Promote Proliferation and Invasiveness of Glioma Cells

    doi: 10.3389/fonc.2020.571181

    Figure Lengend Snippet: CD147 Silencing Inhibited the Proliferation of Xenograft Tumors Induced by Chronic Psychological Stress in Nude Mice. (A) The growth of transplanted tumors in nude mice (n=5). (B) epinephrine (EPI) and norepinephrine (NE) concentrations in the serum of nude mice with transplanted tumors were detected by ELISA, and the stress hormone levels were not affected after CD147 silencing. (C) Determination of lactic acid in the tumor tissues of nude mice. The expression of CD147, MMP-2, and MMP-9 in tumor tissues of nude mice were detected by western blotting. (D) Evaluated by Western blots and (E) Quantified. (left to right). CD147, MMP-2, and MMP-9 expression levels were increased in nude mice with glioma and psychological stress treatment. Data are expressed as the mean ± sd. *P < 0.05. **P < 0.01 vs Con. # P < 0.05. ## P < 0.01 vs Stress.

    Article Snippet: The same amount of protein was loaded onto an SDS-PAGE gel, transferred to a nitrocellulose (NC) membrane, and blocked with 50 g/L non-fat milk for 1 h. The membrane was then incubated with the following antibodies at 4°C: rabbit anti-CD147 antibody (MAB972-100, R@D, 1:3,000) and rabbit anti-ERK1/2 antibody (Cell Signaling Technology, 1:5,000), rabbit anti-phospho-ERK1/2 antibody (Cell Signaling Technology, 1:5,000), rabbit anti-Sp1 antibody (sc-14027, Santa Cruz Biotechnology, 1:2,000), rabbit anti-MMP2 antibody (ab86607, abcam, 1:3,000) rabbit anti-MMP9 antibody (ab236494, abcam, 1:2,000), and mouse anti-β-Actin (sc-8432; Santa Cruz Biotechnology,1:5,000).

    Techniques: Enzyme-linked Immunosorbent Assay, Expressing, Western Blot

    CD147 Knockdown Reduced the Expression and Secretion of MMP-2 and MMP-9 Induced by norepinephrine (NE) in glioma Cells. (A) Detect the relative expression of CD147 in human glioma cell lines including HEB, U251, LN229, U87, and SHG44 by PCR. (B) Two glioma cells were incubated with different concentrations of NE for 1, 2, 3, 4, and 5 day. CCK-8 assay demonstrated that NE promoted the proliferation of glioma cells in a concentration-dependent and time-dependent manner. (C) NE increased expression of CD147 in a concentration-dependent manner. (D) The expression of CD147, MMP-2, and MMP-9 proteins was detected by western blotting. NE promoted the expression of CD147, MMP-2, and MMP-9. (E, F) qPCR confirmed that NE promoted the expression of MMP-2 and MMP-9, which were inhibited by CD147 knockdown. (G, H) Western blotting analysis showed that the expression of MMP-2 and MMP-9 protein in LN229 cells and U87 cells were decreased after transfection with shRNA-CD147. (I, J) Gelatinase assay showed that NE promoted matrix metalloproteinases (MMPs) secretion in two glioma cells, which was inhibited by CD147 knockdown. shRNA-Con was the negative control; data are expressed as the mean ± SD. *P < 0.05. **P < 0.01 vs Con (0 μmol/L NE). # P < 0.05. ## P < 0.01 vs 10 μmol/L NE.

    Journal: Frontiers in Oncology

    Article Title: Psychological Stress Up-Regulates CD147 Expression Through Beta-Arrestin1/ERK to Promote Proliferation and Invasiveness of Glioma Cells

    doi: 10.3389/fonc.2020.571181

    Figure Lengend Snippet: CD147 Knockdown Reduced the Expression and Secretion of MMP-2 and MMP-9 Induced by norepinephrine (NE) in glioma Cells. (A) Detect the relative expression of CD147 in human glioma cell lines including HEB, U251, LN229, U87, and SHG44 by PCR. (B) Two glioma cells were incubated with different concentrations of NE for 1, 2, 3, 4, and 5 day. CCK-8 assay demonstrated that NE promoted the proliferation of glioma cells in a concentration-dependent and time-dependent manner. (C) NE increased expression of CD147 in a concentration-dependent manner. (D) The expression of CD147, MMP-2, and MMP-9 proteins was detected by western blotting. NE promoted the expression of CD147, MMP-2, and MMP-9. (E, F) qPCR confirmed that NE promoted the expression of MMP-2 and MMP-9, which were inhibited by CD147 knockdown. (G, H) Western blotting analysis showed that the expression of MMP-2 and MMP-9 protein in LN229 cells and U87 cells were decreased after transfection with shRNA-CD147. (I, J) Gelatinase assay showed that NE promoted matrix metalloproteinases (MMPs) secretion in two glioma cells, which was inhibited by CD147 knockdown. shRNA-Con was the negative control; data are expressed as the mean ± SD. *P < 0.05. **P < 0.01 vs Con (0 μmol/L NE). # P < 0.05. ## P < 0.01 vs 10 μmol/L NE.

    Article Snippet: The same amount of protein was loaded onto an SDS-PAGE gel, transferred to a nitrocellulose (NC) membrane, and blocked with 50 g/L non-fat milk for 1 h. The membrane was then incubated with the following antibodies at 4°C: rabbit anti-CD147 antibody (MAB972-100, R@D, 1:3,000) and rabbit anti-ERK1/2 antibody (Cell Signaling Technology, 1:5,000), rabbit anti-phospho-ERK1/2 antibody (Cell Signaling Technology, 1:5,000), rabbit anti-Sp1 antibody (sc-14027, Santa Cruz Biotechnology, 1:2,000), rabbit anti-MMP2 antibody (ab86607, abcam, 1:3,000) rabbit anti-MMP9 antibody (ab236494, abcam, 1:2,000), and mouse anti-β-Actin (sc-8432; Santa Cruz Biotechnology,1:5,000).

    Techniques: Expressing, Incubation, CCK-8 Assay, Concentration Assay, Western Blot, Transfection, shRNA, Negative Control

    CD147 Knockout Inhibited the Proliferation, Invasiveness, and Migration of LN229 and U87 Cells. (A) Migration ability of LN229 and U87 cells were detected by scratch assay. (B) Representative images of the invasion ability of and U87 cells [control group, norepinephrine (NE) group, shRNACD147 group, shRNA CD147 + NE group and shRNA Con] in the Matrigel invasion assays ( × 200). Quantification of invaded cells showed that interference with CD147 expression significantly inhibited the invasion of Matrigel in NE -induced LN229 and U87 cells. (C) Colony formation assay. Interference with CD147 expression significantly inhibited the formation of LN229 and U87 cell clones induced by NE (10 μmol/L). (D) CCK-8 assay (at 0, 24, 48, 72, and 96 h) in two glioma cells induced by NE(10μmol/L). CD147-interference significantly inhibited the proliferation of two glioma cells induced by NE. (E) Detection of CD147 silencing effect by Western blot and quantified. Data are expressed as the mean ± sd. *P < 0.05. **P < 0.01 vs Con (0 μmol/L NE); # P < 0.05. ## P < 0.01 vs 10 μmol/L NE.

    Journal: Frontiers in Oncology

    Article Title: Psychological Stress Up-Regulates CD147 Expression Through Beta-Arrestin1/ERK to Promote Proliferation and Invasiveness of Glioma Cells

    doi: 10.3389/fonc.2020.571181

    Figure Lengend Snippet: CD147 Knockout Inhibited the Proliferation, Invasiveness, and Migration of LN229 and U87 Cells. (A) Migration ability of LN229 and U87 cells were detected by scratch assay. (B) Representative images of the invasion ability of and U87 cells [control group, norepinephrine (NE) group, shRNACD147 group, shRNA CD147 + NE group and shRNA Con] in the Matrigel invasion assays ( × 200). Quantification of invaded cells showed that interference with CD147 expression significantly inhibited the invasion of Matrigel in NE -induced LN229 and U87 cells. (C) Colony formation assay. Interference with CD147 expression significantly inhibited the formation of LN229 and U87 cell clones induced by NE (10 μmol/L). (D) CCK-8 assay (at 0, 24, 48, 72, and 96 h) in two glioma cells induced by NE(10μmol/L). CD147-interference significantly inhibited the proliferation of two glioma cells induced by NE. (E) Detection of CD147 silencing effect by Western blot and quantified. Data are expressed as the mean ± sd. *P < 0.05. **P < 0.01 vs Con (0 μmol/L NE); # P < 0.05. ## P < 0.01 vs 10 μmol/L NE.

    Article Snippet: The same amount of protein was loaded onto an SDS-PAGE gel, transferred to a nitrocellulose (NC) membrane, and blocked with 50 g/L non-fat milk for 1 h. The membrane was then incubated with the following antibodies at 4°C: rabbit anti-CD147 antibody (MAB972-100, R@D, 1:3,000) and rabbit anti-ERK1/2 antibody (Cell Signaling Technology, 1:5,000), rabbit anti-phospho-ERK1/2 antibody (Cell Signaling Technology, 1:5,000), rabbit anti-Sp1 antibody (sc-14027, Santa Cruz Biotechnology, 1:2,000), rabbit anti-MMP2 antibody (ab86607, abcam, 1:3,000) rabbit anti-MMP9 antibody (ab236494, abcam, 1:2,000), and mouse anti-β-Actin (sc-8432; Santa Cruz Biotechnology,1:5,000).

    Techniques: Knock-Out, Migration, Wound Healing Assay, shRNA, Expressing, Colony Assay, Clone Assay, CCK-8 Assay, Western Blot

    The β-adrenergic Receptors/β-arrestin1/ERK Signaling Pathway Regulated CD147 Expression. (A) Propranolol and U0126 reduced tumor size in vivo . (B) U0126 and Propranolol blocked the expression of CD147 induced by stress. (C) U0126 and Propranolol blocked norepinephrine (NE)-induced CD147 expression. (D) ERK1/2 signaling regulated CD147 expression in LN229 and (E) U87 cells downstream of β-AR. Cells were treated with NE (10 μmol/L) for 16 h. The effect of U0126 (10 μmol/L) on NE-induced CD147 expression was monitored by western blotting and quantified. (F) The production of lactic acid in extracellular and intracellular compartments of glioma cells under the effect of NE. The ERK1/2 inhibitor U0126 (10 μmol/L) inhibited NE-induced lactate release in LN229 cells (G) and U87 cells (H) , which was also inhibited by propranolol, shRNACD147, and si-β-arrestin1. Data are expressed as the mean ± SD. *P < 0.05. **P < 0.01 vs NE (0 μmol/L); # P < 0.05. ## P < 0.01 vs NE (10 μmol/L) or stress.

    Journal: Frontiers in Oncology

    Article Title: Psychological Stress Up-Regulates CD147 Expression Through Beta-Arrestin1/ERK to Promote Proliferation and Invasiveness of Glioma Cells

    doi: 10.3389/fonc.2020.571181

    Figure Lengend Snippet: The β-adrenergic Receptors/β-arrestin1/ERK Signaling Pathway Regulated CD147 Expression. (A) Propranolol and U0126 reduced tumor size in vivo . (B) U0126 and Propranolol blocked the expression of CD147 induced by stress. (C) U0126 and Propranolol blocked norepinephrine (NE)-induced CD147 expression. (D) ERK1/2 signaling regulated CD147 expression in LN229 and (E) U87 cells downstream of β-AR. Cells were treated with NE (10 μmol/L) for 16 h. The effect of U0126 (10 μmol/L) on NE-induced CD147 expression was monitored by western blotting and quantified. (F) The production of lactic acid in extracellular and intracellular compartments of glioma cells under the effect of NE. The ERK1/2 inhibitor U0126 (10 μmol/L) inhibited NE-induced lactate release in LN229 cells (G) and U87 cells (H) , which was also inhibited by propranolol, shRNACD147, and si-β-arrestin1. Data are expressed as the mean ± SD. *P < 0.05. **P < 0.01 vs NE (0 μmol/L); # P < 0.05. ## P < 0.01 vs NE (10 μmol/L) or stress.

    Article Snippet: The same amount of protein was loaded onto an SDS-PAGE gel, transferred to a nitrocellulose (NC) membrane, and blocked with 50 g/L non-fat milk for 1 h. The membrane was then incubated with the following antibodies at 4°C: rabbit anti-CD147 antibody (MAB972-100, R@D, 1:3,000) and rabbit anti-ERK1/2 antibody (Cell Signaling Technology, 1:5,000), rabbit anti-phospho-ERK1/2 antibody (Cell Signaling Technology, 1:5,000), rabbit anti-Sp1 antibody (sc-14027, Santa Cruz Biotechnology, 1:2,000), rabbit anti-MMP2 antibody (ab86607, abcam, 1:3,000) rabbit anti-MMP9 antibody (ab236494, abcam, 1:2,000), and mouse anti-β-Actin (sc-8432; Santa Cruz Biotechnology,1:5,000).

    Techniques: Expressing, In Vivo, Western Blot

    The Transcription Factor Sp1 Mediated the norepinephrine (NE)-Induced High Expression of CD147. (A) Schematic diagram of luciferase assay for different lengths of CD147 promoter activity, *P<0.05, **p<0.01 compared with the empty PGL4.16 vector. (B) Luciferase activity of different truncated human CD147 promoters after stimulation with 10 μmol/L NE. (C) Schematic diagram of the mutation in the node of Sp1 in the CD147 promoter. (D) Detection of 10 μmol/L NE-induced luciferase activity of CD147-P, CD147-M1, CD147-M2, CD147-M3, and CD147-M4 co-transfected with Sp1. (E) The effect of the β-adrenergic receptor inhibitor propranolol (10 μmol/L), the PKA inhibitor H89 (10 μmol/L), the ERK inhibitor U0126 (10 μmol/L), si-β-arrestin1, and si-β-arrestin2 on Sp1- mediated CD147-P (-245/+51) luciferase activity. Luciferase activity was normalized to that of renilla luciferase, *P < 0.05, **P < 0.01, compared with 0μmol/L NE; # P < 0.05, ## P < 0.01 compared with Sp1-CD147-P (-245/+51)+10 μmol/L NE.

    Journal: Frontiers in Oncology

    Article Title: Psychological Stress Up-Regulates CD147 Expression Through Beta-Arrestin1/ERK to Promote Proliferation and Invasiveness of Glioma Cells

    doi: 10.3389/fonc.2020.571181

    Figure Lengend Snippet: The Transcription Factor Sp1 Mediated the norepinephrine (NE)-Induced High Expression of CD147. (A) Schematic diagram of luciferase assay for different lengths of CD147 promoter activity, *P<0.05, **p<0.01 compared with the empty PGL4.16 vector. (B) Luciferase activity of different truncated human CD147 promoters after stimulation with 10 μmol/L NE. (C) Schematic diagram of the mutation in the node of Sp1 in the CD147 promoter. (D) Detection of 10 μmol/L NE-induced luciferase activity of CD147-P, CD147-M1, CD147-M2, CD147-M3, and CD147-M4 co-transfected with Sp1. (E) The effect of the β-adrenergic receptor inhibitor propranolol (10 μmol/L), the PKA inhibitor H89 (10 μmol/L), the ERK inhibitor U0126 (10 μmol/L), si-β-arrestin1, and si-β-arrestin2 on Sp1- mediated CD147-P (-245/+51) luciferase activity. Luciferase activity was normalized to that of renilla luciferase, *P < 0.05, **P < 0.01, compared with 0μmol/L NE; # P < 0.05, ## P < 0.01 compared with Sp1-CD147-P (-245/+51)+10 μmol/L NE.

    Article Snippet: The same amount of protein was loaded onto an SDS-PAGE gel, transferred to a nitrocellulose (NC) membrane, and blocked with 50 g/L non-fat milk for 1 h. The membrane was then incubated with the following antibodies at 4°C: rabbit anti-CD147 antibody (MAB972-100, R@D, 1:3,000) and rabbit anti-ERK1/2 antibody (Cell Signaling Technology, 1:5,000), rabbit anti-phospho-ERK1/2 antibody (Cell Signaling Technology, 1:5,000), rabbit anti-Sp1 antibody (sc-14027, Santa Cruz Biotechnology, 1:2,000), rabbit anti-MMP2 antibody (ab86607, abcam, 1:3,000) rabbit anti-MMP9 antibody (ab236494, abcam, 1:2,000), and mouse anti-β-Actin (sc-8432; Santa Cruz Biotechnology,1:5,000).

    Techniques: Expressing, Luciferase, Activity Assay, Plasmid Preparation, Mutagenesis, Transfection

    Norepinephrine (NE) Regulated CD147 Expression by Activating the β-AR/β-Arrestin1/ERK/Sp1 Pathway. (A) Expression of CD147 and Sp1 protein and statistical analysis (B) and mRNA in LN229 and U87 cells after transfection with Sp1 siRNA. (C) Effects of U0126, si-β-arrestin1 or Propranolol on NE-induced Sp1 expression in LN229 and U87 cells. (D) Schematic diagram of how NE regulates the expression of CD147 through the β- adrenergic receptor-β-arrestin1-ERK-Sp1 pathway. *P < 0.05, **P < 0.01, compared with 0 μmol/L NE; # P < 0.05, ## P < 0.01 compared with 10 μmol/L NE.

    Journal: Frontiers in Oncology

    Article Title: Psychological Stress Up-Regulates CD147 Expression Through Beta-Arrestin1/ERK to Promote Proliferation and Invasiveness of Glioma Cells

    doi: 10.3389/fonc.2020.571181

    Figure Lengend Snippet: Norepinephrine (NE) Regulated CD147 Expression by Activating the β-AR/β-Arrestin1/ERK/Sp1 Pathway. (A) Expression of CD147 and Sp1 protein and statistical analysis (B) and mRNA in LN229 and U87 cells after transfection with Sp1 siRNA. (C) Effects of U0126, si-β-arrestin1 or Propranolol on NE-induced Sp1 expression in LN229 and U87 cells. (D) Schematic diagram of how NE regulates the expression of CD147 through the β- adrenergic receptor-β-arrestin1-ERK-Sp1 pathway. *P < 0.05, **P < 0.01, compared with 0 μmol/L NE; # P < 0.05, ## P < 0.01 compared with 10 μmol/L NE.

    Article Snippet: The same amount of protein was loaded onto an SDS-PAGE gel, transferred to a nitrocellulose (NC) membrane, and blocked with 50 g/L non-fat milk for 1 h. The membrane was then incubated with the following antibodies at 4°C: rabbit anti-CD147 antibody (MAB972-100, R@D, 1:3,000) and rabbit anti-ERK1/2 antibody (Cell Signaling Technology, 1:5,000), rabbit anti-phospho-ERK1/2 antibody (Cell Signaling Technology, 1:5,000), rabbit anti-Sp1 antibody (sc-14027, Santa Cruz Biotechnology, 1:2,000), rabbit anti-MMP2 antibody (ab86607, abcam, 1:3,000) rabbit anti-MMP9 antibody (ab236494, abcam, 1:2,000), and mouse anti-β-Actin (sc-8432; Santa Cruz Biotechnology,1:5,000).

    Techniques: Expressing, Transfection