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adai microarray data set  (Genentech inc)

 
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    Genentech inc adai microarray data set
    (A) <t>Microarray</t> analysis demonstrates that SIX1 overexpression leads to increased VEGFC mRNA in both MCF7-SIX1 cells and MCF7-SIX1 tumors. (B) Quantitation of VEGFC gene expression in MCF7-Ctrl and MCF7-SIX1 using real-time PCR. (C) SIX1 induces VEGFC promoter activity. VEGFC promoter-luciferase reporter constructs were transiently transfected into MCF7 cells, along with increasing amounts of SIX1 and a constant amount of the SIX1 cofactor, EYA2. Luciferase activity was analyzed after 48 hours. (D) ChIP was performed to detect SIX1 presence on the VEGFC promoter in MCF7 cells transfected with SIX1 and EYA2. Protein-DNA complexes were precipitated with a SIX1-specific antibody as well as a control rabbit IgG antibody, after which real-time PCR was performed with primers that flank 5 predicted SIX1 binding sites within the VEGFC promoter (red circles denote the TGATAC binding sites; green triangles denote the ATCCTGA binding sites) as well as 1 upstream region with no predicted SIX1 binding site as a negative control. Dashed line indicates the background non-specific binding of SIX1 and x axis units are base pairs upstream of transcription start site. (E) Functional VEGF-C secreted by MCF7-Ctrl and MCF7-SIX1 cells was measured by ELISA and Western blot analysis (3 clonal isolates of MCF7-Ctrl cells [lanes 1–3] and 3 clonal isolates of MCF7-SIX1 cells [lanes 4–6]) in conditioned medium after serum starvation for 48 hours. (F) MCF7-SIX1 tumors express higher levels of VEGF-C in vivo compared with the MCF7-Ctrl tumors. Immunostaining was used to detect VEGF-C and VEGF-D. Original magnification, ×400. *P < 0.05; **P < 0.01.
    Adai Microarray Data Set, supplied by Genentech inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/adai microarray data set/product/Genentech inc
    Average 90 stars, based on 1 article reviews
    adai microarray data set - by Bioz Stars, 2026-06
    90/100 stars

    Images

    1) Product Images from "SIX1 induces lymphangiogenesis and metastasis via upregulation of VEGF-C in mouse models of breast cancer"

    Article Title: SIX1 induces lymphangiogenesis and metastasis via upregulation of VEGF-C in mouse models of breast cancer

    Journal: The Journal of Clinical Investigation

    doi: 10.1172/JCI59858

    (A) Microarray analysis demonstrates that SIX1 overexpression leads to increased VEGFC mRNA in both MCF7-SIX1 cells and MCF7-SIX1 tumors. (B) Quantitation of VEGFC gene expression in MCF7-Ctrl and MCF7-SIX1 using real-time PCR. (C) SIX1 induces VEGFC promoter activity. VEGFC promoter-luciferase reporter constructs were transiently transfected into MCF7 cells, along with increasing amounts of SIX1 and a constant amount of the SIX1 cofactor, EYA2. Luciferase activity was analyzed after 48 hours. (D) ChIP was performed to detect SIX1 presence on the VEGFC promoter in MCF7 cells transfected with SIX1 and EYA2. Protein-DNA complexes were precipitated with a SIX1-specific antibody as well as a control rabbit IgG antibody, after which real-time PCR was performed with primers that flank 5 predicted SIX1 binding sites within the VEGFC promoter (red circles denote the TGATAC binding sites; green triangles denote the ATCCTGA binding sites) as well as 1 upstream region with no predicted SIX1 binding site as a negative control. Dashed line indicates the background non-specific binding of SIX1 and x axis units are base pairs upstream of transcription start site. (E) Functional VEGF-C secreted by MCF7-Ctrl and MCF7-SIX1 cells was measured by ELISA and Western blot analysis (3 clonal isolates of MCF7-Ctrl cells [lanes 1–3] and 3 clonal isolates of MCF7-SIX1 cells [lanes 4–6]) in conditioned medium after serum starvation for 48 hours. (F) MCF7-SIX1 tumors express higher levels of VEGF-C in vivo compared with the MCF7-Ctrl tumors. Immunostaining was used to detect VEGF-C and VEGF-D. Original magnification, ×400. *P < 0.05; **P < 0.01.
    Figure Legend Snippet: (A) Microarray analysis demonstrates that SIX1 overexpression leads to increased VEGFC mRNA in both MCF7-SIX1 cells and MCF7-SIX1 tumors. (B) Quantitation of VEGFC gene expression in MCF7-Ctrl and MCF7-SIX1 using real-time PCR. (C) SIX1 induces VEGFC promoter activity. VEGFC promoter-luciferase reporter constructs were transiently transfected into MCF7 cells, along with increasing amounts of SIX1 and a constant amount of the SIX1 cofactor, EYA2. Luciferase activity was analyzed after 48 hours. (D) ChIP was performed to detect SIX1 presence on the VEGFC promoter in MCF7 cells transfected with SIX1 and EYA2. Protein-DNA complexes were precipitated with a SIX1-specific antibody as well as a control rabbit IgG antibody, after which real-time PCR was performed with primers that flank 5 predicted SIX1 binding sites within the VEGFC promoter (red circles denote the TGATAC binding sites; green triangles denote the ATCCTGA binding sites) as well as 1 upstream region with no predicted SIX1 binding site as a negative control. Dashed line indicates the background non-specific binding of SIX1 and x axis units are base pairs upstream of transcription start site. (E) Functional VEGF-C secreted by MCF7-Ctrl and MCF7-SIX1 cells was measured by ELISA and Western blot analysis (3 clonal isolates of MCF7-Ctrl cells [lanes 1–3] and 3 clonal isolates of MCF7-SIX1 cells [lanes 4–6]) in conditioned medium after serum starvation for 48 hours. (F) MCF7-SIX1 tumors express higher levels of VEGF-C in vivo compared with the MCF7-Ctrl tumors. Immunostaining was used to detect VEGF-C and VEGF-D. Original magnification, ×400. *P < 0.05; **P < 0.01.

    Techniques Used: Microarray, Over Expression, Quantitation Assay, Gene Expression, Real-time Polymerase Chain Reaction, Activity Assay, Luciferase, Construct, Transfection, Control, Binding Assay, Negative Control, Functional Assay, Enzyme-linked Immunosorbent Assay, Western Blot, In Vivo, Immunostaining

    (A) SIX1 and VEGFC expression values were retrieved from an Oncomine microarray data set (as indicated in the figure) and were plotted according to different types of cell lines or by expression value. X and y axes of the right panel indicate mRNA expression analyzed on Affymetrix U133 Plus 2.0 microarrays. (B) Representative positive and negative staining of SIX1 and VEGF-C on human breast cancer tissue sections. Original magnification, ×100. (C) Model depicting the mechanism by which SIX1 promotes metastatic dissemination. Overexpression of SIX1 leads to increased VEGF-C and stimulates lymphangiogenesis, allowing for increased escape of tumor cells through the lymphatics and increased distant metastasis. However, SIX1 is also able to augment the later stages of metastasis of cancer cells that have traveled through the vasculature, thus contributing to metastatic spread via multiple mechanisms. An extension of this finding is that while inhibitors of the VEGF-C/VEGFR3 axis may prevent lymphatic spread, inhibitors of SIX1 are expected to inhibit metastasis at multiple stages, serving as powerful antimetastatic agents.
    Figure Legend Snippet: (A) SIX1 and VEGFC expression values were retrieved from an Oncomine microarray data set (as indicated in the figure) and were plotted according to different types of cell lines or by expression value. X and y axes of the right panel indicate mRNA expression analyzed on Affymetrix U133 Plus 2.0 microarrays. (B) Representative positive and negative staining of SIX1 and VEGF-C on human breast cancer tissue sections. Original magnification, ×100. (C) Model depicting the mechanism by which SIX1 promotes metastatic dissemination. Overexpression of SIX1 leads to increased VEGF-C and stimulates lymphangiogenesis, allowing for increased escape of tumor cells through the lymphatics and increased distant metastasis. However, SIX1 is also able to augment the later stages of metastasis of cancer cells that have traveled through the vasculature, thus contributing to metastatic spread via multiple mechanisms. An extension of this finding is that while inhibitors of the VEGF-C/VEGFR3 axis may prevent lymphatic spread, inhibitors of SIX1 are expected to inhibit metastasis at multiple stages, serving as powerful antimetastatic agents.

    Techniques Used: Expressing, Microarray, Negative Staining, Over Expression



    Similar Products

    adai microarray data set  (Genentech inc)
    90
    Genentech inc adai microarray data set
    (A) <t>Microarray</t> analysis demonstrates that SIX1 overexpression leads to increased VEGFC mRNA in both MCF7-SIX1 cells and MCF7-SIX1 tumors. (B) Quantitation of VEGFC gene expression in MCF7-Ctrl and MCF7-SIX1 using real-time PCR. (C) SIX1 induces VEGFC promoter activity. VEGFC promoter-luciferase reporter constructs were transiently transfected into MCF7 cells, along with increasing amounts of SIX1 and a constant amount of the SIX1 cofactor, EYA2. Luciferase activity was analyzed after 48 hours. (D) ChIP was performed to detect SIX1 presence on the VEGFC promoter in MCF7 cells transfected with SIX1 and EYA2. Protein-DNA complexes were precipitated with a SIX1-specific antibody as well as a control rabbit IgG antibody, after which real-time PCR was performed with primers that flank 5 predicted SIX1 binding sites within the VEGFC promoter (red circles denote the TGATAC binding sites; green triangles denote the ATCCTGA binding sites) as well as 1 upstream region with no predicted SIX1 binding site as a negative control. Dashed line indicates the background non-specific binding of SIX1 and x axis units are base pairs upstream of transcription start site. (E) Functional VEGF-C secreted by MCF7-Ctrl and MCF7-SIX1 cells was measured by ELISA and Western blot analysis (3 clonal isolates of MCF7-Ctrl cells [lanes 1–3] and 3 clonal isolates of MCF7-SIX1 cells [lanes 4–6]) in conditioned medium after serum starvation for 48 hours. (F) MCF7-SIX1 tumors express higher levels of VEGF-C in vivo compared with the MCF7-Ctrl tumors. Immunostaining was used to detect VEGF-C and VEGF-D. Original magnification, ×400. *P < 0.05; **P < 0.01.
    Adai Microarray Data Set, supplied by Genentech inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/adai microarray data set/product/Genentech inc
    Average 90 stars, based on 1 article reviews
    adai microarray data set - by Bioz Stars, 2026-06
    90/100 stars
    		  Buy from Supplier

    Image Search Results


    (A) Microarray analysis demonstrates that SIX1 overexpression leads to increased VEGFC mRNA in both MCF7-SIX1 cells and MCF7-SIX1 tumors. (B) Quantitation of VEGFC gene expression in MCF7-Ctrl and MCF7-SIX1 using real-time PCR. (C) SIX1 induces VEGFC promoter activity. VEGFC promoter-luciferase reporter constructs were transiently transfected into MCF7 cells, along with increasing amounts of SIX1 and a constant amount of the SIX1 cofactor, EYA2. Luciferase activity was analyzed after 48 hours. (D) ChIP was performed to detect SIX1 presence on the VEGFC promoter in MCF7 cells transfected with SIX1 and EYA2. Protein-DNA complexes were precipitated with a SIX1-specific antibody as well as a control rabbit IgG antibody, after which real-time PCR was performed with primers that flank 5 predicted SIX1 binding sites within the VEGFC promoter (red circles denote the TGATAC binding sites; green triangles denote the ATCCTGA binding sites) as well as 1 upstream region with no predicted SIX1 binding site as a negative control. Dashed line indicates the background non-specific binding of SIX1 and x axis units are base pairs upstream of transcription start site. (E) Functional VEGF-C secreted by MCF7-Ctrl and MCF7-SIX1 cells was measured by ELISA and Western blot analysis (3 clonal isolates of MCF7-Ctrl cells [lanes 1–3] and 3 clonal isolates of MCF7-SIX1 cells [lanes 4–6]) in conditioned medium after serum starvation for 48 hours. (F) MCF7-SIX1 tumors express higher levels of VEGF-C in vivo compared with the MCF7-Ctrl tumors. Immunostaining was used to detect VEGF-C and VEGF-D. Original magnification, ×400. *P < 0.05; **P < 0.01.

    Journal: The Journal of Clinical Investigation

    Article Title: SIX1 induces lymphangiogenesis and metastasis via upregulation of VEGF-C in mouse models of breast cancer

    doi: 10.1172/JCI59858

    Figure Lengend Snippet: (A) Microarray analysis demonstrates that SIX1 overexpression leads to increased VEGFC mRNA in both MCF7-SIX1 cells and MCF7-SIX1 tumors. (B) Quantitation of VEGFC gene expression in MCF7-Ctrl and MCF7-SIX1 using real-time PCR. (C) SIX1 induces VEGFC promoter activity. VEGFC promoter-luciferase reporter constructs were transiently transfected into MCF7 cells, along with increasing amounts of SIX1 and a constant amount of the SIX1 cofactor, EYA2. Luciferase activity was analyzed after 48 hours. (D) ChIP was performed to detect SIX1 presence on the VEGFC promoter in MCF7 cells transfected with SIX1 and EYA2. Protein-DNA complexes were precipitated with a SIX1-specific antibody as well as a control rabbit IgG antibody, after which real-time PCR was performed with primers that flank 5 predicted SIX1 binding sites within the VEGFC promoter (red circles denote the TGATAC binding sites; green triangles denote the ATCCTGA binding sites) as well as 1 upstream region with no predicted SIX1 binding site as a negative control. Dashed line indicates the background non-specific binding of SIX1 and x axis units are base pairs upstream of transcription start site. (E) Functional VEGF-C secreted by MCF7-Ctrl and MCF7-SIX1 cells was measured by ELISA and Western blot analysis (3 clonal isolates of MCF7-Ctrl cells [lanes 1–3] and 3 clonal isolates of MCF7-SIX1 cells [lanes 4–6]) in conditioned medium after serum starvation for 48 hours. (F) MCF7-SIX1 tumors express higher levels of VEGF-C in vivo compared with the MCF7-Ctrl tumors. Immunostaining was used to detect VEGF-C and VEGF-D. Original magnification, ×400. *P < 0.05; **P < 0.01.

    Article Snippet: Using Oncomine, expression values for SIX1 and VEGFC were retrieved from the Adai microarray data set (Genentech), and the expression data were plotted to perform a correlation analysis between SIX1 and VEGFC in breast cancer cell lines representing different histologic subtypes of breast cancer (Figure A).

    Techniques: Microarray, Over Expression, Quantitation Assay, Gene Expression, Real-time Polymerase Chain Reaction, Activity Assay, Luciferase, Construct, Transfection, Control, Binding Assay, Negative Control, Functional Assay, Enzyme-linked Immunosorbent Assay, Western Blot, In Vivo, Immunostaining

    (A) SIX1 and VEGFC expression values were retrieved from an Oncomine microarray data set (as indicated in the figure) and were plotted according to different types of cell lines or by expression value. X and y axes of the right panel indicate mRNA expression analyzed on Affymetrix U133 Plus 2.0 microarrays. (B) Representative positive and negative staining of SIX1 and VEGF-C on human breast cancer tissue sections. Original magnification, ×100. (C) Model depicting the mechanism by which SIX1 promotes metastatic dissemination. Overexpression of SIX1 leads to increased VEGF-C and stimulates lymphangiogenesis, allowing for increased escape of tumor cells through the lymphatics and increased distant metastasis. However, SIX1 is also able to augment the later stages of metastasis of cancer cells that have traveled through the vasculature, thus contributing to metastatic spread via multiple mechanisms. An extension of this finding is that while inhibitors of the VEGF-C/VEGFR3 axis may prevent lymphatic spread, inhibitors of SIX1 are expected to inhibit metastasis at multiple stages, serving as powerful antimetastatic agents.

    Journal: The Journal of Clinical Investigation

    Article Title: SIX1 induces lymphangiogenesis and metastasis via upregulation of VEGF-C in mouse models of breast cancer

    doi: 10.1172/JCI59858

    Figure Lengend Snippet: (A) SIX1 and VEGFC expression values were retrieved from an Oncomine microarray data set (as indicated in the figure) and were plotted according to different types of cell lines or by expression value. X and y axes of the right panel indicate mRNA expression analyzed on Affymetrix U133 Plus 2.0 microarrays. (B) Representative positive and negative staining of SIX1 and VEGF-C on human breast cancer tissue sections. Original magnification, ×100. (C) Model depicting the mechanism by which SIX1 promotes metastatic dissemination. Overexpression of SIX1 leads to increased VEGF-C and stimulates lymphangiogenesis, allowing for increased escape of tumor cells through the lymphatics and increased distant metastasis. However, SIX1 is also able to augment the later stages of metastasis of cancer cells that have traveled through the vasculature, thus contributing to metastatic spread via multiple mechanisms. An extension of this finding is that while inhibitors of the VEGF-C/VEGFR3 axis may prevent lymphatic spread, inhibitors of SIX1 are expected to inhibit metastasis at multiple stages, serving as powerful antimetastatic agents.

    Article Snippet: Using Oncomine, expression values for SIX1 and VEGFC were retrieved from the Adai microarray data set (Genentech), and the expression data were plotted to perform a correlation analysis between SIX1 and VEGFC in breast cancer cell lines representing different histologic subtypes of breast cancer (Figure A).

    Techniques: Expressing, Microarray, Negative Staining, Over Expression