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pe anti-mouse cd147 antibody  (Thermo Fisher)


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    Structured Review

    Thermo Fisher pe anti-mouse cd147 antibody
    Pe Anti Mouse Cd147 Antibody, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pe+anti-mouse+cd147+antibody/pmc03255577-209-21-27
    Average 90 stars, based on 1 article reviews
    pe anti-mouse cd147 antibody - by Bioz Stars, 2026-09
    90/100 stars

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    Related Articles

    Isolation:

    Article Title: Short-interfering RNAs Induce Retinal Degeneration via TLR3 and IRF3
    Article Snippet: Suspensions of C57BL/6J RPE/choroid cells (10 6 ) were isolated and incubated with APC anti-mouse CD31 antibody (20 μg/ml; BD) and PE anti-mouse CD147 antibody (20 μg/ml; eBioscience) to identify CD147 + CD31 - RPE cells.

    Incubation:

    Article Title: Short-interfering RNAs Induce Retinal Degeneration via TLR3 and IRF3
    Article Snippet: Suspensions of C57BL/6J RPE/choroid cells (10 6 ) were isolated and incubated with APC anti-mouse CD31 antibody (20 μg/ml; BD) and PE anti-mouse CD147 antibody (20 μg/ml; eBioscience) to identify CD147 + CD31 - RPE cells.



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    Figure 2. <t>CD147</t> specific shRNA results in the reduction of CD147 mRNA and protein levels in HT29 cells. The expression levels of CD147, MCT1 and MCT4 in HT29 cells after CD147 silencing. Relative mRNA levels were analysed by quantitative RT-PCR. β-actin was used as normalization control. As shown in (A) and (C), the mRNA expression of CD147 and MCT1 were significantly downregulated (p<0.01) by HT29/shRNA compared with the control group in HT29 cells. (B) Τhe mRNA expression of MCT4 had no significant change (p>0.05). The graphs are representative of three separate experiments. (D) The CD147, MCT1 and MCT4 protein expression levels by western blotting. The control group used β-actin. The results show that the protein expression levels of CD147 and MCT1 were significantly downregulated by HT29/shRNA in cells (p<0.01). There was no significant change of MCT4 protein expression (p>0.05).
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    Thermo Fisher pe anti-mouse cd147 antibody
    Figure 2. <t>CD147</t> specific shRNA results in the reduction of CD147 mRNA and protein levels in HT29 cells. The expression levels of CD147, MCT1 and MCT4 in HT29 cells after CD147 silencing. Relative mRNA levels were analysed by quantitative RT-PCR. β-actin was used as normalization control. As shown in (A) and (C), the mRNA expression of CD147 and MCT1 were significantly downregulated (p<0.01) by HT29/shRNA compared with the control group in HT29 cells. (B) Τhe mRNA expression of MCT4 had no significant change (p>0.05). The graphs are representative of three separate experiments. (D) The CD147, MCT1 and MCT4 protein expression levels by western blotting. The control group used β-actin. The results show that the protein expression levels of CD147 and MCT1 were significantly downregulated by HT29/shRNA in cells (p<0.01). There was no significant change of MCT4 protein expression (p>0.05).
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    Figure 1. Silencing of <t>CD147</t> downregulates VEGF-A expression in Hepa1-6 cells by RNAi approach. The Hepa1-6 cells were transfected with CD147 siRNA and control siRNA. Total RNA was extracted and analyzed by RT-PCR using primers specific to CD147, VEGF-A and GAPDH (A). Cells collected on the indicated day (RNAi-3, 3 days; RNAi-7, 7 days) were lysed, and the expressions of CD147 and VEGF-A were analyzed by western-blot analysis using anti-Axl or anti-VEGF-A antibodies (B). GAPDH was also examined and served as controls for sample loading. (C) CD147 expression did not recover to original level until 12 days after siRNA transfection by RT-PCR.
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    Image Search Results


    Fig. 1 MS analysis of emmprin complexes identified CD73 and CD99. Proteins forming complexes with emmprin were identified from cancer cells alone or from co-cultures of cancer cells and fibroblasts, and were analyzed by immunoprecipitation, cross-linking, and mass spectrometric (MS) protein identification. A total of 548 protein molecules were identified using MS. Overlap between proteins identified in different conditions (tumor cell only or three molecular weight regions under co-culture conditions #1–3) is shown. CD73 and CD99 identified in the overlap of all three co- culture conditions were selected for investigation of their effect on regulation of MMP-2 production

    Journal: BMC cancer

    Article Title: CD73 complexes with emmprin to regulate MMP-2 production from co-cultured sarcoma cells and fibroblasts.

    doi: 10.1186/s12885-019-6127-x

    Figure Lengend Snippet: Fig. 1 MS analysis of emmprin complexes identified CD73 and CD99. Proteins forming complexes with emmprin were identified from cancer cells alone or from co-cultures of cancer cells and fibroblasts, and were analyzed by immunoprecipitation, cross-linking, and mass spectrometric (MS) protein identification. A total of 548 protein molecules were identified using MS. Overlap between proteins identified in different conditions (tumor cell only or three molecular weight regions under co-culture conditions #1–3) is shown. CD73 and CD99 identified in the overlap of all three co- culture conditions were selected for investigation of their effect on regulation of MMP-2 production

    Article Snippet: SDS-PAGE and immunoblotting were performed using 4–15% gradient gel (Bio-Rad, Hercules, CA) and antibodies against emmprin (mouse monoclonal, R&D System, Flanders, NJ), anti-CD73 (rabbit monoclonal, Cell Signaling, Danvers, MA), MMP-2 (monoclonal antibody, Daiichi Fine Chemical, Toyama, Japan) and MT1-MMP (Millipore, Bedford, MA).

    Techniques: Immunoprecipitation, Molecular Weight, Co-Culture Assay

    Fig. 2 CD99 and CD73 form complexes with emmprin. a Complex formation between emmprin and CD99 was identified by immunoprecipitation and immunoblotting, performed in co-cultures of tumor cells and fibroblasts. Arrow indicates emmprin-CD99 complex. b Complex formation between emmprin and CD73 was identified by immunoprecipitation and immunoblotting, performed in co-cultures of tumor cells and fibroblasts. Arrow indicates emmprin-CD73 complex.

    Journal: BMC cancer

    Article Title: CD73 complexes with emmprin to regulate MMP-2 production from co-cultured sarcoma cells and fibroblasts.

    doi: 10.1186/s12885-019-6127-x

    Figure Lengend Snippet: Fig. 2 CD99 and CD73 form complexes with emmprin. a Complex formation between emmprin and CD99 was identified by immunoprecipitation and immunoblotting, performed in co-cultures of tumor cells and fibroblasts. Arrow indicates emmprin-CD99 complex. b Complex formation between emmprin and CD73 was identified by immunoprecipitation and immunoblotting, performed in co-cultures of tumor cells and fibroblasts. Arrow indicates emmprin-CD73 complex.

    Article Snippet: SDS-PAGE and immunoblotting were performed using 4–15% gradient gel (Bio-Rad, Hercules, CA) and antibodies against emmprin (mouse monoclonal, R&D System, Flanders, NJ), anti-CD73 (rabbit monoclonal, Cell Signaling, Danvers, MA), MMP-2 (monoclonal antibody, Daiichi Fine Chemical, Toyama, Japan) and MT1-MMP (Millipore, Bedford, MA).

    Techniques: Immunoprecipitation, Western Blot

    Fig. 5 Colocalization of emmprin/CD73 detected by immunofluorescent staining and in situ proximity ligation assay. Cytoplasmic CD73 (green) expression was observed in fibroblasts, tumor cells and co-culture cells. Membranous emmprin expression (red) was observed in tumor cells and co-cultured cells. Nuclei were stained with DAPI (blue). CD73 and emmprin were colocalized in tumor cells (b) and co-cultured cells (c). The green arrow points to fibroblasts expresssing green florescence (CD73); The yellow arrow points to tumor cells expressed yellow florescence (emmprin and CD73) (c). CD73 siRNA treatment causes downregulation of CD73 cytoplasmic expression, although, membranous emmprin expression was retained in co-cultured cells (d). The fluorescent red spots observed using in situ proximity ligation assay (PLA), indicating protein- protein colocalization in cells, confirmed the interaction between CD73 and emmprin. The detected dimers (emmprin/CD73) are represented as red dots in co-cultured cells (g). In cells transfected with CD73 siRNA prior to in situ PLA for emmmprin-CD73 interaction, CD73 siRNA treatment caused downregulation of red dots (h). Immunofluorescent staining, IF (a-d); In situ proximity ligation assay, PLA (e-h); fibroblast only (a, e); tumor cell only (b, f); co-culture (c-d, g-h)

    Journal: BMC cancer

    Article Title: CD73 complexes with emmprin to regulate MMP-2 production from co-cultured sarcoma cells and fibroblasts.

    doi: 10.1186/s12885-019-6127-x

    Figure Lengend Snippet: Fig. 5 Colocalization of emmprin/CD73 detected by immunofluorescent staining and in situ proximity ligation assay. Cytoplasmic CD73 (green) expression was observed in fibroblasts, tumor cells and co-culture cells. Membranous emmprin expression (red) was observed in tumor cells and co-cultured cells. Nuclei were stained with DAPI (blue). CD73 and emmprin were colocalized in tumor cells (b) and co-cultured cells (c). The green arrow points to fibroblasts expresssing green florescence (CD73); The yellow arrow points to tumor cells expressed yellow florescence (emmprin and CD73) (c). CD73 siRNA treatment causes downregulation of CD73 cytoplasmic expression, although, membranous emmprin expression was retained in co-cultured cells (d). The fluorescent red spots observed using in situ proximity ligation assay (PLA), indicating protein- protein colocalization in cells, confirmed the interaction between CD73 and emmprin. The detected dimers (emmprin/CD73) are represented as red dots in co-cultured cells (g). In cells transfected with CD73 siRNA prior to in situ PLA for emmmprin-CD73 interaction, CD73 siRNA treatment caused downregulation of red dots (h). Immunofluorescent staining, IF (a-d); In situ proximity ligation assay, PLA (e-h); fibroblast only (a, e); tumor cell only (b, f); co-culture (c-d, g-h)

    Article Snippet: SDS-PAGE and immunoblotting were performed using 4–15% gradient gel (Bio-Rad, Hercules, CA) and antibodies against emmprin (mouse monoclonal, R&D System, Flanders, NJ), anti-CD73 (rabbit monoclonal, Cell Signaling, Danvers, MA), MMP-2 (monoclonal antibody, Daiichi Fine Chemical, Toyama, Japan) and MT1-MMP (Millipore, Bedford, MA).

    Techniques: Staining, In Situ, Proximity Ligation Assay, Expressing, Co-Culture Assay, Cell Culture, Transfection

    Fig. 7 Expression of CD73 and emmprin in epithelioid sarcoma. The hematoxylin and eosin (H&E) section shows proliferation of severely atypical polygonal cells with enlarged hyperchromatic nuclei, forming irregular nests, accompanied by fibroblastic cells and fibrous stroma (a). Immunohistochemical (b-c) and fluorescent immunohistochemical (d-f) expression of CD73 and emmprin in epithelioid sarcoma specimen was examined. Both tumor cells and surrounding stromal cells were positive for CD73 (b). Membranous emmprin expression was observed only in tumor cells (c). Cytoplasmic CD73 (green) expression was observed in fibroblasts and in tumor cells (e). Membranous emmprin expression (red) was observed in tumor cells (f). Marger of figures (e) and (f). The green arrow, indicates fibroblasts expressing green florescence (CD73); The Yellow arrow, indicates tumor cells expressing yellow florescence (emmprin and CD73) (d). CD73 and emmprin were colocalized in tumor cells (e). Nuclei were stained with DAPI (blue). Expression of CD73 and emmprin was examined immunohistochemically in a total of ten tumors. All tumors show similar expression pattern (Additional file 6: Table S1)

    Journal: BMC cancer

    Article Title: CD73 complexes with emmprin to regulate MMP-2 production from co-cultured sarcoma cells and fibroblasts.

    doi: 10.1186/s12885-019-6127-x

    Figure Lengend Snippet: Fig. 7 Expression of CD73 and emmprin in epithelioid sarcoma. The hematoxylin and eosin (H&E) section shows proliferation of severely atypical polygonal cells with enlarged hyperchromatic nuclei, forming irregular nests, accompanied by fibroblastic cells and fibrous stroma (a). Immunohistochemical (b-c) and fluorescent immunohistochemical (d-f) expression of CD73 and emmprin in epithelioid sarcoma specimen was examined. Both tumor cells and surrounding stromal cells were positive for CD73 (b). Membranous emmprin expression was observed only in tumor cells (c). Cytoplasmic CD73 (green) expression was observed in fibroblasts and in tumor cells (e). Membranous emmprin expression (red) was observed in tumor cells (f). Marger of figures (e) and (f). The green arrow, indicates fibroblasts expressing green florescence (CD73); The Yellow arrow, indicates tumor cells expressing yellow florescence (emmprin and CD73) (d). CD73 and emmprin were colocalized in tumor cells (e). Nuclei were stained with DAPI (blue). Expression of CD73 and emmprin was examined immunohistochemically in a total of ten tumors. All tumors show similar expression pattern (Additional file 6: Table S1)

    Article Snippet: SDS-PAGE and immunoblotting were performed using 4–15% gradient gel (Bio-Rad, Hercules, CA) and antibodies against emmprin (mouse monoclonal, R&D System, Flanders, NJ), anti-CD73 (rabbit monoclonal, Cell Signaling, Danvers, MA), MMP-2 (monoclonal antibody, Daiichi Fine Chemical, Toyama, Japan) and MT1-MMP (Millipore, Bedford, MA).

    Techniques: Expressing, Immunohistochemical staining, Staining

    Fig. 8 A pictorial representation of the interaction between emmprin on tumor cells and CD73 on fibroblasts. Emmprin mainly exists on tumor cells, and CD73 exists both on tumor cells and fibroblasts. Emmprin forms a complex with CD73, and regulates MMP-2 production in co-cultures of tumor cells and fibroblasts. Pro- MMP-2 produced by fibroblasts is probably activated by MT1-MMP expressed on tumor cells

    Journal: BMC cancer

    Article Title: CD73 complexes with emmprin to regulate MMP-2 production from co-cultured sarcoma cells and fibroblasts.

    doi: 10.1186/s12885-019-6127-x

    Figure Lengend Snippet: Fig. 8 A pictorial representation of the interaction between emmprin on tumor cells and CD73 on fibroblasts. Emmprin mainly exists on tumor cells, and CD73 exists both on tumor cells and fibroblasts. Emmprin forms a complex with CD73, and regulates MMP-2 production in co-cultures of tumor cells and fibroblasts. Pro- MMP-2 produced by fibroblasts is probably activated by MT1-MMP expressed on tumor cells

    Article Snippet: SDS-PAGE and immunoblotting were performed using 4–15% gradient gel (Bio-Rad, Hercules, CA) and antibodies against emmprin (mouse monoclonal, R&D System, Flanders, NJ), anti-CD73 (rabbit monoclonal, Cell Signaling, Danvers, MA), MMP-2 (monoclonal antibody, Daiichi Fine Chemical, Toyama, Japan) and MT1-MMP (Millipore, Bedford, MA).

    Techniques: Produced

    Figure 2. CD147 specific shRNA results in the reduction of CD147 mRNA and protein levels in HT29 cells. The expression levels of CD147, MCT1 and MCT4 in HT29 cells after CD147 silencing. Relative mRNA levels were analysed by quantitative RT-PCR. β-actin was used as normalization control. As shown in (A) and (C), the mRNA expression of CD147 and MCT1 were significantly downregulated (p<0.01) by HT29/shRNA compared with the control group in HT29 cells. (B) Τhe mRNA expression of MCT4 had no significant change (p>0.05). The graphs are representative of three separate experiments. (D) The CD147, MCT1 and MCT4 protein expression levels by western blotting. The control group used β-actin. The results show that the protein expression levels of CD147 and MCT1 were significantly downregulated by HT29/shRNA in cells (p<0.01). There was no significant change of MCT4 protein expression (p>0.05).

    Journal: International journal of oncology

    Article Title: Downregulation of CD147 expression by RNA interference inhibits HT29 cell proliferation, invasion and tumorigenicity in vitro and in vivo.

    doi: 10.3892/ijo.2013.2108

    Figure Lengend Snippet: Figure 2. CD147 specific shRNA results in the reduction of CD147 mRNA and protein levels in HT29 cells. The expression levels of CD147, MCT1 and MCT4 in HT29 cells after CD147 silencing. Relative mRNA levels were analysed by quantitative RT-PCR. β-actin was used as normalization control. As shown in (A) and (C), the mRNA expression of CD147 and MCT1 were significantly downregulated (p<0.01) by HT29/shRNA compared with the control group in HT29 cells. (B) Τhe mRNA expression of MCT4 had no significant change (p>0.05). The graphs are representative of three separate experiments. (D) The CD147, MCT1 and MCT4 protein expression levels by western blotting. The control group used β-actin. The results show that the protein expression levels of CD147 and MCT1 were significantly downregulated by HT29/shRNA in cells (p<0.01). There was no significant change of MCT4 protein expression (p>0.05).

    Article Snippet: Immunohistochemistry analysis used goat anti-mouse CD147 polyclonal antibody (1:50 dilution, Santa Cruz Biotechnology) to detect CD147 protein expression.

    Techniques: shRNA, Expressing, Quantitative RT-PCR, Control, Western Blot

    Figure 3. Gelatin zymography analysis of the activity of MMP-2 and MMP-9 in HT29 cells after CD147 silencing. Cells were incubated for 24 h and con ditioned media were used for the measurement of MMP-2 and MMP-9 protein levels by gelatin zymography. (A) Images of the MMP-2 and MMP-9 bands representative of three independent experiments. (B) Quantitative analysis of the MMP-2 bands. *p<0.01 compared with HT29 and HT29/shRNA-control. (C) Quantitative analysis of the MMP-9 bands. *p<0.01 compared with HT29.

    Journal: International journal of oncology

    Article Title: Downregulation of CD147 expression by RNA interference inhibits HT29 cell proliferation, invasion and tumorigenicity in vitro and in vivo.

    doi: 10.3892/ijo.2013.2108

    Figure Lengend Snippet: Figure 3. Gelatin zymography analysis of the activity of MMP-2 and MMP-9 in HT29 cells after CD147 silencing. Cells were incubated for 24 h and con ditioned media were used for the measurement of MMP-2 and MMP-9 protein levels by gelatin zymography. (A) Images of the MMP-2 and MMP-9 bands representative of three independent experiments. (B) Quantitative analysis of the MMP-2 bands. *p<0.01 compared with HT29 and HT29/shRNA-control. (C) Quantitative analysis of the MMP-9 bands. *p<0.01 compared with HT29.

    Article Snippet: Immunohistochemistry analysis used goat anti-mouse CD147 polyclonal antibody (1:50 dilution, Santa Cruz Biotechnology) to detect CD147 protein expression.

    Techniques: Zymography, Activity Assay, Incubation, shRNA, Control

    Figure 4. Intracellular lactate analysis in HT29 cells after CD147 silencing. The data show that the intracellular lactate concentration after transfection with HT29/shRNA was increased, *p<0.01 compared with HT29.

    Journal: International journal of oncology

    Article Title: Downregulation of CD147 expression by RNA interference inhibits HT29 cell proliferation, invasion and tumorigenicity in vitro and in vivo.

    doi: 10.3892/ijo.2013.2108

    Figure Lengend Snippet: Figure 4. Intracellular lactate analysis in HT29 cells after CD147 silencing. The data show that the intracellular lactate concentration after transfection with HT29/shRNA was increased, *p<0.01 compared with HT29.

    Article Snippet: Immunohistochemistry analysis used goat anti-mouse CD147 polyclonal antibody (1:50 dilution, Santa Cruz Biotechnology) to detect CD147 protein expression.

    Techniques: Concentration Assay, Transfection, shRNA

    Figure 6. Invasive ability of HT29 cells on Matrigel after CD147 silencing. (A) Crystal violet staining results of lower surface filters show the cells invading the Matrigel (x400). (B) The number of cells that invaded through the chamber was evaluated in 3 fields for each experimental group and averaged. The invading cells of each experimental group was counted as the average of the sum of 10 fields of vision under a microscope. *p<0.05 compared with HT29.

    Journal: International journal of oncology

    Article Title: Downregulation of CD147 expression by RNA interference inhibits HT29 cell proliferation, invasion and tumorigenicity in vitro and in vivo.

    doi: 10.3892/ijo.2013.2108

    Figure Lengend Snippet: Figure 6. Invasive ability of HT29 cells on Matrigel after CD147 silencing. (A) Crystal violet staining results of lower surface filters show the cells invading the Matrigel (x400). (B) The number of cells that invaded through the chamber was evaluated in 3 fields for each experimental group and averaged. The invading cells of each experimental group was counted as the average of the sum of 10 fields of vision under a microscope. *p<0.05 compared with HT29.

    Article Snippet: Immunohistochemistry analysis used goat anti-mouse CD147 polyclonal antibody (1:50 dilution, Santa Cruz Biotechnology) to detect CD147 protein expression.

    Techniques: Staining, Microscopy

    Figure 7. Multidrug chemosensitivity analysis in HT29 cells after CD147 silencing. Cells were treated with cisplatin with varying concentrations: 0.1, 1 and 10 µM for 48 h. Cell viability was determined by the WST-8 assay. CD147 silencing significantly increased the chemosensitivity of HT29 cells to cisplatin at 0.1, 1 and 10 µM compared with the control groups (p<0.01). These experiments were repeated in three separate experiments. Cells were treated with paclitaxel, gemcitabine or oxaliplatin at varying concentrations: 0.1, 1 and 10 µM for 48 h and determined by the WST-8 assay. There was no significant change of the chemosensitivity induced by CD147 silencing to paclitaxel, gemcitabine, and oxaliplatin in HT29 cells (p>0.05).

    Journal: International journal of oncology

    Article Title: Downregulation of CD147 expression by RNA interference inhibits HT29 cell proliferation, invasion and tumorigenicity in vitro and in vivo.

    doi: 10.3892/ijo.2013.2108

    Figure Lengend Snippet: Figure 7. Multidrug chemosensitivity analysis in HT29 cells after CD147 silencing. Cells were treated with cisplatin with varying concentrations: 0.1, 1 and 10 µM for 48 h. Cell viability was determined by the WST-8 assay. CD147 silencing significantly increased the chemosensitivity of HT29 cells to cisplatin at 0.1, 1 and 10 µM compared with the control groups (p<0.01). These experiments were repeated in three separate experiments. Cells were treated with paclitaxel, gemcitabine or oxaliplatin at varying concentrations: 0.1, 1 and 10 µM for 48 h and determined by the WST-8 assay. There was no significant change of the chemosensitivity induced by CD147 silencing to paclitaxel, gemcitabine, and oxaliplatin in HT29 cells (p>0.05).

    Article Snippet: Immunohistochemistry analysis used goat anti-mouse CD147 polyclonal antibody (1:50 dilution, Santa Cruz Biotechnology) to detect CD147 protein expression.

    Techniques: Control

    Figure 8. CD147 specific shRNA results on tumor formation in vivo and the expression of CD147 in tumor tissues. (A) The average size of the tumor in each group was measured every 5 days, by the formula: volume = 1/2 x (length x width2). *p<0.01 compared with HT29 group. (B) Immunohistochemistry staining in tumors to detect the CD147 protein expression (x400). The CD147 protein expression is shown in three different groups (x400). *p<0.01 compared with HT29 group. The data were obtained from three independent experiments. Histological analysis with H&E staining was performed in implanted tumors (x400).

    Journal: International journal of oncology

    Article Title: Downregulation of CD147 expression by RNA interference inhibits HT29 cell proliferation, invasion and tumorigenicity in vitro and in vivo.

    doi: 10.3892/ijo.2013.2108

    Figure Lengend Snippet: Figure 8. CD147 specific shRNA results on tumor formation in vivo and the expression of CD147 in tumor tissues. (A) The average size of the tumor in each group was measured every 5 days, by the formula: volume = 1/2 x (length x width2). *p<0.01 compared with HT29 group. (B) Immunohistochemistry staining in tumors to detect the CD147 protein expression (x400). The CD147 protein expression is shown in three different groups (x400). *p<0.01 compared with HT29 group. The data were obtained from three independent experiments. Histological analysis with H&E staining was performed in implanted tumors (x400).

    Article Snippet: Immunohistochemistry analysis used goat anti-mouse CD147 polyclonal antibody (1:50 dilution, Santa Cruz Biotechnology) to detect CD147 protein expression.

    Techniques: shRNA, In Vivo, Expressing, Immunohistochemistry, Staining

    Figure 1. Silencing of CD147 downregulates VEGF-A expression in Hepa1-6 cells by RNAi approach. The Hepa1-6 cells were transfected with CD147 siRNA and control siRNA. Total RNA was extracted and analyzed by RT-PCR using primers specific to CD147, VEGF-A and GAPDH (A). Cells collected on the indicated day (RNAi-3, 3 days; RNAi-7, 7 days) were lysed, and the expressions of CD147 and VEGF-A were analyzed by western-blot analysis using anti-Axl or anti-VEGF-A antibodies (B). GAPDH was also examined and served as controls for sample loading. (C) CD147 expression did not recover to original level until 12 days after siRNA transfection by RT-PCR.

    Journal: IUBMB life

    Article Title: CD147 regulates vascular endothelial growth factor-A expression, tumorigenicity, and chemosensitivity to curcumin in hepatocellular carcinoma.

    doi: 10.1002/iub.11

    Figure Lengend Snippet: Figure 1. Silencing of CD147 downregulates VEGF-A expression in Hepa1-6 cells by RNAi approach. The Hepa1-6 cells were transfected with CD147 siRNA and control siRNA. Total RNA was extracted and analyzed by RT-PCR using primers specific to CD147, VEGF-A and GAPDH (A). Cells collected on the indicated day (RNAi-3, 3 days; RNAi-7, 7 days) were lysed, and the expressions of CD147 and VEGF-A were analyzed by western-blot analysis using anti-Axl or anti-VEGF-A antibodies (B). GAPDH was also examined and served as controls for sample loading. (C) CD147 expression did not recover to original level until 12 days after siRNA transfection by RT-PCR.

    Article Snippet: Rabbit anti-mouse CD147 polyclonal antibody (1:50 dilution, Santa Cruz Biotech) was used in standard indirect immunoperoxidase procedures.

    Techniques: Expressing, Transfection, Control, Reverse Transcription Polymerase Chain Reaction, Western Blot

    Figure 2. Silencing of CD147 impedes Hepa1-6 cells proliferation and anchorage-independent growth in vitro. A: Cells were har- vested at 24, 48, 72, 96, and 120 hours posttransfection, and cell proliferation was measured by MTT assay. Decreased growth abil- ity was detected in CD147/RNAi cells (RNAi-3, 3 days; RNAi-7, 7 days) compared with RNAi control cells. B: Colony-forming activities of CD147/RNAi cells in soft agar. The cell colonies were photographed (3100). C: Colony formation numbers were com- pared between transfected and control RNAi cells. Significant downregulation of colony formation numbers was confirmed in CD147/RNAi cells compared with control RNAi cells (*p \ 0.05). The data were obtained from three independent experiments.

    Journal: IUBMB life

    Article Title: CD147 regulates vascular endothelial growth factor-A expression, tumorigenicity, and chemosensitivity to curcumin in hepatocellular carcinoma.

    doi: 10.1002/iub.11

    Figure Lengend Snippet: Figure 2. Silencing of CD147 impedes Hepa1-6 cells proliferation and anchorage-independent growth in vitro. A: Cells were har- vested at 24, 48, 72, 96, and 120 hours posttransfection, and cell proliferation was measured by MTT assay. Decreased growth abil- ity was detected in CD147/RNAi cells (RNAi-3, 3 days; RNAi-7, 7 days) compared with RNAi control cells. B: Colony-forming activities of CD147/RNAi cells in soft agar. The cell colonies were photographed (3100). C: Colony formation numbers were com- pared between transfected and control RNAi cells. Significant downregulation of colony formation numbers was confirmed in CD147/RNAi cells compared with control RNAi cells (*p \ 0.05). The data were obtained from three independent experiments.

    Article Snippet: Rabbit anti-mouse CD147 polyclonal antibody (1:50 dilution, Santa Cruz Biotech) was used in standard indirect immunoperoxidase procedures.

    Techniques: In Vitro, MTT Assay, Control, Transfection

    Figure 3. Silencing of CD147 in the Hepa1-6 cells inhibits tumorigenicity in nude mice. A: Four groups of nude mice were injected subcutaneously with Hepa1-6, RNAi control, and CD147/RNAi cells (RNAi-3, 3 days; RNAi-7, 7 days). After 3 weeks, tumors were excised, weighed, sized and photographed. B and C: CD147/RNAi groups showed a significant decrease in mean tu- mor weight (n 5 10) and volume (n 5 10) (*p \ 0.05), compared with control groups. D: Histological analysis was performed in implanted tumors generated from Hepa1-6, RNAi control, and CD147/RNAi cells with H&E staining (RNAi-3, 3 days; RNAi-7, 7 days), respectively, 3400. E: CD147 protein expression was determined by immunohistochemistry staining in solid tumors derived from Hepa1-6, RNAi control and CD147/RNAi cells (3400). Differences in CD147 protein expression were shown. The data were obtained from three independent experiments.

    Journal: IUBMB life

    Article Title: CD147 regulates vascular endothelial growth factor-A expression, tumorigenicity, and chemosensitivity to curcumin in hepatocellular carcinoma.

    doi: 10.1002/iub.11

    Figure Lengend Snippet: Figure 3. Silencing of CD147 in the Hepa1-6 cells inhibits tumorigenicity in nude mice. A: Four groups of nude mice were injected subcutaneously with Hepa1-6, RNAi control, and CD147/RNAi cells (RNAi-3, 3 days; RNAi-7, 7 days). After 3 weeks, tumors were excised, weighed, sized and photographed. B and C: CD147/RNAi groups showed a significant decrease in mean tu- mor weight (n 5 10) and volume (n 5 10) (*p \ 0.05), compared with control groups. D: Histological analysis was performed in implanted tumors generated from Hepa1-6, RNAi control, and CD147/RNAi cells with H&E staining (RNAi-3, 3 days; RNAi-7, 7 days), respectively, 3400. E: CD147 protein expression was determined by immunohistochemistry staining in solid tumors derived from Hepa1-6, RNAi control and CD147/RNAi cells (3400). Differences in CD147 protein expression were shown. The data were obtained from three independent experiments.

    Article Snippet: Rabbit anti-mouse CD147 polyclonal antibody (1:50 dilution, Santa Cruz Biotech) was used in standard indirect immunoperoxidase procedures.

    Techniques: Injection, Control, Generated, Staining, Expressing, Immunohistochemistry, Derivative Assay

    Figure 4. Silencing of CD147 in the Hepa1-6 cells increases the chemosensitivity to curcumin. Hepa1-6, RNAi control, and CD147/RNAi cells (RNAi-3, 3 days; RNAi-7, 7 days) were treated with various concentrations of curcumin. Cell viability was determined by MTT chronometry. Cell survival rate (%) was calculated as A570 (curcumin1)/A570 (curcumin2) 3 100%. The data were obtained from three independent experiments (*p \ 0.05).

    Journal: IUBMB life

    Article Title: CD147 regulates vascular endothelial growth factor-A expression, tumorigenicity, and chemosensitivity to curcumin in hepatocellular carcinoma.

    doi: 10.1002/iub.11

    Figure Lengend Snippet: Figure 4. Silencing of CD147 in the Hepa1-6 cells increases the chemosensitivity to curcumin. Hepa1-6, RNAi control, and CD147/RNAi cells (RNAi-3, 3 days; RNAi-7, 7 days) were treated with various concentrations of curcumin. Cell viability was determined by MTT chronometry. Cell survival rate (%) was calculated as A570 (curcumin1)/A570 (curcumin2) 3 100%. The data were obtained from three independent experiments (*p \ 0.05).

    Article Snippet: Rabbit anti-mouse CD147 polyclonal antibody (1:50 dilution, Santa Cruz Biotech) was used in standard indirect immunoperoxidase procedures.

    Techniques: Control