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epha2 open reading frame orf expression  (Genecopoeia)


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    Genecopoeia epha2 open reading frame orf expression
    <t>EPHA2</t> is correlated with poor clinical outcome in TNBC and is a predicted target of miR-200a. (A) Kaplan–Meier survival plots show that high level of EPHA2 mRNA is significantly correlated to a lower overall survival in a cohort of basal-like patients (N = 343). This correlation is not significant for Luminal B (N = 495), or HER2-positive (N = 111) subtype patients. For Luminal A (N = 651) patients, high levels of EPHA2 correlate with better survival. (B) A potential target site for miR-200a was identified in the 3′UTR sequence of EPHA2 at nucleotides 716–737, using target prediction software TargetScan. Eight nucleotides within the seed sequence of miR-200a showed complete complementarity with the 3′UTR sequence of EPHA2. These nucleotides were 100% conserved between various vertebrate species. (C) Western blotting of undifferentiated HC11 cells transfected with miR-200a mimic (25nM) or control in a single (left), or double transfection (right), shows decreased levels of EPHA2 protein by miR-200a. β-Actin was used as a loading control. (D) Significant reductions of EPHA2 mRNA levels were noted within 24h after miR-200a mimic (25nM) treatment in MDA-MB-231 and SUM159 cells, compared to control mimic. (E) Western blotting of MDA-MB-231 and SUM159 cells, 48h after transfection with miR-200a mimic (25nM) or control mimic, shows that miR-200a reduced expression of EPHA2 protein in both cell lines. β-Actin was used as a loading control. Student’s t-test, two-tailed distribution was performed and P ≤ 0.05 was considered statistically significant.
    Epha2 Open Reading Frame Orf Expression, supplied by Genecopoeia, used in various techniques. Bioz Stars score: 94/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/orf+expression+clone+for+epha2/ORF+expression+clone+for+EPHA2/pmc05975720-59-5-18
    Average 94 stars, based on 5 article reviews
    epha2 open reading frame orf expression - by Bioz Stars, 2026-09
    94/100 stars

    Images

    1) Product Images from "miR-200a inhibits migration of triple-negative breast cancer cells through direct repression of the EPHA2 oncogene"

    Article Title: miR-200a inhibits migration of triple-negative breast cancer cells through direct repression of the EPHA2 oncogene

    Journal: Carcinogenesis

    doi: 10.1093/carcin/bgv087

    EPHA2 is correlated with poor clinical outcome in TNBC and is a predicted target of miR-200a. (A) Kaplan–Meier survival plots show that high level of EPHA2 mRNA is significantly correlated to a lower overall survival in a cohort of basal-like patients (N = 343). This correlation is not significant for Luminal B (N = 495), or HER2-positive (N = 111) subtype patients. For Luminal A (N = 651) patients, high levels of EPHA2 correlate with better survival. (B) A potential target site for miR-200a was identified in the 3′UTR sequence of EPHA2 at nucleotides 716–737, using target prediction software TargetScan. Eight nucleotides within the seed sequence of miR-200a showed complete complementarity with the 3′UTR sequence of EPHA2. These nucleotides were 100% conserved between various vertebrate species. (C) Western blotting of undifferentiated HC11 cells transfected with miR-200a mimic (25nM) or control in a single (left), or double transfection (right), shows decreased levels of EPHA2 protein by miR-200a. β-Actin was used as a loading control. (D) Significant reductions of EPHA2 mRNA levels were noted within 24h after miR-200a mimic (25nM) treatment in MDA-MB-231 and SUM159 cells, compared to control mimic. (E) Western blotting of MDA-MB-231 and SUM159 cells, 48h after transfection with miR-200a mimic (25nM) or control mimic, shows that miR-200a reduced expression of EPHA2 protein in both cell lines. β-Actin was used as a loading control. Student’s t-test, two-tailed distribution was performed and P ≤ 0.05 was considered statistically significant.
    Figure Legend Snippet: EPHA2 is correlated with poor clinical outcome in TNBC and is a predicted target of miR-200a. (A) Kaplan–Meier survival plots show that high level of EPHA2 mRNA is significantly correlated to a lower overall survival in a cohort of basal-like patients (N = 343). This correlation is not significant for Luminal B (N = 495), or HER2-positive (N = 111) subtype patients. For Luminal A (N = 651) patients, high levels of EPHA2 correlate with better survival. (B) A potential target site for miR-200a was identified in the 3′UTR sequence of EPHA2 at nucleotides 716–737, using target prediction software TargetScan. Eight nucleotides within the seed sequence of miR-200a showed complete complementarity with the 3′UTR sequence of EPHA2. These nucleotides were 100% conserved between various vertebrate species. (C) Western blotting of undifferentiated HC11 cells transfected with miR-200a mimic (25nM) or control in a single (left), or double transfection (right), shows decreased levels of EPHA2 protein by miR-200a. β-Actin was used as a loading control. (D) Significant reductions of EPHA2 mRNA levels were noted within 24h after miR-200a mimic (25nM) treatment in MDA-MB-231 and SUM159 cells, compared to control mimic. (E) Western blotting of MDA-MB-231 and SUM159 cells, 48h after transfection with miR-200a mimic (25nM) or control mimic, shows that miR-200a reduced expression of EPHA2 protein in both cell lines. β-Actin was used as a loading control. Student’s t-test, two-tailed distribution was performed and P ≤ 0.05 was considered statistically significant.

    Techniques Used: Sequencing, Software, Western Blot, Transfection, Control, Expressing, Two Tailed Test

    miR-200a directly targets the 3′UTR of EPHA2. (A) The constructs contain EPHA2 3′UTR sequence encompassing the predicted miR-200a site or control with (a) this site mutated, and (b) no 3′UTR sequence, cloned into luciferase reporter vectors. The constructs contains hLuc and hRLuc under the control of Sv40 and CMV promoter. hRLuc is endogenous control of construct expression. (B) HEK239 cells were transfected with plasmid containing WT or mutated EPHA2 3′UTR, or control plasmid, and either miR-200a mimic, control mimic or miR-9 mimic. Luciferase activity was measured 24h post transfection. Only the construct containing the predicted target site significantly decreased its luciferase activity, and only when miR-200a was added. (C) EPHA2 mRNA levels were reduced also in HEK239 cells. The cells were transfected with miR-200a mimic (25nM) or control mimic and collected 24h post transfection. EPHA2 and housekeeping gene 36B4 mRNA levels were measured using qPCR and data analyzed using the ΔΔCT method. For significance, Student’s t-test, two-tailed distribution was used.
    Figure Legend Snippet: miR-200a directly targets the 3′UTR of EPHA2. (A) The constructs contain EPHA2 3′UTR sequence encompassing the predicted miR-200a site or control with (a) this site mutated, and (b) no 3′UTR sequence, cloned into luciferase reporter vectors. The constructs contains hLuc and hRLuc under the control of Sv40 and CMV promoter. hRLuc is endogenous control of construct expression. (B) HEK239 cells were transfected with plasmid containing WT or mutated EPHA2 3′UTR, or control plasmid, and either miR-200a mimic, control mimic or miR-9 mimic. Luciferase activity was measured 24h post transfection. Only the construct containing the predicted target site significantly decreased its luciferase activity, and only when miR-200a was added. (C) EPHA2 mRNA levels were reduced also in HEK239 cells. The cells were transfected with miR-200a mimic (25nM) or control mimic and collected 24h post transfection. EPHA2 and housekeeping gene 36B4 mRNA levels were measured using qPCR and data analyzed using the ΔΔCT method. For significance, Student’s t-test, two-tailed distribution was used.

    Techniques Used: Construct, Sequencing, Control, Clone Assay, Luciferase, Expressing, Transfection, Plasmid Preparation, Activity Assay, Two Tailed Test

    miR-200a reduces migration of TNBC cells through EPHA2 regulation. (A) The effect of miR-200a and EPHA2 on migration was measured in MDA-MB-231 and SUM159 cells. Cells transfected with miR-200a mimic (50nM), si-EPHA2 (100nM), EPHA2-ORF (800ng) or corresponding control for 48h were subjected to wound-healing assay. Images were taken at 0 and 12h (or 9h) after wound introduction. The white line highlights the wound edge at 0 and 12h (or 9h). (B) Quantification of relative cell migration in MDA-MB-231 and SUM159 transfected as shown in A. Distance of gap closure was measured using ImageJ. Data are presented as mean ± SD from two independent experiments. Unpaired two-tailed student’s t-test was used for significant testing, and presented as *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001. (C) Overexpression of EPHA2 rescued the anti-migratory effect of miR-200a in MDA-MB-231 and SUM159 cells. Cells were cotransfected with miR-200a mimic and EPHA2-ORF or control ORF and subjected to wound-healing assay.
    Figure Legend Snippet: miR-200a reduces migration of TNBC cells through EPHA2 regulation. (A) The effect of miR-200a and EPHA2 on migration was measured in MDA-MB-231 and SUM159 cells. Cells transfected with miR-200a mimic (50nM), si-EPHA2 (100nM), EPHA2-ORF (800ng) or corresponding control for 48h were subjected to wound-healing assay. Images were taken at 0 and 12h (or 9h) after wound introduction. The white line highlights the wound edge at 0 and 12h (or 9h). (B) Quantification of relative cell migration in MDA-MB-231 and SUM159 transfected as shown in A. Distance of gap closure was measured using ImageJ. Data are presented as mean ± SD from two independent experiments. Unpaired two-tailed student’s t-test was used for significant testing, and presented as *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001. (C) Overexpression of EPHA2 rescued the anti-migratory effect of miR-200a in MDA-MB-231 and SUM159 cells. Cells were cotransfected with miR-200a mimic and EPHA2-ORF or control ORF and subjected to wound-healing assay.

    Techniques Used: Migration, Transfection, Control, Wound Healing Assay, Two Tailed Test, Over Expression

    EPHA2 does not affect E-cadherin levels but increases AMPK phosphorylation. (A) E-cadherin levels are independent on EPHA2 in TNBC cells. MDA-MB-231 and SUM159 cells were transfected with miR-200a mimic (50nM), s-iEPHA2 or corresponding control were subjected to western blot for E-cadherin. β-Actin was used as a loading control. (B) AMPK phosphorylation is enhanced by miR-200a-EPHA2 pathway. MDA-MB-231 cells were transfected and followed by western blot for pAMPK and total AMPK. (C) Inhibition of AMPK promotes cell migration in TNBC cells. Cells were treated with Compound C for 8h followed by wound-healing assay. Images were taken at 0 and 12h after wound introduction and relative migration distance was quantified using ImageJ.
    Figure Legend Snippet: EPHA2 does not affect E-cadherin levels but increases AMPK phosphorylation. (A) E-cadherin levels are independent on EPHA2 in TNBC cells. MDA-MB-231 and SUM159 cells were transfected with miR-200a mimic (50nM), s-iEPHA2 or corresponding control were subjected to western blot for E-cadherin. β-Actin was used as a loading control. (B) AMPK phosphorylation is enhanced by miR-200a-EPHA2 pathway. MDA-MB-231 cells were transfected and followed by western blot for pAMPK and total AMPK. (C) Inhibition of AMPK promotes cell migration in TNBC cells. Cells were treated with Compound C for 8h followed by wound-healing assay. Images were taken at 0 and 12h after wound introduction and relative migration distance was quantified using ImageJ.

    Techniques Used: Phospho-proteomics, Transfection, Control, Western Blot, Inhibition, Migration, Wound Healing Assay

    Model illustrating how miR-200a regulates TNBC migration. (A) Differentiated epithelial cells expressing E-cadherin, EPHA2 and Ephrin. (B) TNBC cells exhibit downregulation of E-cadherin and lack of Ephrin along with a migratory and invasive phenotype. (C) miR-200a regulates both the E-cadherin and EPHA2 pathways, resulting in increased levels of E-cadherin and reduced levels of EPHA2 along with inhibited migratory and invasive capacities. (D) Proposed pathways that miR-200a can repress migration through dual pathways: by direct targeting the 3′UTR of EPHA2 (solid lines, as demonstrated in this study) and through the indirect upregulation of the E-cadherin (dashed lines, as reported in literature).
    Figure Legend Snippet: Model illustrating how miR-200a regulates TNBC migration. (A) Differentiated epithelial cells expressing E-cadherin, EPHA2 and Ephrin. (B) TNBC cells exhibit downregulation of E-cadherin and lack of Ephrin along with a migratory and invasive phenotype. (C) miR-200a regulates both the E-cadherin and EPHA2 pathways, resulting in increased levels of E-cadherin and reduced levels of EPHA2 along with inhibited migratory and invasive capacities. (D) Proposed pathways that miR-200a can repress migration through dual pathways: by direct targeting the 3′UTR of EPHA2 (solid lines, as demonstrated in this study) and through the indirect upregulation of the E-cadherin (dashed lines, as reported in literature).

    Techniques Used: Migration, Expressing

    Related Articles

    Transfection:

    Article Title: Reduction of Circulating Cancer Cells and Metastases in Breast-Cancer Models by a Potent EphA2-Agonistic Peptide–Drug Conjugate
    Article Snippet: 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 18 CO2. Cells were transfected with EphA2 lentiviral plasmid (EX-A0125-Lv105) using the LentiPac HIV Expression Packing Kit (GeneCopoeia, Inc.) to produce lentivirus particles according to manufacturer’s protocol. After two days, viral particles were collected and filtered. Stable EphA2 over-expressing HEK 293T/17 cells wer

    Agarose Gel Electrophoresis:

    Article Title: Reduction of Circulating Cancer Cells and Metastases in Breast-Cancer Models by a Potent EphA2-Agonistic Peptide–Drug Conjugate
    Article Snippet: 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 18 CO2. Cells were transfected with EphA2 lentiviral plasmid (EX-A0125-Lv105) using the LentiPac HIV Expression Packing Kit (GeneCopoeia, Inc.) to produce lentivirus particles according to manufacturer’s protocol. After two days, viral particles were collected and filtered. Stable EphA2 over-expressing HEK 293T/17 cells wer

    Expression Vector:

    Article Title: Reduction of Circulating Cancer Cells and Metastases in Breast-Cancer Models by a Potent EphA2-Agonistic Peptide–Drug Conjugate
    Article Snippet: 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 18 CO2. Cells were transfected with EphA2 lentiviral plasmid (EX-A0125-Lv105) using the LentiPac HIV Expression Packing Kit (GeneCopoeia, Inc.) to produce lentivirus particles according to manufacturer’s protocol. After two days, viral particles were collected and filtered. Stable EphA2 over-expressing HEK 293T/17 cells wer

    Expressing:

    Article Title: Reduction of Circulating Cancer Cells and Metastases in Breast-Cancer Models by a Potent EphA2-Agonistic Peptide–Drug Conjugate
    Article Snippet: 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 18 CO2. Cells were transfected with EphA2 lentiviral plasmid (EX-A0125-Lv105) using the LentiPac HIV Expression Packing Kit (GeneCopoeia, Inc.) to produce lentivirus particles according to manufacturer’s protocol. After two days, viral particles were collected and filtered. Stable EphA2 over-expressing HEK 293T/17 cells wer

    Plasmid Preparation:

    Article Title: Reduction of Circulating Cancer Cells and Metastases in Breast-Cancer Models by a Potent EphA2-Agonistic Peptide–Drug Conjugate
    Article Snippet: 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 18 CO2. Cells were transfected with EphA2 lentiviral plasmid (EX-A0125-Lv105) using the LentiPac HIV Expression Packing Kit (GeneCopoeia, Inc.) to produce lentivirus particles according to manufacturer’s protocol. After two days, viral particles were collected and filtered. Stable EphA2 over-expressing HEK 293T/17 cells wer

    Cell Culture:

    Article Title: Reduction of Circulating Cancer Cells and Metastases in Breast-Cancer Models by a Potent EphA2-Agonistic Peptide–Drug Conjugate
    Article Snippet: 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 18 CO2. Cells were transfected with EphA2 lentiviral plasmid (EX-A0125-Lv105) using the LentiPac HIV Expression Packing Kit (GeneCopoeia, Inc.) to produce lentivirus particles according to manufacturer’s protocol. After two days, viral particles were collected and filtered. Stable EphA2 over-expressing HEK 293T/17 cells wer

    Control:

    Article Title: Reduction of Circulating Cancer Cells and Metastases in Breast-Cancer Models by a Potent EphA2-Agonistic Peptide–Drug Conjugate
    Article Snippet: 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 18 CO2. Cells were transfected with EphA2 lentiviral plasmid (EX-A0125-Lv105) using the LentiPac HIV Expression Packing Kit (GeneCopoeia, Inc.) to produce lentivirus particles according to manufacturer’s protocol. After two days, viral particles were collected and filtered. Stable EphA2 over-expressing HEK 293T/17 cells wer

    Construct:

    Article Title: Reduction of Circulating Cancer Cells and Metastases in Breast-Cancer Models by a Potent EphA2-Agonistic Peptide–Drug Conjugate
    Article Snippet: 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 18 CO2. Cells were transfected with EphA2 lentiviral plasmid (EX-A0125-Lv105) using the LentiPac HIV Expression Packing Kit (GeneCopoeia, Inc.) to produce lentivirus particles according to manufacturer’s protocol. After two days, viral particles were collected and filtered. Stable EphA2 over-expressing HEK 293T/17 cells wer

    Transgenic Assay:

    Article Title: Reduction of Circulating Cancer Cells and Metastases in Breast-Cancer Models by a Potent EphA2-Agonistic Peptide–Drug Conjugate
    Article Snippet: 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 18 CO2. Cells were transfected with EphA2 lentiviral plasmid (EX-A0125-Lv105) using the LentiPac HIV Expression Packing Kit (GeneCopoeia, Inc.) to produce lentivirus particles according to manufacturer’s protocol. After two days, viral particles were collected and filtered. Stable EphA2 over-expressing HEK 293T/17 cells wer

    Sequencing:

    Article Title: Reduction of Circulating Cancer Cells and Metastases in Breast-Cancer Models by a Potent EphA2-Agonistic Peptide–Drug Conjugate
    Article Snippet: 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 18 CO2. Cells were transfected with EphA2 lentiviral plasmid (EX-A0125-Lv105) using the LentiPac HIV Expression Packing Kit (GeneCopoeia, Inc.) to produce lentivirus particles according to manufacturer’s protocol. After two days, viral particles were collected and filtered. Stable EphA2 over-expressing HEK 293T/17 cells wer



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    <t>EPHA2</t> is correlated with poor clinical outcome in TNBC and is a predicted target of miR-200a. (A) Kaplan–Meier survival plots show that high level of EPHA2 mRNA is significantly correlated to a lower overall survival in a cohort of basal-like patients (N = 343). This correlation is not significant for Luminal B (N = 495), or HER2-positive (N = 111) subtype patients. For Luminal A (N = 651) patients, high levels of EPHA2 correlate with better survival. (B) A potential target site for miR-200a was identified in the 3′UTR sequence of EPHA2 at nucleotides 716–737, using target prediction software TargetScan. Eight nucleotides within the seed sequence of miR-200a showed complete complementarity with the 3′UTR sequence of EPHA2. These nucleotides were 100% conserved between various vertebrate species. (C) Western blotting of undifferentiated HC11 cells transfected with miR-200a mimic (25nM) or control in a single (left), or double transfection (right), shows decreased levels of EPHA2 protein by miR-200a. β-Actin was used as a loading control. (D) Significant reductions of EPHA2 mRNA levels were noted within 24h after miR-200a mimic (25nM) treatment in MDA-MB-231 and SUM159 cells, compared to control mimic. (E) Western blotting of MDA-MB-231 and SUM159 cells, 48h after transfection with miR-200a mimic (25nM) or control mimic, shows that miR-200a reduced expression of EPHA2 protein in both cell lines. β-Actin was used as a loading control. Student’s t-test, two-tailed distribution was performed and P ≤ 0.05 was considered statistically significant.
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    <t>EPHA2</t> is correlated with poor clinical outcome in TNBC and is a predicted target of miR-200a. (A) Kaplan–Meier survival plots show that high level of EPHA2 mRNA is significantly correlated to a lower overall survival in a cohort of basal-like patients (N = 343). This correlation is not significant for Luminal B (N = 495), or HER2-positive (N = 111) subtype patients. For Luminal A (N = 651) patients, high levels of EPHA2 correlate with better survival. (B) A potential target site for miR-200a was identified in the 3′UTR sequence of EPHA2 at nucleotides 716–737, using target prediction software TargetScan. Eight nucleotides within the seed sequence of miR-200a showed complete complementarity with the 3′UTR sequence of EPHA2. These nucleotides were 100% conserved between various vertebrate species. (C) Western blotting of undifferentiated HC11 cells transfected with miR-200a mimic (25nM) or control in a single (left), or double transfection (right), shows decreased levels of EPHA2 protein by miR-200a. β-Actin was used as a loading control. (D) Significant reductions of EPHA2 mRNA levels were noted within 24h after miR-200a mimic (25nM) treatment in MDA-MB-231 and SUM159 cells, compared to control mimic. (E) Western blotting of MDA-MB-231 and SUM159 cells, 48h after transfection with miR-200a mimic (25nM) or control mimic, shows that miR-200a reduced expression of EPHA2 protein in both cell lines. β-Actin was used as a loading control. Student’s t-test, two-tailed distribution was performed and P ≤ 0.05 was considered statistically significant.
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    Image Search Results


    EPHA2 is correlated with poor clinical outcome in TNBC and is a predicted target of miR-200a. (A) Kaplan–Meier survival plots show that high level of EPHA2 mRNA is significantly correlated to a lower overall survival in a cohort of basal-like patients (N = 343). This correlation is not significant for Luminal B (N = 495), or HER2-positive (N = 111) subtype patients. For Luminal A (N = 651) patients, high levels of EPHA2 correlate with better survival. (B) A potential target site for miR-200a was identified in the 3′UTR sequence of EPHA2 at nucleotides 716–737, using target prediction software TargetScan. Eight nucleotides within the seed sequence of miR-200a showed complete complementarity with the 3′UTR sequence of EPHA2. These nucleotides were 100% conserved between various vertebrate species. (C) Western blotting of undifferentiated HC11 cells transfected with miR-200a mimic (25nM) or control in a single (left), or double transfection (right), shows decreased levels of EPHA2 protein by miR-200a. β-Actin was used as a loading control. (D) Significant reductions of EPHA2 mRNA levels were noted within 24h after miR-200a mimic (25nM) treatment in MDA-MB-231 and SUM159 cells, compared to control mimic. (E) Western blotting of MDA-MB-231 and SUM159 cells, 48h after transfection with miR-200a mimic (25nM) or control mimic, shows that miR-200a reduced expression of EPHA2 protein in both cell lines. β-Actin was used as a loading control. Student’s t-test, two-tailed distribution was performed and P ≤ 0.05 was considered statistically significant.

    Journal: Carcinogenesis

    Article Title: miR-200a inhibits migration of triple-negative breast cancer cells through direct repression of the EPHA2 oncogene

    doi: 10.1093/carcin/bgv087

    Figure Lengend Snippet: EPHA2 is correlated with poor clinical outcome in TNBC and is a predicted target of miR-200a. (A) Kaplan–Meier survival plots show that high level of EPHA2 mRNA is significantly correlated to a lower overall survival in a cohort of basal-like patients (N = 343). This correlation is not significant for Luminal B (N = 495), or HER2-positive (N = 111) subtype patients. For Luminal A (N = 651) patients, high levels of EPHA2 correlate with better survival. (B) A potential target site for miR-200a was identified in the 3′UTR sequence of EPHA2 at nucleotides 716–737, using target prediction software TargetScan. Eight nucleotides within the seed sequence of miR-200a showed complete complementarity with the 3′UTR sequence of EPHA2. These nucleotides were 100% conserved between various vertebrate species. (C) Western blotting of undifferentiated HC11 cells transfected with miR-200a mimic (25nM) or control in a single (left), or double transfection (right), shows decreased levels of EPHA2 protein by miR-200a. β-Actin was used as a loading control. (D) Significant reductions of EPHA2 mRNA levels were noted within 24h after miR-200a mimic (25nM) treatment in MDA-MB-231 and SUM159 cells, compared to control mimic. (E) Western blotting of MDA-MB-231 and SUM159 cells, 48h after transfection with miR-200a mimic (25nM) or control mimic, shows that miR-200a reduced expression of EPHA2 protein in both cell lines. β-Actin was used as a loading control. Student’s t-test, two-tailed distribution was performed and P ≤ 0.05 was considered statistically significant.

    Article Snippet: To overexpress EPHA2, 800ng of EPHA2 open reading frame (ORF) expression clone and negative control vector (both from Genecopoeia, Rockville, MD, USA) were transfected using Lipofectamine 2000 (Invitrogen, Grand Island, NY, USA) according to the manufacturer instruction.

    Techniques: Sequencing, Software, Western Blot, Transfection, Control, Expressing, Two Tailed Test

    miR-200a directly targets the 3′UTR of EPHA2. (A) The constructs contain EPHA2 3′UTR sequence encompassing the predicted miR-200a site or control with (a) this site mutated, and (b) no 3′UTR sequence, cloned into luciferase reporter vectors. The constructs contains hLuc and hRLuc under the control of Sv40 and CMV promoter. hRLuc is endogenous control of construct expression. (B) HEK239 cells were transfected with plasmid containing WT or mutated EPHA2 3′UTR, or control plasmid, and either miR-200a mimic, control mimic or miR-9 mimic. Luciferase activity was measured 24h post transfection. Only the construct containing the predicted target site significantly decreased its luciferase activity, and only when miR-200a was added. (C) EPHA2 mRNA levels were reduced also in HEK239 cells. The cells were transfected with miR-200a mimic (25nM) or control mimic and collected 24h post transfection. EPHA2 and housekeeping gene 36B4 mRNA levels were measured using qPCR and data analyzed using the ΔΔCT method. For significance, Student’s t-test, two-tailed distribution was used.

    Journal: Carcinogenesis

    Article Title: miR-200a inhibits migration of triple-negative breast cancer cells through direct repression of the EPHA2 oncogene

    doi: 10.1093/carcin/bgv087

    Figure Lengend Snippet: miR-200a directly targets the 3′UTR of EPHA2. (A) The constructs contain EPHA2 3′UTR sequence encompassing the predicted miR-200a site or control with (a) this site mutated, and (b) no 3′UTR sequence, cloned into luciferase reporter vectors. The constructs contains hLuc and hRLuc under the control of Sv40 and CMV promoter. hRLuc is endogenous control of construct expression. (B) HEK239 cells were transfected with plasmid containing WT or mutated EPHA2 3′UTR, or control plasmid, and either miR-200a mimic, control mimic or miR-9 mimic. Luciferase activity was measured 24h post transfection. Only the construct containing the predicted target site significantly decreased its luciferase activity, and only when miR-200a was added. (C) EPHA2 mRNA levels were reduced also in HEK239 cells. The cells were transfected with miR-200a mimic (25nM) or control mimic and collected 24h post transfection. EPHA2 and housekeeping gene 36B4 mRNA levels were measured using qPCR and data analyzed using the ΔΔCT method. For significance, Student’s t-test, two-tailed distribution was used.

    Article Snippet: To overexpress EPHA2, 800ng of EPHA2 open reading frame (ORF) expression clone and negative control vector (both from Genecopoeia, Rockville, MD, USA) were transfected using Lipofectamine 2000 (Invitrogen, Grand Island, NY, USA) according to the manufacturer instruction.

    Techniques: Construct, Sequencing, Control, Clone Assay, Luciferase, Expressing, Transfection, Plasmid Preparation, Activity Assay, Two Tailed Test

    miR-200a reduces migration of TNBC cells through EPHA2 regulation. (A) The effect of miR-200a and EPHA2 on migration was measured in MDA-MB-231 and SUM159 cells. Cells transfected with miR-200a mimic (50nM), si-EPHA2 (100nM), EPHA2-ORF (800ng) or corresponding control for 48h were subjected to wound-healing assay. Images were taken at 0 and 12h (or 9h) after wound introduction. The white line highlights the wound edge at 0 and 12h (or 9h). (B) Quantification of relative cell migration in MDA-MB-231 and SUM159 transfected as shown in A. Distance of gap closure was measured using ImageJ. Data are presented as mean ± SD from two independent experiments. Unpaired two-tailed student’s t-test was used for significant testing, and presented as *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001. (C) Overexpression of EPHA2 rescued the anti-migratory effect of miR-200a in MDA-MB-231 and SUM159 cells. Cells were cotransfected with miR-200a mimic and EPHA2-ORF or control ORF and subjected to wound-healing assay.

    Journal: Carcinogenesis

    Article Title: miR-200a inhibits migration of triple-negative breast cancer cells through direct repression of the EPHA2 oncogene

    doi: 10.1093/carcin/bgv087

    Figure Lengend Snippet: miR-200a reduces migration of TNBC cells through EPHA2 regulation. (A) The effect of miR-200a and EPHA2 on migration was measured in MDA-MB-231 and SUM159 cells. Cells transfected with miR-200a mimic (50nM), si-EPHA2 (100nM), EPHA2-ORF (800ng) or corresponding control for 48h were subjected to wound-healing assay. Images were taken at 0 and 12h (or 9h) after wound introduction. The white line highlights the wound edge at 0 and 12h (or 9h). (B) Quantification of relative cell migration in MDA-MB-231 and SUM159 transfected as shown in A. Distance of gap closure was measured using ImageJ. Data are presented as mean ± SD from two independent experiments. Unpaired two-tailed student’s t-test was used for significant testing, and presented as *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001. (C) Overexpression of EPHA2 rescued the anti-migratory effect of miR-200a in MDA-MB-231 and SUM159 cells. Cells were cotransfected with miR-200a mimic and EPHA2-ORF or control ORF and subjected to wound-healing assay.

    Article Snippet: To overexpress EPHA2, 800ng of EPHA2 open reading frame (ORF) expression clone and negative control vector (both from Genecopoeia, Rockville, MD, USA) were transfected using Lipofectamine 2000 (Invitrogen, Grand Island, NY, USA) according to the manufacturer instruction.

    Techniques: Migration, Transfection, Control, Wound Healing Assay, Two Tailed Test, Over Expression

    EPHA2 does not affect E-cadherin levels but increases AMPK phosphorylation. (A) E-cadherin levels are independent on EPHA2 in TNBC cells. MDA-MB-231 and SUM159 cells were transfected with miR-200a mimic (50nM), s-iEPHA2 or corresponding control were subjected to western blot for E-cadherin. β-Actin was used as a loading control. (B) AMPK phosphorylation is enhanced by miR-200a-EPHA2 pathway. MDA-MB-231 cells were transfected and followed by western blot for pAMPK and total AMPK. (C) Inhibition of AMPK promotes cell migration in TNBC cells. Cells were treated with Compound C for 8h followed by wound-healing assay. Images were taken at 0 and 12h after wound introduction and relative migration distance was quantified using ImageJ.

    Journal: Carcinogenesis

    Article Title: miR-200a inhibits migration of triple-negative breast cancer cells through direct repression of the EPHA2 oncogene

    doi: 10.1093/carcin/bgv087

    Figure Lengend Snippet: EPHA2 does not affect E-cadherin levels but increases AMPK phosphorylation. (A) E-cadherin levels are independent on EPHA2 in TNBC cells. MDA-MB-231 and SUM159 cells were transfected with miR-200a mimic (50nM), s-iEPHA2 or corresponding control were subjected to western blot for E-cadherin. β-Actin was used as a loading control. (B) AMPK phosphorylation is enhanced by miR-200a-EPHA2 pathway. MDA-MB-231 cells were transfected and followed by western blot for pAMPK and total AMPK. (C) Inhibition of AMPK promotes cell migration in TNBC cells. Cells were treated with Compound C for 8h followed by wound-healing assay. Images were taken at 0 and 12h after wound introduction and relative migration distance was quantified using ImageJ.

    Article Snippet: To overexpress EPHA2, 800ng of EPHA2 open reading frame (ORF) expression clone and negative control vector (both from Genecopoeia, Rockville, MD, USA) were transfected using Lipofectamine 2000 (Invitrogen, Grand Island, NY, USA) according to the manufacturer instruction.

    Techniques: Phospho-proteomics, Transfection, Control, Western Blot, Inhibition, Migration, Wound Healing Assay

    Model illustrating how miR-200a regulates TNBC migration. (A) Differentiated epithelial cells expressing E-cadherin, EPHA2 and Ephrin. (B) TNBC cells exhibit downregulation of E-cadherin and lack of Ephrin along with a migratory and invasive phenotype. (C) miR-200a regulates both the E-cadherin and EPHA2 pathways, resulting in increased levels of E-cadherin and reduced levels of EPHA2 along with inhibited migratory and invasive capacities. (D) Proposed pathways that miR-200a can repress migration through dual pathways: by direct targeting the 3′UTR of EPHA2 (solid lines, as demonstrated in this study) and through the indirect upregulation of the E-cadherin (dashed lines, as reported in literature).

    Journal: Carcinogenesis

    Article Title: miR-200a inhibits migration of triple-negative breast cancer cells through direct repression of the EPHA2 oncogene

    doi: 10.1093/carcin/bgv087

    Figure Lengend Snippet: Model illustrating how miR-200a regulates TNBC migration. (A) Differentiated epithelial cells expressing E-cadherin, EPHA2 and Ephrin. (B) TNBC cells exhibit downregulation of E-cadherin and lack of Ephrin along with a migratory and invasive phenotype. (C) miR-200a regulates both the E-cadherin and EPHA2 pathways, resulting in increased levels of E-cadherin and reduced levels of EPHA2 along with inhibited migratory and invasive capacities. (D) Proposed pathways that miR-200a can repress migration through dual pathways: by direct targeting the 3′UTR of EPHA2 (solid lines, as demonstrated in this study) and through the indirect upregulation of the E-cadherin (dashed lines, as reported in literature).

    Article Snippet: To overexpress EPHA2, 800ng of EPHA2 open reading frame (ORF) expression clone and negative control vector (both from Genecopoeia, Rockville, MD, USA) were transfected using Lipofectamine 2000 (Invitrogen, Grand Island, NY, USA) according to the manufacturer instruction.

    Techniques: Migration, Expressing