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etv7 plasmid  (Thermo Fisher)


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    Structured Review

    Thermo Fisher etv7 plasmid
    Elevated plasma exosomal miR-361-3p promotes the malignant progression of BC in mice. A Upper panel : A schematic diagram of the animal experiments. Lower panel : A T47D cell xenograft model in female BALB/c nude mice was established. Mice exhibiting a high abundance of plasma exosomal miR-361-3p, as well as control mice, were obtained through the tail vein injection of EXO-miR-361-3p or EXO-miR-NC, respectively. B Differences in volume, weight and growth rate of murine tumors in the EXO-miR-361-3p group compared to the control group. C H&E staining of murine tumor tissues (×40). D – F Compare the expression levels of miR-361-3p, ETV7 , <t>BATF2</t> , and the PAI-1/ERK pathway in excised tumors of the two groups of mice. G Proposed model of exosomal miR-361-3p targeting ETVT and BATF2 to upregulate the PAI-1/ERK pathway, leading to increased viability in BC cells. (* P < 0.05, ** P < 0.01, *** P < 0.001)
    Etv7 Plasmid, 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/result/etv7 plasmid/product/Thermo Fisher
    Average 90 stars, based on 1 article reviews
    etv7 plasmid - by Bioz Stars, 2026-02
    90/100 stars

    Images

    1) Product Images from "Exosomal miR-361-3p promotes the viability of breast cancer cells by targeting ETV7 and BATF2 to upregulate the PAI-1/ERK pathway"

    Article Title: Exosomal miR-361-3p promotes the viability of breast cancer cells by targeting ETV7 and BATF2 to upregulate the PAI-1/ERK pathway

    Journal: Journal of Translational Medicine

    doi: 10.1186/s12967-024-04914-4

    Elevated plasma exosomal miR-361-3p promotes the malignant progression of BC in mice. A Upper panel : A schematic diagram of the animal experiments. Lower panel : A T47D cell xenograft model in female BALB/c nude mice was established. Mice exhibiting a high abundance of plasma exosomal miR-361-3p, as well as control mice, were obtained through the tail vein injection of EXO-miR-361-3p or EXO-miR-NC, respectively. B Differences in volume, weight and growth rate of murine tumors in the EXO-miR-361-3p group compared to the control group. C H&E staining of murine tumor tissues (×40). D – F Compare the expression levels of miR-361-3p, ETV7 , BATF2 , and the PAI-1/ERK pathway in excised tumors of the two groups of mice. G Proposed model of exosomal miR-361-3p targeting ETVT and BATF2 to upregulate the PAI-1/ERK pathway, leading to increased viability in BC cells. (* P < 0.05, ** P < 0.01, *** P < 0.001)
    Figure Legend Snippet: Elevated plasma exosomal miR-361-3p promotes the malignant progression of BC in mice. A Upper panel : A schematic diagram of the animal experiments. Lower panel : A T47D cell xenograft model in female BALB/c nude mice was established. Mice exhibiting a high abundance of plasma exosomal miR-361-3p, as well as control mice, were obtained through the tail vein injection of EXO-miR-361-3p or EXO-miR-NC, respectively. B Differences in volume, weight and growth rate of murine tumors in the EXO-miR-361-3p group compared to the control group. C H&E staining of murine tumor tissues (×40). D – F Compare the expression levels of miR-361-3p, ETV7 , BATF2 , and the PAI-1/ERK pathway in excised tumors of the two groups of mice. G Proposed model of exosomal miR-361-3p targeting ETVT and BATF2 to upregulate the PAI-1/ERK pathway, leading to increased viability in BC cells. (* P < 0.05, ** P < 0.01, *** P < 0.001)

    Techniques Used: Clinical Proteomics, Control, Injection, Staining, Expressing

    ETV7 and BATF2 are two new targets of miR-361-3p. A The GO analysis revealed distinct pathways enriched by genes that are either downregulated or upregulated in BC cells overexpressing miR-361-3p. B Intersection of our RNA-seq results (displayed as a heatmap) and miRNA target prediction algorithms from 2 databases. C – D miR-361-3p putative targeting sites in the wild-type and mutant ETV7 3'UTR and BATF2 3'UTR, and luciferase activity assays were performed to confirm the direct binding efficiency of miR-361-3p and its targets ETV7 and BATF2. E – F Relative protein expression of ETV7 and BATF2 after coculturing BC cells with EXO-miR-361-3p/EXO-miR-NC. (* P < 0.05)
    Figure Legend Snippet: ETV7 and BATF2 are two new targets of miR-361-3p. A The GO analysis revealed distinct pathways enriched by genes that are either downregulated or upregulated in BC cells overexpressing miR-361-3p. B Intersection of our RNA-seq results (displayed as a heatmap) and miRNA target prediction algorithms from 2 databases. C – D miR-361-3p putative targeting sites in the wild-type and mutant ETV7 3'UTR and BATF2 3'UTR, and luciferase activity assays were performed to confirm the direct binding efficiency of miR-361-3p and its targets ETV7 and BATF2. E – F Relative protein expression of ETV7 and BATF2 after coculturing BC cells with EXO-miR-361-3p/EXO-miR-NC. (* P < 0.05)

    Techniques Used: RNA Sequencing, Mutagenesis, Luciferase, Activity Assay, Binding Assay, Expressing

    ETV7 and BATF2 negatively regulate the PAI-1/ERK pathway as well as the proliferation and migration of BC cells. A Relative protein expression of PAI-1, p-ERK and T-ERK after coculturing BC cells with EXO-miR-361-3p/EXO-miR-NC. B , F Relative expression of ETV7, BATF2, PAI-1 and p-ERK/T-ERK protein after ETV7 and/or BATF2 knockdown or overexpression (* P < 0.05, ** P < 0.01, *** P < 0.001). CellTiter-Glo assays ( C , G ), wound healing assays ( D , H ) and Transwell assays ( E , I ) were performed to test the effect of ETV7 and/or BATF2 knockdown or overexpression on BC cell proliferation and metastasis. Scale bars, 100 μm
    Figure Legend Snippet: ETV7 and BATF2 negatively regulate the PAI-1/ERK pathway as well as the proliferation and migration of BC cells. A Relative protein expression of PAI-1, p-ERK and T-ERK after coculturing BC cells with EXO-miR-361-3p/EXO-miR-NC. B , F Relative expression of ETV7, BATF2, PAI-1 and p-ERK/T-ERK protein after ETV7 and/or BATF2 knockdown or overexpression (* P < 0.05, ** P < 0.01, *** P < 0.001). CellTiter-Glo assays ( C , G ), wound healing assays ( D , H ) and Transwell assays ( E , I ) were performed to test the effect of ETV7 and/or BATF2 knockdown or overexpression on BC cell proliferation and metastasis. Scale bars, 100 μm

    Techniques Used: Migration, Expressing, Knockdown, Over Expression



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    Elevated plasma exosomal miR-361-3p promotes the malignant progression of BC in mice. A Upper panel : A schematic diagram of the animal experiments. Lower panel : A T47D cell xenograft model in female BALB/c nude mice was established. Mice exhibiting a high abundance of plasma exosomal miR-361-3p, as well as control mice, were obtained through the tail vein injection of EXO-miR-361-3p or EXO-miR-NC, respectively. B Differences in volume, weight and growth rate of murine tumors in the EXO-miR-361-3p group compared to the control group. C H&E staining of murine tumor tissues (×40). D – F Compare the expression levels of miR-361-3p, ETV7 , <t>BATF2</t> , and the PAI-1/ERK pathway in excised tumors of the two groups of mice. G Proposed model of exosomal miR-361-3p targeting ETVT and BATF2 to upregulate the PAI-1/ERK pathway, leading to increased viability in BC cells. (* P < 0.05, ** P < 0.01, *** P < 0.001)
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    Image Search Results


    Elevated plasma exosomal miR-361-3p promotes the malignant progression of BC in mice. A Upper panel : A schematic diagram of the animal experiments. Lower panel : A T47D cell xenograft model in female BALB/c nude mice was established. Mice exhibiting a high abundance of plasma exosomal miR-361-3p, as well as control mice, were obtained through the tail vein injection of EXO-miR-361-3p or EXO-miR-NC, respectively. B Differences in volume, weight and growth rate of murine tumors in the EXO-miR-361-3p group compared to the control group. C H&E staining of murine tumor tissues (×40). D – F Compare the expression levels of miR-361-3p, ETV7 , BATF2 , and the PAI-1/ERK pathway in excised tumors of the two groups of mice. G Proposed model of exosomal miR-361-3p targeting ETVT and BATF2 to upregulate the PAI-1/ERK pathway, leading to increased viability in BC cells. (* P < 0.05, ** P < 0.01, *** P < 0.001)

    Journal: Journal of Translational Medicine

    Article Title: Exosomal miR-361-3p promotes the viability of breast cancer cells by targeting ETV7 and BATF2 to upregulate the PAI-1/ERK pathway

    doi: 10.1186/s12967-024-04914-4

    Figure Lengend Snippet: Elevated plasma exosomal miR-361-3p promotes the malignant progression of BC in mice. A Upper panel : A schematic diagram of the animal experiments. Lower panel : A T47D cell xenograft model in female BALB/c nude mice was established. Mice exhibiting a high abundance of plasma exosomal miR-361-3p, as well as control mice, were obtained through the tail vein injection of EXO-miR-361-3p or EXO-miR-NC, respectively. B Differences in volume, weight and growth rate of murine tumors in the EXO-miR-361-3p group compared to the control group. C H&E staining of murine tumor tissues (×40). D – F Compare the expression levels of miR-361-3p, ETV7 , BATF2 , and the PAI-1/ERK pathway in excised tumors of the two groups of mice. G Proposed model of exosomal miR-361-3p targeting ETVT and BATF2 to upregulate the PAI-1/ERK pathway, leading to increased viability in BC cells. (* P < 0.05, ** P < 0.01, *** P < 0.001)

    Article Snippet: Human ETVT cDNA plasmid ( ETV7 plasmid), BATF2 cDNA plasmid ( BATF2 plasmid), PAI-1 cDNA plasmid ( PAI-1 plasmid) and negative control plasmid (control plasmid) were transfected into cells using Lipofectamine 2000 (Invitrogen; Thermo Fisher Scientific, Inc.).

    Techniques: Clinical Proteomics, Control, Injection, Staining, Expressing

    ETV7 and BATF2 are two new targets of miR-361-3p. A The GO analysis revealed distinct pathways enriched by genes that are either downregulated or upregulated in BC cells overexpressing miR-361-3p. B Intersection of our RNA-seq results (displayed as a heatmap) and miRNA target prediction algorithms from 2 databases. C – D miR-361-3p putative targeting sites in the wild-type and mutant ETV7 3'UTR and BATF2 3'UTR, and luciferase activity assays were performed to confirm the direct binding efficiency of miR-361-3p and its targets ETV7 and BATF2. E – F Relative protein expression of ETV7 and BATF2 after coculturing BC cells with EXO-miR-361-3p/EXO-miR-NC. (* P < 0.05)

    Journal: Journal of Translational Medicine

    Article Title: Exosomal miR-361-3p promotes the viability of breast cancer cells by targeting ETV7 and BATF2 to upregulate the PAI-1/ERK pathway

    doi: 10.1186/s12967-024-04914-4

    Figure Lengend Snippet: ETV7 and BATF2 are two new targets of miR-361-3p. A The GO analysis revealed distinct pathways enriched by genes that are either downregulated or upregulated in BC cells overexpressing miR-361-3p. B Intersection of our RNA-seq results (displayed as a heatmap) and miRNA target prediction algorithms from 2 databases. C – D miR-361-3p putative targeting sites in the wild-type and mutant ETV7 3'UTR and BATF2 3'UTR, and luciferase activity assays were performed to confirm the direct binding efficiency of miR-361-3p and its targets ETV7 and BATF2. E – F Relative protein expression of ETV7 and BATF2 after coculturing BC cells with EXO-miR-361-3p/EXO-miR-NC. (* P < 0.05)

    Article Snippet: Human ETVT cDNA plasmid ( ETV7 plasmid), BATF2 cDNA plasmid ( BATF2 plasmid), PAI-1 cDNA plasmid ( PAI-1 plasmid) and negative control plasmid (control plasmid) were transfected into cells using Lipofectamine 2000 (Invitrogen; Thermo Fisher Scientific, Inc.).

    Techniques: RNA Sequencing, Mutagenesis, Luciferase, Activity Assay, Binding Assay, Expressing

    ETV7 and BATF2 negatively regulate the PAI-1/ERK pathway as well as the proliferation and migration of BC cells. A Relative protein expression of PAI-1, p-ERK and T-ERK after coculturing BC cells with EXO-miR-361-3p/EXO-miR-NC. B , F Relative expression of ETV7, BATF2, PAI-1 and p-ERK/T-ERK protein after ETV7 and/or BATF2 knockdown or overexpression (* P < 0.05, ** P < 0.01, *** P < 0.001). CellTiter-Glo assays ( C , G ), wound healing assays ( D , H ) and Transwell assays ( E , I ) were performed to test the effect of ETV7 and/or BATF2 knockdown or overexpression on BC cell proliferation and metastasis. Scale bars, 100 μm

    Journal: Journal of Translational Medicine

    Article Title: Exosomal miR-361-3p promotes the viability of breast cancer cells by targeting ETV7 and BATF2 to upregulate the PAI-1/ERK pathway

    doi: 10.1186/s12967-024-04914-4

    Figure Lengend Snippet: ETV7 and BATF2 negatively regulate the PAI-1/ERK pathway as well as the proliferation and migration of BC cells. A Relative protein expression of PAI-1, p-ERK and T-ERK after coculturing BC cells with EXO-miR-361-3p/EXO-miR-NC. B , F Relative expression of ETV7, BATF2, PAI-1 and p-ERK/T-ERK protein after ETV7 and/or BATF2 knockdown or overexpression (* P < 0.05, ** P < 0.01, *** P < 0.001). CellTiter-Glo assays ( C , G ), wound healing assays ( D , H ) and Transwell assays ( E , I ) were performed to test the effect of ETV7 and/or BATF2 knockdown or overexpression on BC cell proliferation and metastasis. Scale bars, 100 μm

    Article Snippet: Human ETVT cDNA plasmid ( ETV7 plasmid), BATF2 cDNA plasmid ( BATF2 plasmid), PAI-1 cDNA plasmid ( PAI-1 plasmid) and negative control plasmid (control plasmid) were transfected into cells using Lipofectamine 2000 (Invitrogen; Thermo Fisher Scientific, Inc.).

    Techniques: Migration, Expressing, Knockdown, Over Expression