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ctr1 sirna si ctr1  (Santa Cruz Biotechnology)


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    Santa Cruz Biotechnology ctr1 sirna si ctr1
    High expressions of <t>Ctr1</t> mRNA and protein in ESCC tissues and cells. A: Representative image of Ctr1 high expression in ESCC tissues by ISH and IHC; ISH and IHC assay for Ctr1 mRNA and protein expressions in 108 cases of ESCC tissues and paired normal esophageal epithelial tissues, Bar=100 μm. B: Semi-quantitative RT-PCR detection for Ctr1 mRNA expression in randomly selected 10 cases of ESCC tissues and paired normal tissues using Ctr1 specific primers. C: Statistical assay for Ctr1 relative level in ESCC tissues and paired normal tissues, * P <0.05, ** P <0.01, *** P <0.001 and **** P <0.0001, compared para-carcinoma tissues. D: qRT-PCR assay for Ctr1 mRNA expression in ESCC cell lines (Kyse70, Eca109, and Kyse450 cells), ** P <0.01 and *** P <0.001, compared with Het-1A cell. E: Western blot analysis for Ctr1 protein expression in ESCC cell lines (Kyse70, Eca109, and Kyse450 cells), and β-actin was used as loading control. F: Relative Ctr1 protein level in various ESCC cell lines (Kyse70, Eca109, and Kyse450 cells), ** P <0.01, compared with Het-1A cell.
    Ctr1 Sirna Si Ctr1, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ctr1+sirna+si+ctr1/pmc09876974-69-7-10?v=Santa+Cruz+Biotechnology
    Average 94 stars, based on 3 article reviews
    ctr1 sirna si ctr1 - by Bioz Stars, 2026-08
    94/100 stars

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    1) Product Images from "Copper transporter Ctr1 contributes to enhancement of the sensitivity of cisplatin in esophageal squamous cell carcinoma"

    Article Title: Copper transporter Ctr1 contributes to enhancement of the sensitivity of cisplatin in esophageal squamous cell carcinoma

    Journal: Translational Oncology

    doi: 10.1016/j.tranon.2023.101626

    High expressions of Ctr1 mRNA and protein in ESCC tissues and cells. A: Representative image of Ctr1 high expression in ESCC tissues by ISH and IHC; ISH and IHC assay for Ctr1 mRNA and protein expressions in 108 cases of ESCC tissues and paired normal esophageal epithelial tissues, Bar=100 μm. B: Semi-quantitative RT-PCR detection for Ctr1 mRNA expression in randomly selected 10 cases of ESCC tissues and paired normal tissues using Ctr1 specific primers. C: Statistical assay for Ctr1 relative level in ESCC tissues and paired normal tissues, * P <0.05, ** P <0.01, *** P <0.001 and **** P <0.0001, compared para-carcinoma tissues. D: qRT-PCR assay for Ctr1 mRNA expression in ESCC cell lines (Kyse70, Eca109, and Kyse450 cells), ** P <0.01 and *** P <0.001, compared with Het-1A cell. E: Western blot analysis for Ctr1 protein expression in ESCC cell lines (Kyse70, Eca109, and Kyse450 cells), and β-actin was used as loading control. F: Relative Ctr1 protein level in various ESCC cell lines (Kyse70, Eca109, and Kyse450 cells), ** P <0.01, compared with Het-1A cell.
    Figure Legend Snippet: High expressions of Ctr1 mRNA and protein in ESCC tissues and cells. A: Representative image of Ctr1 high expression in ESCC tissues by ISH and IHC; ISH and IHC assay for Ctr1 mRNA and protein expressions in 108 cases of ESCC tissues and paired normal esophageal epithelial tissues, Bar=100 μm. B: Semi-quantitative RT-PCR detection for Ctr1 mRNA expression in randomly selected 10 cases of ESCC tissues and paired normal tissues using Ctr1 specific primers. C: Statistical assay for Ctr1 relative level in ESCC tissues and paired normal tissues, * P <0.05, ** P <0.01, *** P <0.001 and **** P <0.0001, compared para-carcinoma tissues. D: qRT-PCR assay for Ctr1 mRNA expression in ESCC cell lines (Kyse70, Eca109, and Kyse450 cells), ** P <0.01 and *** P <0.001, compared with Het-1A cell. E: Western blot analysis for Ctr1 protein expression in ESCC cell lines (Kyse70, Eca109, and Kyse450 cells), and β-actin was used as loading control. F: Relative Ctr1 protein level in various ESCC cell lines (Kyse70, Eca109, and Kyse450 cells), ** P <0.01, compared with Het-1A cell.

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

    The expressions of Ctr1 mRNA and protein in ESCC tissues and normal tissues.
    Figure Legend Snippet: The expressions of Ctr1 mRNA and protein in ESCC tissues and normal tissues.

    Techniques Used:

    The associations of Ctr1 mRNA and protein expressions with clinicopathological features in ESCC.
    Figure Legend Snippet: The associations of Ctr1 mRNA and protein expressions with clinicopathological features in ESCC.

    Techniques Used:

    The Ctr1 downregulation reduces the sensitivity of cisplatin in ESCC cells. A: Ctr1 siRNA significantly suppressed Ctr1 mRNA expression at 24 h, 48 h and 72 h in various ESCC cells (Eca109, Kyse70 and Kyse450), si-Con and si-Ctr1 were transfected to Eca109, Kyse70 and Kyse450 cells by Lipofectamine™ 2000, and Semi-quantitative RT-PCR was used to determine the relative level of Ctr1 at 24 h, 48 h and 72 h after transfection, ** P <0.01 and *** P <0.001, compared with control group and si-Con group. B: Western blot was performed to investigate the Ctr1 protein expression at 24 h, 48 h and 72 h after transfection with si-Ctr1 and si-Con in different ESCC cells (Eca109, Kyse70 and Kyse450), and β-actin was employed as a loading control. C: The relative level of Ctr1 was counted using the rate of Ctr1 protein level to β-actin level in diverse ESCC cells (Eca109, Kyse70 and Kyse450), * P <0.05, ** P <0.01 and *** P <0.001, compared with control group and si-Con group. D: The Ctr1 downregulation reduced the cytotoxicity of cisplatin in distinct ESCC cells. ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and CCK-8 was used to determine cell viability, * P <0.05, ** P <0.01, *** P <0.001 and **** P <0.0001, indicating statistical significance, compared with si-Con.
    Figure Legend Snippet: The Ctr1 downregulation reduces the sensitivity of cisplatin in ESCC cells. A: Ctr1 siRNA significantly suppressed Ctr1 mRNA expression at 24 h, 48 h and 72 h in various ESCC cells (Eca109, Kyse70 and Kyse450), si-Con and si-Ctr1 were transfected to Eca109, Kyse70 and Kyse450 cells by Lipofectamine™ 2000, and Semi-quantitative RT-PCR was used to determine the relative level of Ctr1 at 24 h, 48 h and 72 h after transfection, ** P <0.01 and *** P <0.001, compared with control group and si-Con group. B: Western blot was performed to investigate the Ctr1 protein expression at 24 h, 48 h and 72 h after transfection with si-Ctr1 and si-Con in different ESCC cells (Eca109, Kyse70 and Kyse450), and β-actin was employed as a loading control. C: The relative level of Ctr1 was counted using the rate of Ctr1 protein level to β-actin level in diverse ESCC cells (Eca109, Kyse70 and Kyse450), * P <0.05, ** P <0.01 and *** P <0.001, compared with control group and si-Con group. D: The Ctr1 downregulation reduced the cytotoxicity of cisplatin in distinct ESCC cells. ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and CCK-8 was used to determine cell viability, * P <0.05, ** P <0.01, *** P <0.001 and **** P <0.0001, indicating statistical significance, compared with si-Con.

    Techniques Used: Expressing, Transfection, Quantitative RT-PCR, Control, Western Blot, CCK-8 Assay

    Ctr1 depletion prominently repressed cell apoptosis evoked by cisplatin in ESCC cells. A: Flow cytometry assay for cell apoptosis in different ESCC cells treated with si-Con, si-Con plus cisplatin, si-Ctr1 as well as si-Ctr1 plus cisplatin; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Flow cytometry was employed to determine cell apoptosis. B: Statistical assay for apoptotic cell numbers in different ESCC cells treated with si-Con, si-Con plus cisplatin, si-Ctr1 as well as si-Ctr1 plus cisplatin, *** P <0.001 and **** P <0.0001, compared with si-Con plus cisplatin group. C: Ctr1 depletion combined cisplatin significantly suppressed the activity of Caspase-3 induced by cisplatin plus si-Con; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Caspase-3 activity kit was utilized to determine the activity of Caspase-3, *** P <0.001, compared with si-Con plus cisplatin group.
    Figure Legend Snippet: Ctr1 depletion prominently repressed cell apoptosis evoked by cisplatin in ESCC cells. A: Flow cytometry assay for cell apoptosis in different ESCC cells treated with si-Con, si-Con plus cisplatin, si-Ctr1 as well as si-Ctr1 plus cisplatin; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Flow cytometry was employed to determine cell apoptosis. B: Statistical assay for apoptotic cell numbers in different ESCC cells treated with si-Con, si-Con plus cisplatin, si-Ctr1 as well as si-Ctr1 plus cisplatin, *** P <0.001 and **** P <0.0001, compared with si-Con plus cisplatin group. C: Ctr1 depletion combined cisplatin significantly suppressed the activity of Caspase-3 induced by cisplatin plus si-Con; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Caspase-3 activity kit was utilized to determine the activity of Caspase-3, *** P <0.001, compared with si-Con plus cisplatin group.

    Techniques Used: Flow Cytometry, Transfection, Activity Assay

    The Ctr1 downregulation meliorated cell migration and invasion abilities inhibited by cisplatin in number of ESCC cells. A: Transwell assay for cell migration in various ESCC cells treated with si-Con, si-Con plus cisplatin, si-Ctr1 and si-Ctr1 plus cisplatin; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Transwell chamber without Matrigel was employed to determine cell migration. B: Statistical assay for migratory cell numbers in different ESCC cells treated with si-Con, si-Con plus cisplatin, si-Ctr1 and si-Ctr1 plus cisplatin, *** P <0.001, compared with si-Con plus cisplatin group. C: Transwell assay for cell invasion in varied ESCC cells treated with si-Con, si-Con plus cisplatin, si-Ctr1 and si-Ctr1 plus cisplatin; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Transwell chamber with Matrigel was used to determine cell invasion. D: Statistical assay for invasive cell numbers in a variety of ESCC cells treated with si-Con, si-Con plus cisplatin, si-Ctr1 and si-Ctr1 plus cisplatin, *** P <0.001, compared with si-Con plus cisplatin group.
    Figure Legend Snippet: The Ctr1 downregulation meliorated cell migration and invasion abilities inhibited by cisplatin in number of ESCC cells. A: Transwell assay for cell migration in various ESCC cells treated with si-Con, si-Con plus cisplatin, si-Ctr1 and si-Ctr1 plus cisplatin; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Transwell chamber without Matrigel was employed to determine cell migration. B: Statistical assay for migratory cell numbers in different ESCC cells treated with si-Con, si-Con plus cisplatin, si-Ctr1 and si-Ctr1 plus cisplatin, *** P <0.001, compared with si-Con plus cisplatin group. C: Transwell assay for cell invasion in varied ESCC cells treated with si-Con, si-Con plus cisplatin, si-Ctr1 and si-Ctr1 plus cisplatin; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Transwell chamber with Matrigel was used to determine cell invasion. D: Statistical assay for invasive cell numbers in a variety of ESCC cells treated with si-Con, si-Con plus cisplatin, si-Ctr1 and si-Ctr1 plus cisplatin, *** P <0.001, compared with si-Con plus cisplatin group.

    Techniques Used: Migration, Transwell Assay, Transfection

    The Ctr1 upregulation potentiated the killing efficacy of cisplatin in ESCC cells. A: pcDNA3.1-Ctr1 remarkablely enhanced the Ctr1 mRNA level at 48 h in various ESCC cells (Eca109, Kyse70 and Kyse450), pcDNA3.1 and pcDNA3.1-Ctr1 were transfected to Eca109, Kyse70 and Kyse450 cells by Lipofectamine™ 2000, and Semi-quantitative RT-PCR was used to determine the relative level of Ctr1 at 48 h after transfection,** P <0.01 and *** P <0.001, compared with control group and pcDNA3.1 group. B: Western blot was performed to investigate the Ctr1 protein expression in a number of ESCC cells 48 h after transfection with pcDNA3.1 and pcDNA3.1-Ctr1, and β-actin was used as a loading control. C: The relative level of Ctr1 protein in untreated ESCC cells, ESCC cells transfected with pcDNA3.1 and pcDNA3.1-Ctr1, ** P <0.01, compared with control group and pcDNA3.1 group. D: CCK-8 was used to examine the cell proliferative ability in different concentration of cisplatin with pcDNA3.1 or pcDNA3.1-Ctr1, ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and CCK-8 was used to determine cell viability, ** P <0.01, *** P <0.001 and **** P <0.0001, indicating statistical significance, compared with pcDNA3.1.
    Figure Legend Snippet: The Ctr1 upregulation potentiated the killing efficacy of cisplatin in ESCC cells. A: pcDNA3.1-Ctr1 remarkablely enhanced the Ctr1 mRNA level at 48 h in various ESCC cells (Eca109, Kyse70 and Kyse450), pcDNA3.1 and pcDNA3.1-Ctr1 were transfected to Eca109, Kyse70 and Kyse450 cells by Lipofectamine™ 2000, and Semi-quantitative RT-PCR was used to determine the relative level of Ctr1 at 48 h after transfection,** P <0.01 and *** P <0.001, compared with control group and pcDNA3.1 group. B: Western blot was performed to investigate the Ctr1 protein expression in a number of ESCC cells 48 h after transfection with pcDNA3.1 and pcDNA3.1-Ctr1, and β-actin was used as a loading control. C: The relative level of Ctr1 protein in untreated ESCC cells, ESCC cells transfected with pcDNA3.1 and pcDNA3.1-Ctr1, ** P <0.01, compared with control group and pcDNA3.1 group. D: CCK-8 was used to examine the cell proliferative ability in different concentration of cisplatin with pcDNA3.1 or pcDNA3.1-Ctr1, ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and CCK-8 was used to determine cell viability, ** P <0.01, *** P <0.001 and **** P <0.0001, indicating statistical significance, compared with pcDNA3.1.

    Techniques Used: Transfection, Quantitative RT-PCR, Control, Western Blot, Expressing, CCK-8 Assay, Concentration Assay

    Ctr1 upregulation combined with cisplatin displayed the synergistic role in the induction of cell apoptosis in ESCC cells. A: Flow cytometry assay for cell apoptosis in different ESCC cells treated with pcDNA3.1, pcDNA3.1 plus cisplatin, pcDNA3.1-Ctr1 and pcDNA3.1-Ctr1 plus cisplatin, ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Flow cytometry was employed to determine cell apoptosis. B: Statistical assay for apoptotic cell numbers in different ESCC cells treated with pcDNA3.1, pcDNA3.1 plus cisplatin, pcDNA3.1-Ctr1 and pcDNA3.1-Ctr1 plus cisplatin, ** P <0.01 and *** P <0.001, compared with pcDNA3.1 plus cisplatin group. C: pcDNA3.1-Ctr1 combined cisplatin significantly promoted the activity of Caspase-3 induced by cisplatin plus pcDNA3.1; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Caspase-3 activity kit was utilized to determine the activity of Caspase-3, ** P <0.01 and *** P <0.001, compared with pcDNA3.1 plus cisplatin group.
    Figure Legend Snippet: Ctr1 upregulation combined with cisplatin displayed the synergistic role in the induction of cell apoptosis in ESCC cells. A: Flow cytometry assay for cell apoptosis in different ESCC cells treated with pcDNA3.1, pcDNA3.1 plus cisplatin, pcDNA3.1-Ctr1 and pcDNA3.1-Ctr1 plus cisplatin, ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Flow cytometry was employed to determine cell apoptosis. B: Statistical assay for apoptotic cell numbers in different ESCC cells treated with pcDNA3.1, pcDNA3.1 plus cisplatin, pcDNA3.1-Ctr1 and pcDNA3.1-Ctr1 plus cisplatin, ** P <0.01 and *** P <0.001, compared with pcDNA3.1 plus cisplatin group. C: pcDNA3.1-Ctr1 combined cisplatin significantly promoted the activity of Caspase-3 induced by cisplatin plus pcDNA3.1; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Caspase-3 activity kit was utilized to determine the activity of Caspase-3, ** P <0.01 and *** P <0.001, compared with pcDNA3.1 plus cisplatin group.

    Techniques Used: Flow Cytometry, Transfection, Activity Assay

    Ctr1 upregulation exerted the synergistic role in the repression of cell migration and invasion with cisplatin in ESCC cells. A: Transwell assay for cell migration in various ESCC cells treated with pcDNA3.1, pcDNA3.1 plus cisplatin, pcDNA3.1-Ctr1 and pcDNA3.1-Ctr1 plus cisplatin; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Transwell chamber without Matrigel was employed to determine cell migration. B: Statistical assay for migratory cell numbers in different ESCC cells treated with pcDNA3.1, pcDNA3.1 plus cisplatin, pcDNA3.1-Ctr1 and pcDNA3.1-Ctr1 plus cisplatin, ** P <0.01 and **** P <0.0001, compared with pcDNA3.1 plus cisplatin group. C: Transwell assay for cell invasion in varied ESCC cells treated with pcDNA3.1, pcDNA3.1 plus cisplatin, pcDNA3.1-Ctr1 and pcDNA3.1-Ctr1 plus cisplatin; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Transwell chamber with Matrigel was employed to determine cell invasion. D: Statistical assay for invasive cell numbers in a variety of ESCC cells treated with pcDNA3.1, pcDNA3.1 plus cisplatin, pcDNA3.1-Ctr1 and pcDNA3.1-Ctr1 plus cisplatin, ** P <0.01 and *** P <0.001, compared with pcDNA3.1 plus cisplatin group.
    Figure Legend Snippet: Ctr1 upregulation exerted the synergistic role in the repression of cell migration and invasion with cisplatin in ESCC cells. A: Transwell assay for cell migration in various ESCC cells treated with pcDNA3.1, pcDNA3.1 plus cisplatin, pcDNA3.1-Ctr1 and pcDNA3.1-Ctr1 plus cisplatin; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Transwell chamber without Matrigel was employed to determine cell migration. B: Statistical assay for migratory cell numbers in different ESCC cells treated with pcDNA3.1, pcDNA3.1 plus cisplatin, pcDNA3.1-Ctr1 and pcDNA3.1-Ctr1 plus cisplatin, ** P <0.01 and **** P <0.0001, compared with pcDNA3.1 plus cisplatin group. C: Transwell assay for cell invasion in varied ESCC cells treated with pcDNA3.1, pcDNA3.1 plus cisplatin, pcDNA3.1-Ctr1 and pcDNA3.1-Ctr1 plus cisplatin; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Transwell chamber with Matrigel was employed to determine cell invasion. D: Statistical assay for invasive cell numbers in a variety of ESCC cells treated with pcDNA3.1, pcDNA3.1 plus cisplatin, pcDNA3.1-Ctr1 and pcDNA3.1-Ctr1 plus cisplatin, ** P <0.01 and *** P <0.001, compared with pcDNA3.1 plus cisplatin group.

    Techniques Used: Migration, Transwell Assay, Transfection



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    ctr1 sirna si ctr1  (Santa Cruz Biotechnology)
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    Santa Cruz Biotechnology ctr1 sirna si ctr1
    High expressions of <t>Ctr1</t> mRNA and protein in ESCC tissues and cells. A: Representative image of Ctr1 high expression in ESCC tissues by ISH and IHC; ISH and IHC assay for Ctr1 mRNA and protein expressions in 108 cases of ESCC tissues and paired normal esophageal epithelial tissues, Bar=100 μm. B: Semi-quantitative RT-PCR detection for Ctr1 mRNA expression in randomly selected 10 cases of ESCC tissues and paired normal tissues using Ctr1 specific primers. C: Statistical assay for Ctr1 relative level in ESCC tissues and paired normal tissues, * P <0.05, ** P <0.01, *** P <0.001 and **** P <0.0001, compared para-carcinoma tissues. D: qRT-PCR assay for Ctr1 mRNA expression in ESCC cell lines (Kyse70, Eca109, and Kyse450 cells), ** P <0.01 and *** P <0.001, compared with Het-1A cell. E: Western blot analysis for Ctr1 protein expression in ESCC cell lines (Kyse70, Eca109, and Kyse450 cells), and β-actin was used as loading control. F: Relative Ctr1 protein level in various ESCC cell lines (Kyse70, Eca109, and Kyse450 cells), ** P <0.01, compared with Het-1A cell.
    Ctr1 Sirna Si Ctr1, supplied by Santa Cruz Biotechnology, 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/product/ctr1+sirna+si+ctr1/pmc09876974-69-7-10?v=Santa+Cruz+Biotechnology
    Average 94 stars, based on 1 article reviews
    ctr1 sirna si ctr1 - by Bioz Stars, 2026-08
    94/100 stars
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    High expressions of Ctr1 mRNA and protein in ESCC tissues and cells. A: Representative image of Ctr1 high expression in ESCC tissues by ISH and IHC; ISH and IHC assay for Ctr1 mRNA and protein expressions in 108 cases of ESCC tissues and paired normal esophageal epithelial tissues, Bar=100 μm. B: Semi-quantitative RT-PCR detection for Ctr1 mRNA expression in randomly selected 10 cases of ESCC tissues and paired normal tissues using Ctr1 specific primers. C: Statistical assay for Ctr1 relative level in ESCC tissues and paired normal tissues, * P <0.05, ** P <0.01, *** P <0.001 and **** P <0.0001, compared para-carcinoma tissues. D: qRT-PCR assay for Ctr1 mRNA expression in ESCC cell lines (Kyse70, Eca109, and Kyse450 cells), ** P <0.01 and *** P <0.001, compared with Het-1A cell. E: Western blot analysis for Ctr1 protein expression in ESCC cell lines (Kyse70, Eca109, and Kyse450 cells), and β-actin was used as loading control. F: Relative Ctr1 protein level in various ESCC cell lines (Kyse70, Eca109, and Kyse450 cells), ** P <0.01, compared with Het-1A cell.

    Journal: Translational Oncology

    Article Title: Copper transporter Ctr1 contributes to enhancement of the sensitivity of cisplatin in esophageal squamous cell carcinoma

    doi: 10.1016/j.tranon.2023.101626

    Figure Lengend Snippet: High expressions of Ctr1 mRNA and protein in ESCC tissues and cells. A: Representative image of Ctr1 high expression in ESCC tissues by ISH and IHC; ISH and IHC assay for Ctr1 mRNA and protein expressions in 108 cases of ESCC tissues and paired normal esophageal epithelial tissues, Bar=100 μm. B: Semi-quantitative RT-PCR detection for Ctr1 mRNA expression in randomly selected 10 cases of ESCC tissues and paired normal tissues using Ctr1 specific primers. C: Statistical assay for Ctr1 relative level in ESCC tissues and paired normal tissues, * P <0.05, ** P <0.01, *** P <0.001 and **** P <0.0001, compared para-carcinoma tissues. D: qRT-PCR assay for Ctr1 mRNA expression in ESCC cell lines (Kyse70, Eca109, and Kyse450 cells), ** P <0.01 and *** P <0.001, compared with Het-1A cell. E: Western blot analysis for Ctr1 protein expression in ESCC cell lines (Kyse70, Eca109, and Kyse450 cells), and β-actin was used as loading control. F: Relative Ctr1 protein level in various ESCC cell lines (Kyse70, Eca109, and Kyse450 cells), ** P <0.01, compared with Het-1A cell.

    Article Snippet: Control siRNA (si-Con) (Santa Cruz company, USA), Ctr1 siRNA (si-Ctr1) (Santa Cruz company, USA), pcDNA3.1 and pcDNA3.1-Ctr1 were transfected to Eca109, Kyse70 and Kyse450 cells by LipofectamineTM 2000 (Invitrogen Life Technologies, Carslbad, CA, USA) according to manufacturer's instruction.

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

    The expressions of Ctr1 mRNA and protein in ESCC tissues and normal tissues.

    Journal: Translational Oncology

    Article Title: Copper transporter Ctr1 contributes to enhancement of the sensitivity of cisplatin in esophageal squamous cell carcinoma

    doi: 10.1016/j.tranon.2023.101626

    Figure Lengend Snippet: The expressions of Ctr1 mRNA and protein in ESCC tissues and normal tissues.

    Article Snippet: Control siRNA (si-Con) (Santa Cruz company, USA), Ctr1 siRNA (si-Ctr1) (Santa Cruz company, USA), pcDNA3.1 and pcDNA3.1-Ctr1 were transfected to Eca109, Kyse70 and Kyse450 cells by LipofectamineTM 2000 (Invitrogen Life Technologies, Carslbad, CA, USA) according to manufacturer's instruction.

    Techniques:

    The associations of Ctr1 mRNA and protein expressions with clinicopathological features in ESCC.

    Journal: Translational Oncology

    Article Title: Copper transporter Ctr1 contributes to enhancement of the sensitivity of cisplatin in esophageal squamous cell carcinoma

    doi: 10.1016/j.tranon.2023.101626

    Figure Lengend Snippet: The associations of Ctr1 mRNA and protein expressions with clinicopathological features in ESCC.

    Article Snippet: Control siRNA (si-Con) (Santa Cruz company, USA), Ctr1 siRNA (si-Ctr1) (Santa Cruz company, USA), pcDNA3.1 and pcDNA3.1-Ctr1 were transfected to Eca109, Kyse70 and Kyse450 cells by LipofectamineTM 2000 (Invitrogen Life Technologies, Carslbad, CA, USA) according to manufacturer's instruction.

    Techniques:

    The Ctr1 downregulation reduces the sensitivity of cisplatin in ESCC cells. A: Ctr1 siRNA significantly suppressed Ctr1 mRNA expression at 24 h, 48 h and 72 h in various ESCC cells (Eca109, Kyse70 and Kyse450), si-Con and si-Ctr1 were transfected to Eca109, Kyse70 and Kyse450 cells by Lipofectamine™ 2000, and Semi-quantitative RT-PCR was used to determine the relative level of Ctr1 at 24 h, 48 h and 72 h after transfection, ** P <0.01 and *** P <0.001, compared with control group and si-Con group. B: Western blot was performed to investigate the Ctr1 protein expression at 24 h, 48 h and 72 h after transfection with si-Ctr1 and si-Con in different ESCC cells (Eca109, Kyse70 and Kyse450), and β-actin was employed as a loading control. C: The relative level of Ctr1 was counted using the rate of Ctr1 protein level to β-actin level in diverse ESCC cells (Eca109, Kyse70 and Kyse450), * P <0.05, ** P <0.01 and *** P <0.001, compared with control group and si-Con group. D: The Ctr1 downregulation reduced the cytotoxicity of cisplatin in distinct ESCC cells. ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and CCK-8 was used to determine cell viability, * P <0.05, ** P <0.01, *** P <0.001 and **** P <0.0001, indicating statistical significance, compared with si-Con.

    Journal: Translational Oncology

    Article Title: Copper transporter Ctr1 contributes to enhancement of the sensitivity of cisplatin in esophageal squamous cell carcinoma

    doi: 10.1016/j.tranon.2023.101626

    Figure Lengend Snippet: The Ctr1 downregulation reduces the sensitivity of cisplatin in ESCC cells. A: Ctr1 siRNA significantly suppressed Ctr1 mRNA expression at 24 h, 48 h and 72 h in various ESCC cells (Eca109, Kyse70 and Kyse450), si-Con and si-Ctr1 were transfected to Eca109, Kyse70 and Kyse450 cells by Lipofectamine™ 2000, and Semi-quantitative RT-PCR was used to determine the relative level of Ctr1 at 24 h, 48 h and 72 h after transfection, ** P <0.01 and *** P <0.001, compared with control group and si-Con group. B: Western blot was performed to investigate the Ctr1 protein expression at 24 h, 48 h and 72 h after transfection with si-Ctr1 and si-Con in different ESCC cells (Eca109, Kyse70 and Kyse450), and β-actin was employed as a loading control. C: The relative level of Ctr1 was counted using the rate of Ctr1 protein level to β-actin level in diverse ESCC cells (Eca109, Kyse70 and Kyse450), * P <0.05, ** P <0.01 and *** P <0.001, compared with control group and si-Con group. D: The Ctr1 downregulation reduced the cytotoxicity of cisplatin in distinct ESCC cells. ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and CCK-8 was used to determine cell viability, * P <0.05, ** P <0.01, *** P <0.001 and **** P <0.0001, indicating statistical significance, compared with si-Con.

    Article Snippet: Control siRNA (si-Con) (Santa Cruz company, USA), Ctr1 siRNA (si-Ctr1) (Santa Cruz company, USA), pcDNA3.1 and pcDNA3.1-Ctr1 were transfected to Eca109, Kyse70 and Kyse450 cells by LipofectamineTM 2000 (Invitrogen Life Technologies, Carslbad, CA, USA) according to manufacturer's instruction.

    Techniques: Expressing, Transfection, Quantitative RT-PCR, Control, Western Blot, CCK-8 Assay

    Ctr1 depletion prominently repressed cell apoptosis evoked by cisplatin in ESCC cells. A: Flow cytometry assay for cell apoptosis in different ESCC cells treated with si-Con, si-Con plus cisplatin, si-Ctr1 as well as si-Ctr1 plus cisplatin; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Flow cytometry was employed to determine cell apoptosis. B: Statistical assay for apoptotic cell numbers in different ESCC cells treated with si-Con, si-Con plus cisplatin, si-Ctr1 as well as si-Ctr1 plus cisplatin, *** P <0.001 and **** P <0.0001, compared with si-Con plus cisplatin group. C: Ctr1 depletion combined cisplatin significantly suppressed the activity of Caspase-3 induced by cisplatin plus si-Con; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Caspase-3 activity kit was utilized to determine the activity of Caspase-3, *** P <0.001, compared with si-Con plus cisplatin group.

    Journal: Translational Oncology

    Article Title: Copper transporter Ctr1 contributes to enhancement of the sensitivity of cisplatin in esophageal squamous cell carcinoma

    doi: 10.1016/j.tranon.2023.101626

    Figure Lengend Snippet: Ctr1 depletion prominently repressed cell apoptosis evoked by cisplatin in ESCC cells. A: Flow cytometry assay for cell apoptosis in different ESCC cells treated with si-Con, si-Con plus cisplatin, si-Ctr1 as well as si-Ctr1 plus cisplatin; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Flow cytometry was employed to determine cell apoptosis. B: Statistical assay for apoptotic cell numbers in different ESCC cells treated with si-Con, si-Con plus cisplatin, si-Ctr1 as well as si-Ctr1 plus cisplatin, *** P <0.001 and **** P <0.0001, compared with si-Con plus cisplatin group. C: Ctr1 depletion combined cisplatin significantly suppressed the activity of Caspase-3 induced by cisplatin plus si-Con; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Caspase-3 activity kit was utilized to determine the activity of Caspase-3, *** P <0.001, compared with si-Con plus cisplatin group.

    Article Snippet: Control siRNA (si-Con) (Santa Cruz company, USA), Ctr1 siRNA (si-Ctr1) (Santa Cruz company, USA), pcDNA3.1 and pcDNA3.1-Ctr1 were transfected to Eca109, Kyse70 and Kyse450 cells by LipofectamineTM 2000 (Invitrogen Life Technologies, Carslbad, CA, USA) according to manufacturer's instruction.

    Techniques: Flow Cytometry, Transfection, Activity Assay

    The Ctr1 downregulation meliorated cell migration and invasion abilities inhibited by cisplatin in number of ESCC cells. A: Transwell assay for cell migration in various ESCC cells treated with si-Con, si-Con plus cisplatin, si-Ctr1 and si-Ctr1 plus cisplatin; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Transwell chamber without Matrigel was employed to determine cell migration. B: Statistical assay for migratory cell numbers in different ESCC cells treated with si-Con, si-Con plus cisplatin, si-Ctr1 and si-Ctr1 plus cisplatin, *** P <0.001, compared with si-Con plus cisplatin group. C: Transwell assay for cell invasion in varied ESCC cells treated with si-Con, si-Con plus cisplatin, si-Ctr1 and si-Ctr1 plus cisplatin; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Transwell chamber with Matrigel was used to determine cell invasion. D: Statistical assay for invasive cell numbers in a variety of ESCC cells treated with si-Con, si-Con plus cisplatin, si-Ctr1 and si-Ctr1 plus cisplatin, *** P <0.001, compared with si-Con plus cisplatin group.

    Journal: Translational Oncology

    Article Title: Copper transporter Ctr1 contributes to enhancement of the sensitivity of cisplatin in esophageal squamous cell carcinoma

    doi: 10.1016/j.tranon.2023.101626

    Figure Lengend Snippet: The Ctr1 downregulation meliorated cell migration and invasion abilities inhibited by cisplatin in number of ESCC cells. A: Transwell assay for cell migration in various ESCC cells treated with si-Con, si-Con plus cisplatin, si-Ctr1 and si-Ctr1 plus cisplatin; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Transwell chamber without Matrigel was employed to determine cell migration. B: Statistical assay for migratory cell numbers in different ESCC cells treated with si-Con, si-Con plus cisplatin, si-Ctr1 and si-Ctr1 plus cisplatin, *** P <0.001, compared with si-Con plus cisplatin group. C: Transwell assay for cell invasion in varied ESCC cells treated with si-Con, si-Con plus cisplatin, si-Ctr1 and si-Ctr1 plus cisplatin; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Transwell chamber with Matrigel was used to determine cell invasion. D: Statistical assay for invasive cell numbers in a variety of ESCC cells treated with si-Con, si-Con plus cisplatin, si-Ctr1 and si-Ctr1 plus cisplatin, *** P <0.001, compared with si-Con plus cisplatin group.

    Article Snippet: Control siRNA (si-Con) (Santa Cruz company, USA), Ctr1 siRNA (si-Ctr1) (Santa Cruz company, USA), pcDNA3.1 and pcDNA3.1-Ctr1 were transfected to Eca109, Kyse70 and Kyse450 cells by LipofectamineTM 2000 (Invitrogen Life Technologies, Carslbad, CA, USA) according to manufacturer's instruction.

    Techniques: Migration, Transwell Assay, Transfection

    The Ctr1 upregulation potentiated the killing efficacy of cisplatin in ESCC cells. A: pcDNA3.1-Ctr1 remarkablely enhanced the Ctr1 mRNA level at 48 h in various ESCC cells (Eca109, Kyse70 and Kyse450), pcDNA3.1 and pcDNA3.1-Ctr1 were transfected to Eca109, Kyse70 and Kyse450 cells by Lipofectamine™ 2000, and Semi-quantitative RT-PCR was used to determine the relative level of Ctr1 at 48 h after transfection,** P <0.01 and *** P <0.001, compared with control group and pcDNA3.1 group. B: Western blot was performed to investigate the Ctr1 protein expression in a number of ESCC cells 48 h after transfection with pcDNA3.1 and pcDNA3.1-Ctr1, and β-actin was used as a loading control. C: The relative level of Ctr1 protein in untreated ESCC cells, ESCC cells transfected with pcDNA3.1 and pcDNA3.1-Ctr1, ** P <0.01, compared with control group and pcDNA3.1 group. D: CCK-8 was used to examine the cell proliferative ability in different concentration of cisplatin with pcDNA3.1 or pcDNA3.1-Ctr1, ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and CCK-8 was used to determine cell viability, ** P <0.01, *** P <0.001 and **** P <0.0001, indicating statistical significance, compared with pcDNA3.1.

    Journal: Translational Oncology

    Article Title: Copper transporter Ctr1 contributes to enhancement of the sensitivity of cisplatin in esophageal squamous cell carcinoma

    doi: 10.1016/j.tranon.2023.101626

    Figure Lengend Snippet: The Ctr1 upregulation potentiated the killing efficacy of cisplatin in ESCC cells. A: pcDNA3.1-Ctr1 remarkablely enhanced the Ctr1 mRNA level at 48 h in various ESCC cells (Eca109, Kyse70 and Kyse450), pcDNA3.1 and pcDNA3.1-Ctr1 were transfected to Eca109, Kyse70 and Kyse450 cells by Lipofectamine™ 2000, and Semi-quantitative RT-PCR was used to determine the relative level of Ctr1 at 48 h after transfection,** P <0.01 and *** P <0.001, compared with control group and pcDNA3.1 group. B: Western blot was performed to investigate the Ctr1 protein expression in a number of ESCC cells 48 h after transfection with pcDNA3.1 and pcDNA3.1-Ctr1, and β-actin was used as a loading control. C: The relative level of Ctr1 protein in untreated ESCC cells, ESCC cells transfected with pcDNA3.1 and pcDNA3.1-Ctr1, ** P <0.01, compared with control group and pcDNA3.1 group. D: CCK-8 was used to examine the cell proliferative ability in different concentration of cisplatin with pcDNA3.1 or pcDNA3.1-Ctr1, ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and CCK-8 was used to determine cell viability, ** P <0.01, *** P <0.001 and **** P <0.0001, indicating statistical significance, compared with pcDNA3.1.

    Article Snippet: Control siRNA (si-Con) (Santa Cruz company, USA), Ctr1 siRNA (si-Ctr1) (Santa Cruz company, USA), pcDNA3.1 and pcDNA3.1-Ctr1 were transfected to Eca109, Kyse70 and Kyse450 cells by LipofectamineTM 2000 (Invitrogen Life Technologies, Carslbad, CA, USA) according to manufacturer's instruction.

    Techniques: Transfection, Quantitative RT-PCR, Control, Western Blot, Expressing, CCK-8 Assay, Concentration Assay

    Ctr1 upregulation combined with cisplatin displayed the synergistic role in the induction of cell apoptosis in ESCC cells. A: Flow cytometry assay for cell apoptosis in different ESCC cells treated with pcDNA3.1, pcDNA3.1 plus cisplatin, pcDNA3.1-Ctr1 and pcDNA3.1-Ctr1 plus cisplatin, ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Flow cytometry was employed to determine cell apoptosis. B: Statistical assay for apoptotic cell numbers in different ESCC cells treated with pcDNA3.1, pcDNA3.1 plus cisplatin, pcDNA3.1-Ctr1 and pcDNA3.1-Ctr1 plus cisplatin, ** P <0.01 and *** P <0.001, compared with pcDNA3.1 plus cisplatin group. C: pcDNA3.1-Ctr1 combined cisplatin significantly promoted the activity of Caspase-3 induced by cisplatin plus pcDNA3.1; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Caspase-3 activity kit was utilized to determine the activity of Caspase-3, ** P <0.01 and *** P <0.001, compared with pcDNA3.1 plus cisplatin group.

    Journal: Translational Oncology

    Article Title: Copper transporter Ctr1 contributes to enhancement of the sensitivity of cisplatin in esophageal squamous cell carcinoma

    doi: 10.1016/j.tranon.2023.101626

    Figure Lengend Snippet: Ctr1 upregulation combined with cisplatin displayed the synergistic role in the induction of cell apoptosis in ESCC cells. A: Flow cytometry assay for cell apoptosis in different ESCC cells treated with pcDNA3.1, pcDNA3.1 plus cisplatin, pcDNA3.1-Ctr1 and pcDNA3.1-Ctr1 plus cisplatin, ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Flow cytometry was employed to determine cell apoptosis. B: Statistical assay for apoptotic cell numbers in different ESCC cells treated with pcDNA3.1, pcDNA3.1 plus cisplatin, pcDNA3.1-Ctr1 and pcDNA3.1-Ctr1 plus cisplatin, ** P <0.01 and *** P <0.001, compared with pcDNA3.1 plus cisplatin group. C: pcDNA3.1-Ctr1 combined cisplatin significantly promoted the activity of Caspase-3 induced by cisplatin plus pcDNA3.1; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Caspase-3 activity kit was utilized to determine the activity of Caspase-3, ** P <0.01 and *** P <0.001, compared with pcDNA3.1 plus cisplatin group.

    Article Snippet: Control siRNA (si-Con) (Santa Cruz company, USA), Ctr1 siRNA (si-Ctr1) (Santa Cruz company, USA), pcDNA3.1 and pcDNA3.1-Ctr1 were transfected to Eca109, Kyse70 and Kyse450 cells by LipofectamineTM 2000 (Invitrogen Life Technologies, Carslbad, CA, USA) according to manufacturer's instruction.

    Techniques: Flow Cytometry, Transfection, Activity Assay

    Ctr1 upregulation exerted the synergistic role in the repression of cell migration and invasion with cisplatin in ESCC cells. A: Transwell assay for cell migration in various ESCC cells treated with pcDNA3.1, pcDNA3.1 plus cisplatin, pcDNA3.1-Ctr1 and pcDNA3.1-Ctr1 plus cisplatin; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Transwell chamber without Matrigel was employed to determine cell migration. B: Statistical assay for migratory cell numbers in different ESCC cells treated with pcDNA3.1, pcDNA3.1 plus cisplatin, pcDNA3.1-Ctr1 and pcDNA3.1-Ctr1 plus cisplatin, ** P <0.01 and **** P <0.0001, compared with pcDNA3.1 plus cisplatin group. C: Transwell assay for cell invasion in varied ESCC cells treated with pcDNA3.1, pcDNA3.1 plus cisplatin, pcDNA3.1-Ctr1 and pcDNA3.1-Ctr1 plus cisplatin; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Transwell chamber with Matrigel was employed to determine cell invasion. D: Statistical assay for invasive cell numbers in a variety of ESCC cells treated with pcDNA3.1, pcDNA3.1 plus cisplatin, pcDNA3.1-Ctr1 and pcDNA3.1-Ctr1 plus cisplatin, ** P <0.01 and *** P <0.001, compared with pcDNA3.1 plus cisplatin group.

    Journal: Translational Oncology

    Article Title: Copper transporter Ctr1 contributes to enhancement of the sensitivity of cisplatin in esophageal squamous cell carcinoma

    doi: 10.1016/j.tranon.2023.101626

    Figure Lengend Snippet: Ctr1 upregulation exerted the synergistic role in the repression of cell migration and invasion with cisplatin in ESCC cells. A: Transwell assay for cell migration in various ESCC cells treated with pcDNA3.1, pcDNA3.1 plus cisplatin, pcDNA3.1-Ctr1 and pcDNA3.1-Ctr1 plus cisplatin; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Transwell chamber without Matrigel was employed to determine cell migration. B: Statistical assay for migratory cell numbers in different ESCC cells treated with pcDNA3.1, pcDNA3.1 plus cisplatin, pcDNA3.1-Ctr1 and pcDNA3.1-Ctr1 plus cisplatin, ** P <0.01 and **** P <0.0001, compared with pcDNA3.1 plus cisplatin group. C: Transwell assay for cell invasion in varied ESCC cells treated with pcDNA3.1, pcDNA3.1 plus cisplatin, pcDNA3.1-Ctr1 and pcDNA3.1-Ctr1 plus cisplatin; ESCC cells (Eca109, Kyse70 and Kyse450) were harvested at 48 h after transfection, different doses of cisplatin was applied to ESCC cells above, and Transwell chamber with Matrigel was employed to determine cell invasion. D: Statistical assay for invasive cell numbers in a variety of ESCC cells treated with pcDNA3.1, pcDNA3.1 plus cisplatin, pcDNA3.1-Ctr1 and pcDNA3.1-Ctr1 plus cisplatin, ** P <0.01 and *** P <0.001, compared with pcDNA3.1 plus cisplatin group.

    Article Snippet: Control siRNA (si-Con) (Santa Cruz company, USA), Ctr1 siRNA (si-Ctr1) (Santa Cruz company, USA), pcDNA3.1 and pcDNA3.1-Ctr1 were transfected to Eca109, Kyse70 and Kyse450 cells by LipofectamineTM 2000 (Invitrogen Life Technologies, Carslbad, CA, USA) according to manufacturer's instruction.

    Techniques: Migration, Transwell Assay, Transfection