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cdh1 human cdna orf  (OriGene)


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    Structured Review

    OriGene cdh1 human cdna orf
    (A) Luciferase reporter plasmids containing the putative wild-type or mutant miR-23a binding sequence in 3’-UTR of <t>CDH1</t> mRNA. (B) HEK293T cells were co-transfected with a control vector or miR-23a and a luciferase reporter construct containing the wild-type or mutant CDH1 3’-UTR. The results were normalized, and the luciferase activity of the control was set to 1. (C and D) Effects of miR-23a dysregulation of CDH1 expression were detected by western blot analysis in MCF-7 and MDA-MB-231 cells. (E) Real-time PCR analysis of CDH1 mRNA expression of the NC and anti-miR-23a-transfected cells treated with or without TGF-β1. *P<0.05, **P<0.01.
    Cdh1 Human Cdna Orf, supplied by OriGene, used in various techniques. Bioz Stars score: 93/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cdh1+human+cdna+orf+clone/E+Cadherin+(CDH1)+(NM_004360)+Human+Tagged+ORF+Clone/pmc05642498-161-0-8
    Average 93 stars, based on 7 article reviews
    cdh1 human cdna orf - by Bioz Stars, 2026-10
    93/100 stars

    Images

    1) Product Images from "MiR-23a promotes TGF-β1-induced EMT and tumor metastasis in breast cancer cells by directly targeting CDH1 and activating Wnt/β-catenin signaling"

    Article Title: MiR-23a promotes TGF-β1-induced EMT and tumor metastasis in breast cancer cells by directly targeting CDH1 and activating Wnt/β-catenin signaling

    Journal: Oncotarget

    doi: 10.18632/oncotarget.18422

    (A) Luciferase reporter plasmids containing the putative wild-type or mutant miR-23a binding sequence in 3’-UTR of CDH1 mRNA. (B) HEK293T cells were co-transfected with a control vector or miR-23a and a luciferase reporter construct containing the wild-type or mutant CDH1 3’-UTR. The results were normalized, and the luciferase activity of the control was set to 1. (C and D) Effects of miR-23a dysregulation of CDH1 expression were detected by western blot analysis in MCF-7 and MDA-MB-231 cells. (E) Real-time PCR analysis of CDH1 mRNA expression of the NC and anti-miR-23a-transfected cells treated with or without TGF-β1. *P<0.05, **P<0.01.
    Figure Legend Snippet: (A) Luciferase reporter plasmids containing the putative wild-type or mutant miR-23a binding sequence in 3’-UTR of CDH1 mRNA. (B) HEK293T cells were co-transfected with a control vector or miR-23a and a luciferase reporter construct containing the wild-type or mutant CDH1 3’-UTR. The results were normalized, and the luciferase activity of the control was set to 1. (C and D) Effects of miR-23a dysregulation of CDH1 expression were detected by western blot analysis in MCF-7 and MDA-MB-231 cells. (E) Real-time PCR analysis of CDH1 mRNA expression of the NC and anti-miR-23a-transfected cells treated with or without TGF-β1. *P<0.05, **P<0.01.

    Techniques Used: Luciferase, Mutagenesis, Binding Assay, Sequencing, Transfection, Control, Plasmid Preparation, Construct, Activity Assay, Expressing, Western Blot, Real-time Polymerase Chain Reaction

    (A) Western blot analysis confirmed the transfection of constructs containing CDH1 ORF in cells treated with TGF-β1. (B) Western blot analysis confirmed the transfection of specific siRNA in miR-23a-silenced cells treated with TGF-β1. (C) Reintroduction of E-cadherin in TGF-β1-treated MDA-MB-231 cells abrogated TGF-β1-induced cell invasion. MiR-23a inhibitor reduced the invasion and migration cells treated by TGF-β1 and siCDH1 restored the cell invasion and migration in miR-23a-silenced cells. (D) Tumor metastasis analysis. The number of metastatic lung nodules in each group of nude mice (n= 6 per group, left panel). Representative photos of nude mice injected with indicated cells and micrographs of HE staining of metastatic tumor tissues (right panel). *P<0.05, **P<0.01.
    Figure Legend Snippet: (A) Western blot analysis confirmed the transfection of constructs containing CDH1 ORF in cells treated with TGF-β1. (B) Western blot analysis confirmed the transfection of specific siRNA in miR-23a-silenced cells treated with TGF-β1. (C) Reintroduction of E-cadherin in TGF-β1-treated MDA-MB-231 cells abrogated TGF-β1-induced cell invasion. MiR-23a inhibitor reduced the invasion and migration cells treated by TGF-β1 and siCDH1 restored the cell invasion and migration in miR-23a-silenced cells. (D) Tumor metastasis analysis. The number of metastatic lung nodules in each group of nude mice (n= 6 per group, left panel). Representative photos of nude mice injected with indicated cells and micrographs of HE staining of metastatic tumor tissues (right panel). *P<0.05, **P<0.01.

    Techniques Used: Western Blot, Transfection, Construct, Migration, Injection, Staining

    (A) Nuclear fraction of indicated cells was analyzed by Western blot. Lamin B1 was used as a loading control. (B) Beta-catenin localization in indicated cells was detected by immunofluorescence staining. (C) Indicated cells were transfected with TOPflash and Renilla pRL-TK plasmids, and subjected to dual –luciferase assays 48h after transfection. Reporter activity was normalized to Renilla luciferase activity. (D and E) Transwell assays were used to detect the quantification of invading cells transfected with indicated siRNAs and luciferase-reported TCF/LEF transcriptional activity in indicated cells were examined. (F) Western blot analysis was used to confirm the transfection of constructs containing CDH1 ORF in miR-23a overexpressed MCF-7 cells (left panel). Quantification of invading cells transfected with indicated construct (middle panel) and luciferase-reported TCF/LEF transcriptional activity in indicated cells (right panel). (G) Luciferase-reported TCF/LEF transcriptional activity in NC, cells treated with TGF-β1 or miR-23a silenced-cells treated with TGF-β1. (H) Schematic representation of a model for the role of miR-23a in the TGF-β-induced tumor metastasis in breast cancer. *P<0.05, **P<0.01.
    Figure Legend Snippet: (A) Nuclear fraction of indicated cells was analyzed by Western blot. Lamin B1 was used as a loading control. (B) Beta-catenin localization in indicated cells was detected by immunofluorescence staining. (C) Indicated cells were transfected with TOPflash and Renilla pRL-TK plasmids, and subjected to dual –luciferase assays 48h after transfection. Reporter activity was normalized to Renilla luciferase activity. (D and E) Transwell assays were used to detect the quantification of invading cells transfected with indicated siRNAs and luciferase-reported TCF/LEF transcriptional activity in indicated cells were examined. (F) Western blot analysis was used to confirm the transfection of constructs containing CDH1 ORF in miR-23a overexpressed MCF-7 cells (left panel). Quantification of invading cells transfected with indicated construct (middle panel) and luciferase-reported TCF/LEF transcriptional activity in indicated cells (right panel). (G) Luciferase-reported TCF/LEF transcriptional activity in NC, cells treated with TGF-β1 or miR-23a silenced-cells treated with TGF-β1. (H) Schematic representation of a model for the role of miR-23a in the TGF-β-induced tumor metastasis in breast cancer. *P<0.05, **P<0.01.

    Techniques Used: Western Blot, Control, Immunofluorescence, Staining, Transfection, Luciferase, Activity Assay, Construct

    Related Articles

    Plasmid Preparation:

    Article Title: SAHA, an HDAC inhibitor, overcomes erlotinib resistance in human pancreatic cancer cells by modulating E-cadherin.
    Article Snippet: Pancreatic cancer is one of the most lethal cancers and remains a major unsolved health problem.. Less than 20% of patients are surgical candidates, and the median survival for non-resected patients is approximately 3 to 4 months.. Despite the existence of many conventional cancer therapies, few targeted therapies have been developed for pancreatic cancer.

    Transfection:

    Article Title: SAHA, an HDAC inhibitor, overcomes erlotinib resistance in human pancreatic cancer cells by modulating E-cadherin.
    Article Snippet: Pancreatic cancer is one of the most lethal cancers and remains a major unsolved health problem.. Less than 20% of patients are surgical candidates, and the median survival for non-resected patients is approximately 3 to 4 months.. Despite the existence of many conventional cancer therapies, few targeted therapies have been developed for pancreatic cancer.

    Transduction:

    Article Title: SAHA, an HDAC inhibitor, overcomes erlotinib resistance in human pancreatic cancer cells by modulating E-cadherin.
    Article Snippet: Pancreatic cancer is one of the most lethal cancers and remains a major unsolved health problem.. Less than 20% of patients are surgical candidates, and the median survival for non-resected patients is approximately 3 to 4 months.. Despite the existence of many conventional cancer therapies, few targeted therapies have been developed for pancreatic cancer.



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    (A) Luciferase reporter plasmids containing the putative wild-type or mutant miR-23a binding sequence in 3’-UTR of <t>CDH1</t> mRNA. (B) HEK293T cells were co-transfected with a control vector or miR-23a and a luciferase reporter construct containing the wild-type or mutant CDH1 3’-UTR. The results were normalized, and the luciferase activity of the control was set to 1. (C and D) Effects of miR-23a dysregulation of CDH1 expression were detected by western blot analysis in MCF-7 and MDA-MB-231 cells. (E) Real-time PCR analysis of CDH1 mRNA expression of the NC and anti-miR-23a-transfected cells treated with or without TGF-β1. *P<0.05, **P<0.01.
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    (A) Luciferase reporter plasmids containing the putative wild-type or mutant miR-23a binding sequence in 3’-UTR of <t>CDH1</t> mRNA. (B) HEK293T cells were co-transfected with a control vector or miR-23a and a luciferase reporter construct containing the wild-type or mutant CDH1 3’-UTR. The results were normalized, and the luciferase activity of the control was set to 1. (C and D) Effects of miR-23a dysregulation of CDH1 expression were detected by western blot analysis in MCF-7 and MDA-MB-231 cells. (E) Real-time PCR analysis of CDH1 mRNA expression of the NC and anti-miR-23a-transfected cells treated with or without TGF-β1. *P<0.05, **P<0.01.
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    Image Search Results


    (A) Luciferase reporter plasmids containing the putative wild-type or mutant miR-23a binding sequence in 3’-UTR of CDH1 mRNA. (B) HEK293T cells were co-transfected with a control vector or miR-23a and a luciferase reporter construct containing the wild-type or mutant CDH1 3’-UTR. The results were normalized, and the luciferase activity of the control was set to 1. (C and D) Effects of miR-23a dysregulation of CDH1 expression were detected by western blot analysis in MCF-7 and MDA-MB-231 cells. (E) Real-time PCR analysis of CDH1 mRNA expression of the NC and anti-miR-23a-transfected cells treated with or without TGF-β1. *P<0.05, **P<0.01.

    Journal: Oncotarget

    Article Title: MiR-23a promotes TGF-β1-induced EMT and tumor metastasis in breast cancer cells by directly targeting CDH1 and activating Wnt/β-catenin signaling

    doi: 10.18632/oncotarget.18422

    Figure Lengend Snippet: (A) Luciferase reporter plasmids containing the putative wild-type or mutant miR-23a binding sequence in 3’-UTR of CDH1 mRNA. (B) HEK293T cells were co-transfected with a control vector or miR-23a and a luciferase reporter construct containing the wild-type or mutant CDH1 3’-UTR. The results were normalized, and the luciferase activity of the control was set to 1. (C and D) Effects of miR-23a dysregulation of CDH1 expression were detected by western blot analysis in MCF-7 and MDA-MB-231 cells. (E) Real-time PCR analysis of CDH1 mRNA expression of the NC and anti-miR-23a-transfected cells treated with or without TGF-β1. *P<0.05, **P<0.01.

    Article Snippet: CDH1 Human cDNA ORF Clone was purchased from Origene (Origene Technologies).

    Techniques: Luciferase, Mutagenesis, Binding Assay, Sequencing, Transfection, Control, Plasmid Preparation, Construct, Activity Assay, Expressing, Western Blot, Real-time Polymerase Chain Reaction

    (A) Western blot analysis confirmed the transfection of constructs containing CDH1 ORF in cells treated with TGF-β1. (B) Western blot analysis confirmed the transfection of specific siRNA in miR-23a-silenced cells treated with TGF-β1. (C) Reintroduction of E-cadherin in TGF-β1-treated MDA-MB-231 cells abrogated TGF-β1-induced cell invasion. MiR-23a inhibitor reduced the invasion and migration cells treated by TGF-β1 and siCDH1 restored the cell invasion and migration in miR-23a-silenced cells. (D) Tumor metastasis analysis. The number of metastatic lung nodules in each group of nude mice (n= 6 per group, left panel). Representative photos of nude mice injected with indicated cells and micrographs of HE staining of metastatic tumor tissues (right panel). *P<0.05, **P<0.01.

    Journal: Oncotarget

    Article Title: MiR-23a promotes TGF-β1-induced EMT and tumor metastasis in breast cancer cells by directly targeting CDH1 and activating Wnt/β-catenin signaling

    doi: 10.18632/oncotarget.18422

    Figure Lengend Snippet: (A) Western blot analysis confirmed the transfection of constructs containing CDH1 ORF in cells treated with TGF-β1. (B) Western blot analysis confirmed the transfection of specific siRNA in miR-23a-silenced cells treated with TGF-β1. (C) Reintroduction of E-cadherin in TGF-β1-treated MDA-MB-231 cells abrogated TGF-β1-induced cell invasion. MiR-23a inhibitor reduced the invasion and migration cells treated by TGF-β1 and siCDH1 restored the cell invasion and migration in miR-23a-silenced cells. (D) Tumor metastasis analysis. The number of metastatic lung nodules in each group of nude mice (n= 6 per group, left panel). Representative photos of nude mice injected with indicated cells and micrographs of HE staining of metastatic tumor tissues (right panel). *P<0.05, **P<0.01.

    Article Snippet: CDH1 Human cDNA ORF Clone was purchased from Origene (Origene Technologies).

    Techniques: Western Blot, Transfection, Construct, Migration, Injection, Staining

    (A) Nuclear fraction of indicated cells was analyzed by Western blot. Lamin B1 was used as a loading control. (B) Beta-catenin localization in indicated cells was detected by immunofluorescence staining. (C) Indicated cells were transfected with TOPflash and Renilla pRL-TK plasmids, and subjected to dual –luciferase assays 48h after transfection. Reporter activity was normalized to Renilla luciferase activity. (D and E) Transwell assays were used to detect the quantification of invading cells transfected with indicated siRNAs and luciferase-reported TCF/LEF transcriptional activity in indicated cells were examined. (F) Western blot analysis was used to confirm the transfection of constructs containing CDH1 ORF in miR-23a overexpressed MCF-7 cells (left panel). Quantification of invading cells transfected with indicated construct (middle panel) and luciferase-reported TCF/LEF transcriptional activity in indicated cells (right panel). (G) Luciferase-reported TCF/LEF transcriptional activity in NC, cells treated with TGF-β1 or miR-23a silenced-cells treated with TGF-β1. (H) Schematic representation of a model for the role of miR-23a in the TGF-β-induced tumor metastasis in breast cancer. *P<0.05, **P<0.01.

    Journal: Oncotarget

    Article Title: MiR-23a promotes TGF-β1-induced EMT and tumor metastasis in breast cancer cells by directly targeting CDH1 and activating Wnt/β-catenin signaling

    doi: 10.18632/oncotarget.18422

    Figure Lengend Snippet: (A) Nuclear fraction of indicated cells was analyzed by Western blot. Lamin B1 was used as a loading control. (B) Beta-catenin localization in indicated cells was detected by immunofluorescence staining. (C) Indicated cells were transfected with TOPflash and Renilla pRL-TK plasmids, and subjected to dual –luciferase assays 48h after transfection. Reporter activity was normalized to Renilla luciferase activity. (D and E) Transwell assays were used to detect the quantification of invading cells transfected with indicated siRNAs and luciferase-reported TCF/LEF transcriptional activity in indicated cells were examined. (F) Western blot analysis was used to confirm the transfection of constructs containing CDH1 ORF in miR-23a overexpressed MCF-7 cells (left panel). Quantification of invading cells transfected with indicated construct (middle panel) and luciferase-reported TCF/LEF transcriptional activity in indicated cells (right panel). (G) Luciferase-reported TCF/LEF transcriptional activity in NC, cells treated with TGF-β1 or miR-23a silenced-cells treated with TGF-β1. (H) Schematic representation of a model for the role of miR-23a in the TGF-β-induced tumor metastasis in breast cancer. *P<0.05, **P<0.01.

    Article Snippet: CDH1 Human cDNA ORF Clone was purchased from Origene (Origene Technologies).

    Techniques: Western Blot, Control, Immunofluorescence, Staining, Transfection, Luciferase, Activity Assay, Construct