anti cyr61  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti cyr61
    Anti Cyr61, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 1 article reviews
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    anti cyr61 - by Bioz Stars, 2023-01
    94/100 stars

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    anti cyr61  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti cyr61
    Anti Cyr61, supplied by Cell Signaling Technology Inc, 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/result/anti cyr61/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
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    cyr61  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc cyr61
    YAP confers resistance to cisplatin in ovarian cancer cells. Notes: ( A ) Cells were treated with different concentrations (0–50 μmol/L) of cisplatin for 48 hours. Cell viability was assessed using the CCK-8 assay. Data represent the mean and standard deviation values from three independent experiments (** P <0.01). ( B ) The 50% maximal inhibitory concentration (IC 50 ) values of cisplatin in the cisplatin-sensitive parent cell line OV2008 and its resistant clone C13K were calculated. Each value represents the mean ± standard deviation values from three independent experiments (** P <0.01). ( C ) The messenger RNA levels of YAP, <t>Cyr61,</t> CTGF, and CCND1 in the cells were examined using a real-time polymerase chain-reaction kit. Data represent the mean and standard deviation values from three independent experiments (** P <0.01). ( D ) Cell lysates were collected for Western blot analyses of the protein levels of YAP, Cyr61, CTGF, and CCND1.
    Cyr61, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 1 article reviews
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    1) Product Images from "YAP induces cisplatin resistance through activation of autophagy in human ovarian carcinoma cells"

    Article Title: YAP induces cisplatin resistance through activation of autophagy in human ovarian carcinoma cells

    Journal: OncoTargets and therapy

    doi: 10.2147/OTT.S102837

    YAP confers resistance to cisplatin in ovarian cancer cells. Notes: ( A ) Cells were treated with different concentrations (0–50 μmol/L) of cisplatin for 48 hours. Cell viability was assessed using the CCK-8 assay. Data represent the mean and standard deviation values from three independent experiments (** P <0.01). ( B ) The 50% maximal inhibitory concentration (IC 50 ) values of cisplatin in the cisplatin-sensitive parent cell line OV2008 and its resistant clone C13K were calculated. Each value represents the mean ± standard deviation values from three independent experiments (** P <0.01). ( C ) The messenger RNA levels of YAP, Cyr61, CTGF, and CCND1 in the cells were examined using a real-time polymerase chain-reaction kit. Data represent the mean and standard deviation values from three independent experiments (** P <0.01). ( D ) Cell lysates were collected for Western blot analyses of the protein levels of YAP, Cyr61, CTGF, and CCND1.
    Figure Legend Snippet: YAP confers resistance to cisplatin in ovarian cancer cells. Notes: ( A ) Cells were treated with different concentrations (0–50 μmol/L) of cisplatin for 48 hours. Cell viability was assessed using the CCK-8 assay. Data represent the mean and standard deviation values from three independent experiments (** P <0.01). ( B ) The 50% maximal inhibitory concentration (IC 50 ) values of cisplatin in the cisplatin-sensitive parent cell line OV2008 and its resistant clone C13K were calculated. Each value represents the mean ± standard deviation values from three independent experiments (** P <0.01). ( C ) The messenger RNA levels of YAP, Cyr61, CTGF, and CCND1 in the cells were examined using a real-time polymerase chain-reaction kit. Data represent the mean and standard deviation values from three independent experiments (** P <0.01). ( D ) Cell lysates were collected for Western blot analyses of the protein levels of YAP, Cyr61, CTGF, and CCND1.

    Techniques Used: CCK-8 Assay, Standard Deviation, Concentration Assay, Real-time Polymerase Chain Reaction, Western Blot

    Effects of YAP knockdown on cisplatin sensitivity in resistant C13K cells via impairment of autophagy. Notes: After C13K cells were transfected with YAP small interfering RNA (siRNA) and control siRNA (37.5 nM) for 48 hours, they were treated with 50 μmol/L cisplatin for 48 hours. ( A ) Cell lysates were collected for Western blot analysis of the protein expression of YAP, Cyr61, CTGF, and CCND1. ( B ) Cell viability was determined using a CCK-8 assay. Data represent the mean and standard deviation values from three independent experiments (** P <0.01). ( C ) The fluorescence intensity of rhodamine 123 in the cells was measured by fluorescence-activated cell sorting. Data shown represent the mean ± standard error values from three independent experiments (** P <0.01 vs the control siRNA group). ( D ) Cells were subjected to annexin V–propidium iodide staining. The apoptosis ratio represents the ratio of the number of cells in early stage apoptosis to that in advanced-stage apoptosis. Quantification of apoptotic cells: mean ± standard deviation values represent those from three independent experiments (** P <0.01). ( E ) Western blot analysis of the expression of cleaved caspase 3 and PARP and the autophagy-related proteins Atg-3 and Atg-5 in the control siRNA and YAP siRNA C13K cells. ( F ) Electron transmission microscopy for the detection of autophagosomes in the control siRNA and YAP siRNA C13K cells; the black arrows indicate the autophagic vacuoles (magnification 10,000×). Scale bars 2 μm.
    Figure Legend Snippet: Effects of YAP knockdown on cisplatin sensitivity in resistant C13K cells via impairment of autophagy. Notes: After C13K cells were transfected with YAP small interfering RNA (siRNA) and control siRNA (37.5 nM) for 48 hours, they were treated with 50 μmol/L cisplatin for 48 hours. ( A ) Cell lysates were collected for Western blot analysis of the protein expression of YAP, Cyr61, CTGF, and CCND1. ( B ) Cell viability was determined using a CCK-8 assay. Data represent the mean and standard deviation values from three independent experiments (** P <0.01). ( C ) The fluorescence intensity of rhodamine 123 in the cells was measured by fluorescence-activated cell sorting. Data shown represent the mean ± standard error values from three independent experiments (** P <0.01 vs the control siRNA group). ( D ) Cells were subjected to annexin V–propidium iodide staining. The apoptosis ratio represents the ratio of the number of cells in early stage apoptosis to that in advanced-stage apoptosis. Quantification of apoptotic cells: mean ± standard deviation values represent those from three independent experiments (** P <0.01). ( E ) Western blot analysis of the expression of cleaved caspase 3 and PARP and the autophagy-related proteins Atg-3 and Atg-5 in the control siRNA and YAP siRNA C13K cells. ( F ) Electron transmission microscopy for the detection of autophagosomes in the control siRNA and YAP siRNA C13K cells; the black arrows indicate the autophagic vacuoles (magnification 10,000×). Scale bars 2 μm.

    Techniques Used: Transfection, Small Interfering RNA, Western Blot, Expressing, CCK-8 Assay, Standard Deviation, Fluorescence, FACS, Staining, Transmission Assay, Microscopy

    cyr61  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc cyr61
    MiR-129-5p mimics repressed YAP and its target gene expression in PC-3 cells. Notes: ( A ) MiR-129-5p overexpression decreased YAP mRNA level in PC-3 cells. ( B ) Western blot showed that YAP protein level was reduced toward miR-129-5p overexpression. ( C ) Quantitative analysis of YAP protein level in ( B ). ( D ) MiR-129-5p overexpression decreased CTGF and <t>CYR61</t> mRNA levels in PC-3 cells. ( E ) Western blot showed that CTGF and <t>CYR61</t> <t>protein</t> levels were reduced toward miR-129-5p overexpression. ( F ) Quantitative analysis of CTGF and CYR61 protein levels in ( E ). ** P <0.01, *** P <0.001.
    Cyr61, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 1 article reviews
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    cyr61 - by Bioz Stars, 2023-01
    94/100 stars

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    1) Product Images from "miR-129-5p inhibits prostate cancer proliferation via targeting ETV1"

    Article Title: miR-129-5p inhibits prostate cancer proliferation via targeting ETV1

    Journal: OncoTargets and therapy

    doi: 10.2147/OTT.S183435

    MiR-129-5p mimics repressed YAP and its target gene expression in PC-3 cells. Notes: ( A ) MiR-129-5p overexpression decreased YAP mRNA level in PC-3 cells. ( B ) Western blot showed that YAP protein level was reduced toward miR-129-5p overexpression. ( C ) Quantitative analysis of YAP protein level in ( B ). ( D ) MiR-129-5p overexpression decreased CTGF and CYR61 mRNA levels in PC-3 cells. ( E ) Western blot showed that CTGF and CYR61 protein levels were reduced toward miR-129-5p overexpression. ( F ) Quantitative analysis of CTGF and CYR61 protein levels in ( E ). ** P <0.01, *** P <0.001.
    Figure Legend Snippet: MiR-129-5p mimics repressed YAP and its target gene expression in PC-3 cells. Notes: ( A ) MiR-129-5p overexpression decreased YAP mRNA level in PC-3 cells. ( B ) Western blot showed that YAP protein level was reduced toward miR-129-5p overexpression. ( C ) Quantitative analysis of YAP protein level in ( B ). ( D ) MiR-129-5p overexpression decreased CTGF and CYR61 mRNA levels in PC-3 cells. ( E ) Western blot showed that CTGF and CYR61 protein levels were reduced toward miR-129-5p overexpression. ( F ) Quantitative analysis of CTGF and CYR61 protein levels in ( E ). ** P <0.01, *** P <0.001.

    Techniques Used: Expressing, Over Expression, Western Blot

    MiR-129-5p downregulation elevated YAP and its target gene expression in RWPE-1 cells. Notes: ( A ) MiR-129-5p downregulation increased YAP mRNA level in RWPE-1 cells. ( B ) Western blot showed that YAP protein level was elevated toward miR-129-5p downregulation. ( C ) Quantitative analysis of YAP protein level in ( B ). ( D ) MiR-129-5p downregulation increased CTGF and CYR61 mRNA levels in RWPE-1 cells. ( E ) Western blot showed that CTGF and CYR61 protein levels were elevated toward miR-129-5p downregulation. ( F ) Quantitative analysis of CTGF and CYR61 protein levels in ( E ). * P <0.05, ** P <0.01, *** P <0.001.
    Figure Legend Snippet: MiR-129-5p downregulation elevated YAP and its target gene expression in RWPE-1 cells. Notes: ( A ) MiR-129-5p downregulation increased YAP mRNA level in RWPE-1 cells. ( B ) Western blot showed that YAP protein level was elevated toward miR-129-5p downregulation. ( C ) Quantitative analysis of YAP protein level in ( B ). ( D ) MiR-129-5p downregulation increased CTGF and CYR61 mRNA levels in RWPE-1 cells. ( E ) Western blot showed that CTGF and CYR61 protein levels were elevated toward miR-129-5p downregulation. ( F ) Quantitative analysis of CTGF and CYR61 protein levels in ( E ). * P <0.05, ** P <0.01, *** P <0.001.

    Techniques Used: Expressing, Western Blot

    cyr61  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc cyr61
    Cyr61, supplied by Cell Signaling Technology Inc, 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/result/cyr61/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
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    cyr61 - by Bioz Stars, 2023-01
    94/100 stars

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    anti human cyr61 monoclonal antibody 093g9  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti human cyr61 monoclonal antibody 093g9
    The level of <t>Cyr61</t> in the HCT-8/L-OHP and HCT116/L-OHP cell lines. (A) and (D) The mRNA level of Cyr61 was determined by RT-PCR. (B) and (E) The protein level of Cyr61 was determined by western blotting. (C) and (F) The concentration of Cyr61 in the cell supernatant was measured by ELISA. The data are expressed as the mean ± SEM values (n=3). *P < 0.05, **P < 0.01.
    Anti Human Cyr61 Monoclonal Antibody 093g9, supplied by Cell Signaling Technology Inc, 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/result/anti human cyr61 monoclonal antibody 093g9/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
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    anti human cyr61 monoclonal antibody 093g9 - by Bioz Stars, 2023-01
    94/100 stars

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    1) Product Images from "Cyr61 mediates oxaliplatin resistance in colorectal cancer cells by regulating Bcl-xL expression"

    Article Title: Cyr61 mediates oxaliplatin resistance in colorectal cancer cells by regulating Bcl-xL expression

    Journal: Journal of Cancer

    doi: 10.7150/jca.48891

    The level of Cyr61 in the HCT-8/L-OHP and HCT116/L-OHP cell lines. (A) and (D) The mRNA level of Cyr61 was determined by RT-PCR. (B) and (E) The protein level of Cyr61 was determined by western blotting. (C) and (F) The concentration of Cyr61 in the cell supernatant was measured by ELISA. The data are expressed as the mean ± SEM values (n=3). *P < 0.05, **P < 0.01.
    Figure Legend Snippet: The level of Cyr61 in the HCT-8/L-OHP and HCT116/L-OHP cell lines. (A) and (D) The mRNA level of Cyr61 was determined by RT-PCR. (B) and (E) The protein level of Cyr61 was determined by western blotting. (C) and (F) The concentration of Cyr61 in the cell supernatant was measured by ELISA. The data are expressed as the mean ± SEM values (n=3). *P < 0.05, **P < 0.01.

    Techniques Used: Reverse Transcription Polymerase Chain Reaction, Western Blot, Concentration Assay, Enzyme-linked Immunosorbent Assay

    Cyr61 knockdown reduces the resistance of L-OHP-resistant CRC cells. (A) and (D) Lentiviral vectors expressing shCyr61 were transduced into HCT-8/L-OHP cells and HCT116/L-OHP cells to knock down Cyr61 expression, and the concentration of Cyr61 in the cell supernatant was detected by ELISA. (B) and (E) shCyr61 and shNC cells from HCT-8/L-OHP cells and HCT116/L-OHP cells were treated with increasing doses of L-OHP for 72 h and subjected to a CCK8 assay; the IC50 of L-OHP in the cells was then calculated using GraphPad Prism 5.0. (C) and (F) HCT-8 and HCT116 cells were preincubated with exogenous Cyr61 (1 µg/ml) for 24 h and were then treated with increasing doses of L-OHP. After incubation for 72 hours and analysis with a CCK8 assay, the IC50 of L-OHP in the cells was calculated using GraphPad Prism 5.0. The data are expressed as the mean ± SEM values (n=3). *P < 0.05, **P < 0.01.
    Figure Legend Snippet: Cyr61 knockdown reduces the resistance of L-OHP-resistant CRC cells. (A) and (D) Lentiviral vectors expressing shCyr61 were transduced into HCT-8/L-OHP cells and HCT116/L-OHP cells to knock down Cyr61 expression, and the concentration of Cyr61 in the cell supernatant was detected by ELISA. (B) and (E) shCyr61 and shNC cells from HCT-8/L-OHP cells and HCT116/L-OHP cells were treated with increasing doses of L-OHP for 72 h and subjected to a CCK8 assay; the IC50 of L-OHP in the cells was then calculated using GraphPad Prism 5.0. (C) and (F) HCT-8 and HCT116 cells were preincubated with exogenous Cyr61 (1 µg/ml) for 24 h and were then treated with increasing doses of L-OHP. After incubation for 72 hours and analysis with a CCK8 assay, the IC50 of L-OHP in the cells was calculated using GraphPad Prism 5.0. The data are expressed as the mean ± SEM values (n=3). *P < 0.05, **P < 0.01.

    Techniques Used: Expressing, Concentration Assay, Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Incubation

    Cyr61 knockdown enhances L-OHP-induced apoptosis in L-OHP-resistant CRC cells . (A) HCT-8/L-OHP-shCyr61 and HCT-8/L-OHP-shNC cells were treated with L-OHP (50 µg/ml) for 72 h, and apoptosis was assessed with a BD FACSCanto II cytometer. (B) HCT116/L-OHP-shCyr61 and HCT116/L-OHP-shNC cells were treated with L-OHP (30 µg/ml) for 72 h, and the percentages of apoptotic cells were determined with a BD FACSCanto II cytometer. The data are expressed as the mean ± SEM values (n=3). *P < 0.05, **P < 0.01.
    Figure Legend Snippet: Cyr61 knockdown enhances L-OHP-induced apoptosis in L-OHP-resistant CRC cells . (A) HCT-8/L-OHP-shCyr61 and HCT-8/L-OHP-shNC cells were treated with L-OHP (50 µg/ml) for 72 h, and apoptosis was assessed with a BD FACSCanto II cytometer. (B) HCT116/L-OHP-shCyr61 and HCT116/L-OHP-shNC cells were treated with L-OHP (30 µg/ml) for 72 h, and the percentages of apoptotic cells were determined with a BD FACSCanto II cytometer. The data are expressed as the mean ± SEM values (n=3). *P < 0.05, **P < 0.01.

    Techniques Used: Cytometry

    Bcl-xL is involved in the effect of Cyr61 on drug resistance. (A) Left panel: Bcl-2, Bcl-xL, XIAP and Survivin mRNA levels in HCT-8/L-OHP and parental HCT-8 cells were determined by real-time PCR; Right panel: Bcl-xL protein levels in HCT-8/L-OHP and parental HCT-8 cells were determined by western blotting. (B) HCT-8/L-OHP-shCyr61 and HCT-8/L-OHP-shNC cells were treated with L-OHP (50 µg/ml) for 72 h, and the protein level of Bcl-xL was detected by western blotting. (C) HCT-8-Cyr61 and HCT-8-NC cells were cultured for 72 h, and the concentration of Cyr61 in the cell supernatant was determined by ELISA. (D) HCT8-Cyr61 and HCT8-NC cells were treated with L-OHP (10 µg/ml) for 72 h, and the protein level of Bcl-xL was determined by western blotting. (E) HCT-8-Cyr61 and HCT-8-NC cells were treated with L-OHP (10 µg/ml), A1155463 (5 µM) (a specific Bcl-xL inhibitor), or L-OHP + A1155463 for 72 h, and apoptosis was analyzed by flow cytometry. (F) Left panel: HCT-8-Cyr61 and HCT-8-NC cells were treated with increasing doses of L-OHP or increasing doses of L-OHP+ A1155463 (5 µM) for 72 h and were then analyzed with a CCK8 assay The IC50 of L-OHP in HCT-8-Cyr61 and HCT-8-NC cells was calculated using GraphPad Prism 5.0. (G) HCT116/L-OHP-shCyr61 and HCT116/L-OHP-shNC cells were treated with L-OHP (30 µg/ml) for 72 h, and the protein level of Bcl-xL was determined by western blotting. (H) HCT116-Cyr61 and HCT116-NC cells were cultured for 72 h, and the concentration of Cyr61 in the cell supernatant was determined by ELISA. (I) HCT116-Cyr61 and HCT116-NC cells were treated with L-OHP (10 µg/ml) for 72 h, and the protein level of Bcl-xL was determined by western blotting. (J) HCT116-Cyr61 and HCT116-NC cells were treated with increasing doses of L-OHP or increasing doses of L-OHP+ A1155463 (5 µM) for 72 h and were then analyzed with a CCK8 assay. Then, the IC50 of L-OHP in HCT116-Cyr61 and HCT116-NC cells was calculated using GraphPad Prism 5.0. The data are expressed as the mean ± SEM values (n=3). *P < 0.05, **P < 0.01.
    Figure Legend Snippet: Bcl-xL is involved in the effect of Cyr61 on drug resistance. (A) Left panel: Bcl-2, Bcl-xL, XIAP and Survivin mRNA levels in HCT-8/L-OHP and parental HCT-8 cells were determined by real-time PCR; Right panel: Bcl-xL protein levels in HCT-8/L-OHP and parental HCT-8 cells were determined by western blotting. (B) HCT-8/L-OHP-shCyr61 and HCT-8/L-OHP-shNC cells were treated with L-OHP (50 µg/ml) for 72 h, and the protein level of Bcl-xL was detected by western blotting. (C) HCT-8-Cyr61 and HCT-8-NC cells were cultured for 72 h, and the concentration of Cyr61 in the cell supernatant was determined by ELISA. (D) HCT8-Cyr61 and HCT8-NC cells were treated with L-OHP (10 µg/ml) for 72 h, and the protein level of Bcl-xL was determined by western blotting. (E) HCT-8-Cyr61 and HCT-8-NC cells were treated with L-OHP (10 µg/ml), A1155463 (5 µM) (a specific Bcl-xL inhibitor), or L-OHP + A1155463 for 72 h, and apoptosis was analyzed by flow cytometry. (F) Left panel: HCT-8-Cyr61 and HCT-8-NC cells were treated with increasing doses of L-OHP or increasing doses of L-OHP+ A1155463 (5 µM) for 72 h and were then analyzed with a CCK8 assay The IC50 of L-OHP in HCT-8-Cyr61 and HCT-8-NC cells was calculated using GraphPad Prism 5.0. (G) HCT116/L-OHP-shCyr61 and HCT116/L-OHP-shNC cells were treated with L-OHP (30 µg/ml) for 72 h, and the protein level of Bcl-xL was determined by western blotting. (H) HCT116-Cyr61 and HCT116-NC cells were cultured for 72 h, and the concentration of Cyr61 in the cell supernatant was determined by ELISA. (I) HCT116-Cyr61 and HCT116-NC cells were treated with L-OHP (10 µg/ml) for 72 h, and the protein level of Bcl-xL was determined by western blotting. (J) HCT116-Cyr61 and HCT116-NC cells were treated with increasing doses of L-OHP or increasing doses of L-OHP+ A1155463 (5 µM) for 72 h and were then analyzed with a CCK8 assay. Then, the IC50 of L-OHP in HCT116-Cyr61 and HCT116-NC cells was calculated using GraphPad Prism 5.0. The data are expressed as the mean ± SEM values (n=3). *P < 0.05, **P < 0.01.

    Techniques Used: Real-time Polymerase Chain Reaction, Western Blot, Cell Culture, Concentration Assay, Enzyme-linked Immunosorbent Assay, Flow Cytometry, CCK-8 Assay

    cyr61  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc cyr61
    Cyr61, supplied by Cell Signaling Technology Inc, 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/result/cyr61/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
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    cyr61 - by Bioz Stars, 2023-01
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    cyr61  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc cyr61
    FGF6 inhibits activation of the Hippo pathway in NRCMs after OGD. (A) Western blot was performed to determine the protein levels of p‐MST1, MST1, p‐LATS1, LATS1, p‐YAP, YAP, CTGF and <t>CYR61</t> in NRCMs in different group. n >4 per group. (B) Western blot analysis the subcellular localization of YAP in NRCMs in different group. Quantitative analysis of expressions of p‐MST1, MST1, p‐LATS1, LATS1, p‐YAP, YAP, CTGF and CYR61 in (A), quantitative analysis of expressions of YAP in nuclear extracts. (C) Representative immunofluorescence (green for YAP, blue for DAPI) analysis subcellular localization of YAP in NRCMs in different group. n = 5 per group. (D) RT‐PCR analysis of the mRNA levels of YAP and CTGF in NRCMs in different group. n = 3 per group. Data represent means ± SEM. Two‐tailed Student's t test. * p <0.05, ** p <0.01, *** p <0.001
    Cyr61, supplied by Cell Signaling Technology Inc, 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/result/cyr61/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
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    1) Product Images from "FGF6 promotes cardiac repair after myocardial infarction by inhibiting the Hippo pathway"

    Article Title: FGF6 promotes cardiac repair after myocardial infarction by inhibiting the Hippo pathway

    Journal: Cell Proliferation

    doi: 10.1111/cpr.13221

    FGF6 inhibits activation of the Hippo pathway in NRCMs after OGD. (A) Western blot was performed to determine the protein levels of p‐MST1, MST1, p‐LATS1, LATS1, p‐YAP, YAP, CTGF and CYR61 in NRCMs in different group. n >4 per group. (B) Western blot analysis the subcellular localization of YAP in NRCMs in different group. Quantitative analysis of expressions of p‐MST1, MST1, p‐LATS1, LATS1, p‐YAP, YAP, CTGF and CYR61 in (A), quantitative analysis of expressions of YAP in nuclear extracts. (C) Representative immunofluorescence (green for YAP, blue for DAPI) analysis subcellular localization of YAP in NRCMs in different group. n = 5 per group. (D) RT‐PCR analysis of the mRNA levels of YAP and CTGF in NRCMs in different group. n = 3 per group. Data represent means ± SEM. Two‐tailed Student's t test. * p <0.05, ** p <0.01, *** p <0.001
    Figure Legend Snippet: FGF6 inhibits activation of the Hippo pathway in NRCMs after OGD. (A) Western blot was performed to determine the protein levels of p‐MST1, MST1, p‐LATS1, LATS1, p‐YAP, YAP, CTGF and CYR61 in NRCMs in different group. n >4 per group. (B) Western blot analysis the subcellular localization of YAP in NRCMs in different group. Quantitative analysis of expressions of p‐MST1, MST1, p‐LATS1, LATS1, p‐YAP, YAP, CTGF and CYR61 in (A), quantitative analysis of expressions of YAP in nuclear extracts. (C) Representative immunofluorescence (green for YAP, blue for DAPI) analysis subcellular localization of YAP in NRCMs in different group. n = 5 per group. (D) RT‐PCR analysis of the mRNA levels of YAP and CTGF in NRCMs in different group. n = 3 per group. Data represent means ± SEM. Two‐tailed Student's t test. * p <0.05, ** p <0.01, *** p <0.001

    Techniques Used: Activation Assay, Western Blot, Immunofluorescence, Reverse Transcription Polymerase Chain Reaction, Two Tailed Test

    FGF6 inhibits activation of the Hippo pathway in CMs after MI. (A) Western blot was performed to determine the protein levels of p‐MST1, MST1, p‐LATS1, LATS1, p‐YAP, YAP, CTGF and CYR61 in the heart from different group mice. n >3 per group. (B) Western blot analysis the subcellular localization of YAP in the heart from different group mice. n = 3 per group. Quantitative analysis of expressions of p‐MST1, MST1, p‐LATS1, LATS1, p‐YAP, YAP, CTGF, and CYR61 in (A), quantitative analysis of expressions of YAP in nuclear extracts. (C) Representative immunofluorescence (green for YAP, blue for DAPI) analysis subcellular localization of YAP in the heart section from different group mice. (D) RT‐PCR analysis of the mRNA levels of YAP and CTGF in the heart from different group. n >3 per group; n = 5 per group. Data represent means ± SEM. Two‐tailed Student's t test. * p <0.05, ** p <0.01, *** p <0.001
    Figure Legend Snippet: FGF6 inhibits activation of the Hippo pathway in CMs after MI. (A) Western blot was performed to determine the protein levels of p‐MST1, MST1, p‐LATS1, LATS1, p‐YAP, YAP, CTGF and CYR61 in the heart from different group mice. n >3 per group. (B) Western blot analysis the subcellular localization of YAP in the heart from different group mice. n = 3 per group. Quantitative analysis of expressions of p‐MST1, MST1, p‐LATS1, LATS1, p‐YAP, YAP, CTGF, and CYR61 in (A), quantitative analysis of expressions of YAP in nuclear extracts. (C) Representative immunofluorescence (green for YAP, blue for DAPI) analysis subcellular localization of YAP in the heart section from different group mice. (D) RT‐PCR analysis of the mRNA levels of YAP and CTGF in the heart from different group. n >3 per group; n = 5 per group. Data represent means ± SEM. Two‐tailed Student's t test. * p <0.05, ** p <0.01, *** p <0.001

    Techniques Used: Activation Assay, Western Blot, Immunofluorescence, Reverse Transcription Polymerase Chain Reaction, Two Tailed Test

    FGF6 protects cardiac function via YAP. (A) Schematic diagram demonstrates the animal experiment design. (B) Western blot was performed and quantitatively analysed to determine the protein levels of CTGF, CYR61 in the hearts of different group mice. n = 4 per group. (C) Representative M‐mode echocardiographic recording obtained from different group mice. n >7 per group. (D) Quantitative analysis of LV ejection fraction (EF), fractional shortening (FS). (E) Masson trichrome staining was performed to detect cardiac fibrosis area of different group mice. Scale bar = 2 mm. n = 5 per group. (F) TTC staining was performed to detect cardiac ischemic area of different group mice. Scale bar = 2 mm. n = 5 per group. (G) Quantitative analysis of cardiac fibrosis area in (E). (H) Quantitative analysis of cardiac ischemic area in (F). Data represent means ± SEM. Two‐tailed Student's t test. * p <0.05, ** p <0.01, *** p <0.001
    Figure Legend Snippet: FGF6 protects cardiac function via YAP. (A) Schematic diagram demonstrates the animal experiment design. (B) Western blot was performed and quantitatively analysed to determine the protein levels of CTGF, CYR61 in the hearts of different group mice. n = 4 per group. (C) Representative M‐mode echocardiographic recording obtained from different group mice. n >7 per group. (D) Quantitative analysis of LV ejection fraction (EF), fractional shortening (FS). (E) Masson trichrome staining was performed to detect cardiac fibrosis area of different group mice. Scale bar = 2 mm. n = 5 per group. (F) TTC staining was performed to detect cardiac ischemic area of different group mice. Scale bar = 2 mm. n = 5 per group. (G) Quantitative analysis of cardiac fibrosis area in (E). (H) Quantitative analysis of cardiac ischemic area in (F). Data represent means ± SEM. Two‐tailed Student's t test. * p <0.05, ** p <0.01, *** p <0.001

    Techniques Used: Western Blot, Staining, Two Tailed Test

    FGF6 inhibits the Hippo pathway via ERK1/2. (A) Western blot was performed to determine the protein levels of p‐ERK1/2, ERK1/2, p‐MST1, MST1, p‐LATS1, LATS1, p‐YAP and YAP in NRCMs in different group. Quantitative analysis of expressions of p‐MST1, MST1, p‐LATS1, LATS1, p‐YAP, YAP, CTGF and CYR61. n >3 per group. (B) Western blot analysis the subcellular localization of YAP in NRCMs in different group. n = 3 per group. Quantitative analysis of expressions of YAP in nuclear extracts. (C) Representative immunofluorescence (green for YAP, blue for DAPI) analysis subcellular localization of YAP in NRCMs in different group. n = 5 per group. Data represent means ± SEM. Two‐tailed Student's t test. * p <0.05, ** p <0.01, *** p <0.001
    Figure Legend Snippet: FGF6 inhibits the Hippo pathway via ERK1/2. (A) Western blot was performed to determine the protein levels of p‐ERK1/2, ERK1/2, p‐MST1, MST1, p‐LATS1, LATS1, p‐YAP and YAP in NRCMs in different group. Quantitative analysis of expressions of p‐MST1, MST1, p‐LATS1, LATS1, p‐YAP, YAP, CTGF and CYR61. n >3 per group. (B) Western blot analysis the subcellular localization of YAP in NRCMs in different group. n = 3 per group. Quantitative analysis of expressions of YAP in nuclear extracts. (C) Representative immunofluorescence (green for YAP, blue for DAPI) analysis subcellular localization of YAP in NRCMs in different group. n = 5 per group. Data represent means ± SEM. Two‐tailed Student's t test. * p <0.05, ** p <0.01, *** p <0.001

    Techniques Used: Western Blot, Immunofluorescence, Two Tailed Test

    anti cyr61  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti cyr61
    Inhibition of geranylgeranyl biosynthesis down-regulates expression of the kinetochore/centromere-related proteins in breast cancer cells. A. The quantitative RT-PCR (qRT-PCR) assay of expression of the mRNA of kinetochore/centromere-related protein in the breast cancer MDA-MB-231 and MDA-MB-453 cells upon treatment with the solvent (DMSO), 10 μM atorvastatin (AT), and 10 μM atorvastatin plus 10 μM geranylgeraniol (AT+GGOH) for 48 hours. Data are from three independent experiments. *P<0.05; **P<0.01. B. The conventional RT-PCR assay of expression of the YAP/TAZ target gene <t>CYR61</t> and the kinetochore/centromere regulatory genes ZWINT and BUB1 (the left panel). The Western blot assay of CYR61 and CENPM upon the treatments (the right panel). C. The immunofluorescent staining assay of the level and nuclear localization of the kinetochore/centromere protein CENPA upon the treatments. Bar, 10 μm.
    Anti Cyr61, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Geranylgeranylation signaling promotes breast cancer cell mitosis via the YAP-activated transcription of kinetochore/centromere genes"

    Article Title: Geranylgeranylation signaling promotes breast cancer cell mitosis via the YAP-activated transcription of kinetochore/centromere genes

    Journal: American Journal of Cancer Research

    doi:

    Inhibition of geranylgeranyl biosynthesis down-regulates expression of the kinetochore/centromere-related proteins in breast cancer cells. A. The quantitative RT-PCR (qRT-PCR) assay of expression of the mRNA of kinetochore/centromere-related protein in the breast cancer MDA-MB-231 and MDA-MB-453 cells upon treatment with the solvent (DMSO), 10 μM atorvastatin (AT), and 10 μM atorvastatin plus 10 μM geranylgeraniol (AT+GGOH) for 48 hours. Data are from three independent experiments. *P<0.05; **P<0.01. B. The conventional RT-PCR assay of expression of the YAP/TAZ target gene CYR61 and the kinetochore/centromere regulatory genes ZWINT and BUB1 (the left panel). The Western blot assay of CYR61 and CENPM upon the treatments (the right panel). C. The immunofluorescent staining assay of the level and nuclear localization of the kinetochore/centromere protein CENPA upon the treatments. Bar, 10 μm.
    Figure Legend Snippet: Inhibition of geranylgeranyl biosynthesis down-regulates expression of the kinetochore/centromere-related proteins in breast cancer cells. A. The quantitative RT-PCR (qRT-PCR) assay of expression of the mRNA of kinetochore/centromere-related protein in the breast cancer MDA-MB-231 and MDA-MB-453 cells upon treatment with the solvent (DMSO), 10 μM atorvastatin (AT), and 10 μM atorvastatin plus 10 μM geranylgeraniol (AT+GGOH) for 48 hours. Data are from three independent experiments. *P<0.05; **P<0.01. B. The conventional RT-PCR assay of expression of the YAP/TAZ target gene CYR61 and the kinetochore/centromere regulatory genes ZWINT and BUB1 (the left panel). The Western blot assay of CYR61 and CENPM upon the treatments (the right panel). C. The immunofluorescent staining assay of the level and nuclear localization of the kinetochore/centromere protein CENPA upon the treatments. Bar, 10 μm.

    Techniques Used: Inhibition, Expressing, Quantitative RT-PCR, Reverse Transcription Polymerase Chain Reaction, Western Blot, Staining

    cyr61  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc cyr61
    Serum <t>CYR61</t> level and its association with severity of COPD. Sera were collected from COPD patients and controls. (A,B) Serum CYR61 level was detected using ELISA. (A) Serum CYR61 level was compared between COPD patients and controls. All data were represented as means ± S.E.M. ( N = 150). (B) Serum CYR61 level was compared among different grades of COPD patients. All data were represented as means ± S.E.M. ( N = 69 for G 1-2 patients, N = 48 for G 3 patients, N = 33 for G 4 patients). (C,D) Pulmonary CYR61 expression was compared between COPD patients and controls. (C) Three representative pictures. (D) Quantitative analysis of CYR61-positive cells in COPD patients and controls. (E,F) Pulmonary CYR61 was compared among different grades of COPD patients. (E) Three representative pictures: arrows indicate CYR61-positive cell; (F) Quantitative analysis of CYR61-positive cells in COPD patients with different grades. All data were represented as means ± S.E.M. ( N = 6). * P < 0.05, ** P < 0.01.
    Cyr61, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Serum CYR61 Is Associated With Airway Inflammation and Is a Potential Biomarker for Severity in Chronic Obstructive Pulmonary Disease"

    Article Title: Serum CYR61 Is Associated With Airway Inflammation and Is a Potential Biomarker for Severity in Chronic Obstructive Pulmonary Disease

    Journal: Frontiers in Medicine

    doi: 10.3389/fmed.2021.781596

    Serum CYR61 level and its association with severity of COPD. Sera were collected from COPD patients and controls. (A,B) Serum CYR61 level was detected using ELISA. (A) Serum CYR61 level was compared between COPD patients and controls. All data were represented as means ± S.E.M. ( N = 150). (B) Serum CYR61 level was compared among different grades of COPD patients. All data were represented as means ± S.E.M. ( N = 69 for G 1-2 patients, N = 48 for G 3 patients, N = 33 for G 4 patients). (C,D) Pulmonary CYR61 expression was compared between COPD patients and controls. (C) Three representative pictures. (D) Quantitative analysis of CYR61-positive cells in COPD patients and controls. (E,F) Pulmonary CYR61 was compared among different grades of COPD patients. (E) Three representative pictures: arrows indicate CYR61-positive cell; (F) Quantitative analysis of CYR61-positive cells in COPD patients with different grades. All data were represented as means ± S.E.M. ( N = 6). * P < 0.05, ** P < 0.01.
    Figure Legend Snippet: Serum CYR61 level and its association with severity of COPD. Sera were collected from COPD patients and controls. (A,B) Serum CYR61 level was detected using ELISA. (A) Serum CYR61 level was compared between COPD patients and controls. All data were represented as means ± S.E.M. ( N = 150). (B) Serum CYR61 level was compared among different grades of COPD patients. All data were represented as means ± S.E.M. ( N = 69 for G 1-2 patients, N = 48 for G 3 patients, N = 33 for G 4 patients). (C,D) Pulmonary CYR61 expression was compared between COPD patients and controls. (C) Three representative pictures. (D) Quantitative analysis of CYR61-positive cells in COPD patients and controls. (E,F) Pulmonary CYR61 was compared among different grades of COPD patients. (E) Three representative pictures: arrows indicate CYR61-positive cell; (F) Quantitative analysis of CYR61-positive cells in COPD patients with different grades. All data were represented as means ± S.E.M. ( N = 6). * P < 0.05, ** P < 0.01.

    Techniques Used: Enzyme-linked Immunosorbent Assay, Expressing

    The correlation between serum CYR61 and lung function indexes in COPD patients. Pulmonary function was measured in 150 COPD patients. Sera were collected and CYR61 was detected using ELISA. Correlation between serum CYR61 and lung function indexes was analyzed. (A) CYR61 vs. FVC(L); (B) CYR61 vs. FEV1(L); (C) CYR61 vs. FEV1/FVC (%); (D) CYR61 vs. FEV1(%).
    Figure Legend Snippet: The correlation between serum CYR61 and lung function indexes in COPD patients. Pulmonary function was measured in 150 COPD patients. Sera were collected and CYR61 was detected using ELISA. Correlation between serum CYR61 and lung function indexes was analyzed. (A) CYR61 vs. FVC(L); (B) CYR61 vs. FEV1(L); (C) CYR61 vs. FEV1/FVC (%); (D) CYR61 vs. FEV1(%).

    Techniques Used: Enzyme-linked Immunosorbent Assay

    Association of serum  CYR61  with lung function.
    Figure Legend Snippet: Association of serum CYR61 with lung function.

    Techniques Used:

    The association between serum CYR61 and pulmonary NF-κB activation in COPD patients. Lung tissues were collected from COPD patients and controls. Pulmonary NF-κB p65 was detected using IHC. (A,B) Pulmonary NF-κB p65-positive nuclei were compared between COPD patients and control subjects. (A) Three representative pictures: arrows indicate p65-positive nuclei; (B) Quantitative analysis of p65-positive nuclei in COPD patients and controls. (C,D) Pulmonary NF-κB p65-positive nuclei were compared among COPD patients with different levels of CYR61. (C) Three representative pictures: arrows indicate p65-positive nuclei; (D) Quantitative analysis of p65-positive nuclei in COPD patients with different levels of CYR61. All data were represented as means ± S.E.M. ( N = 6). * P < 0.05, ** P < 0.01.
    Figure Legend Snippet: The association between serum CYR61 and pulmonary NF-κB activation in COPD patients. Lung tissues were collected from COPD patients and controls. Pulmonary NF-κB p65 was detected using IHC. (A,B) Pulmonary NF-κB p65-positive nuclei were compared between COPD patients and control subjects. (A) Three representative pictures: arrows indicate p65-positive nuclei; (B) Quantitative analysis of p65-positive nuclei in COPD patients and controls. (C,D) Pulmonary NF-κB p65-positive nuclei were compared among COPD patients with different levels of CYR61. (C) Three representative pictures: arrows indicate p65-positive nuclei; (D) Quantitative analysis of p65-positive nuclei in COPD patients with different levels of CYR61. All data were represented as means ± S.E.M. ( N = 6). * P < 0.05, ** P < 0.01.

    Techniques Used: Activation Assay

    The association of serum CYR61 level with serum inflammatory cytokines in COPD patients. Sera were collected from 150 COPD patients and 150 control subjects. Serum CYR61 and inflammatory cytokines were detected using ELISA. (A,D) Association between serum CYR61 and MCP-1 was analyzed among all subjects. (A) Serum MCP-1 was compared among subjects with different levels of CYR61. (D) Correlation analysis between serum CYR61 and MCP-1. (B,E) Association between serum CYR61 and MCP-1 was analyzed among COPD patients. (B) Serum MCP-1 was compared among COPD patients with different levels of CYR61. (E) Correlation analysis between serum CYR61 and MCP-1. (C,F) Association between serum CYR61 and MCP-1 was analyzed among control subjects. (C) Serum MCP-1 was compared among control subjects with different levels of CYR61. (F) Correlation analysis between serum CYR61 and MCP-1. (G,J) Association between serum CYR61 and TNF-α was analyzed among all subjects. (G) Serum TNF-α was compared among subjects with different levels of CYR61. (J) Correlation analysis between serum CYR61 and TNF-α. (H,K) Association between serum CYR61 and TNF-α was analyzed among COPD patients. (H) Serum TNF-α was compared among COPD patients with different levels of CYR61. (K) Correlation analysis between serum CYR61 and TNF-α. (I,L) Association between serum CYR61 and TNF-α was analyzed among control subjects. (I) Serum TNF-α was compared among control subjects with different levels of CYR61. (L) Correlation analysis between serum CYR61 and TNF-α. * P < 0.05, ** P < 0.01.
    Figure Legend Snippet: The association of serum CYR61 level with serum inflammatory cytokines in COPD patients. Sera were collected from 150 COPD patients and 150 control subjects. Serum CYR61 and inflammatory cytokines were detected using ELISA. (A,D) Association between serum CYR61 and MCP-1 was analyzed among all subjects. (A) Serum MCP-1 was compared among subjects with different levels of CYR61. (D) Correlation analysis between serum CYR61 and MCP-1. (B,E) Association between serum CYR61 and MCP-1 was analyzed among COPD patients. (B) Serum MCP-1 was compared among COPD patients with different levels of CYR61. (E) Correlation analysis between serum CYR61 and MCP-1. (C,F) Association between serum CYR61 and MCP-1 was analyzed among control subjects. (C) Serum MCP-1 was compared among control subjects with different levels of CYR61. (F) Correlation analysis between serum CYR61 and MCP-1. (G,J) Association between serum CYR61 and TNF-α was analyzed among all subjects. (G) Serum TNF-α was compared among subjects with different levels of CYR61. (J) Correlation analysis between serum CYR61 and TNF-α. (H,K) Association between serum CYR61 and TNF-α was analyzed among COPD patients. (H) Serum TNF-α was compared among COPD patients with different levels of CYR61. (K) Correlation analysis between serum CYR61 and TNF-α. (I,L) Association between serum CYR61 and TNF-α was analyzed among control subjects. (I) Serum TNF-α was compared among control subjects with different levels of CYR61. (L) Correlation analysis between serum CYR61 and TNF-α. * P < 0.05, ** P < 0.01.

    Techniques Used: Enzyme-linked Immunosorbent Assay

    Associations of serum  CYR61  with MCP-1 and TNF-α.
    Figure Legend Snippet: Associations of serum CYR61 with MCP-1 and TNF-α.

    Techniques Used:

    Association of serum  CYR61  and hospital stays in COPD patients.
    Figure Legend Snippet: Association of serum CYR61 and hospital stays in COPD patients.

    Techniques Used:

    angiogenic inducer 61 cyr61  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc angiogenic inducer 61 cyr61
    The cell function analysis are all chemically synthesized interference lncRNA and eukaryotic plasmid-mediated lncRNA transient transfection. These have limited gene silencing and overexpression efficiency and show that the correlation between LNC01508 and OC cisplatin resistance is not highly significant. Furthermore, the effect of eukaryotic plasmid-mediated lncRNA overexpression is better than the chemical synthesis of lncRNA. This suggests a stable transfection in vitro to provide knockout and overexpression effects. (A) qPCR detects a lower LINC01508 expression, and the CCK-8 assay measures the cell viability. IC 50 values in LINC01508 inhibition OV2008 cells. (B) qPCR inspects a higher LINC01508 expression, and the CCK-8 assay measures the cell viability. IC 50 values in LINC01508 overexpression C13K cells. (C and D) Colony formation assays were conducted to determine the cell proliferation ability for transfected OC cells. (E and F) GAPDH, <t>Cyr61,</t> ERCC1, and p-AKT protein levels were determined by Western blot. All experiments are repeated in triplicated, and data are shown as mean±SE. lncRNA, long non-coding RNAs; OC, ovarian cancer; qPCR, quantitative real-time polymerase chain reaction; CCK-8, cell counting kit-8; IC 50 , half maximal inhibitory concentration; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; Cyr61, cysteine-rich angiogenic inducer 61; ERCC1, excision repair cross complementing‐group 1; p-AKT, phospho-AKT; SE, standard error. * p<0.05; † p<0.01.
    Angiogenic Inducer 61 Cyr61, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Downregulation of LINC01508 contributes to cisplatin resistance in ovarian cancer via the regulation of the Hippo-YAP pathway"

    Article Title: Downregulation of LINC01508 contributes to cisplatin resistance in ovarian cancer via the regulation of the Hippo-YAP pathway

    Journal: Journal of Gynecologic Oncology

    doi: 10.3802/jgo.2021.32.e77

    The cell function analysis are all chemically synthesized interference lncRNA and eukaryotic plasmid-mediated lncRNA transient transfection. These have limited gene silencing and overexpression efficiency and show that the correlation between LNC01508 and OC cisplatin resistance is not highly significant. Furthermore, the effect of eukaryotic plasmid-mediated lncRNA overexpression is better than the chemical synthesis of lncRNA. This suggests a stable transfection in vitro to provide knockout and overexpression effects. (A) qPCR detects a lower LINC01508 expression, and the CCK-8 assay measures the cell viability. IC 50 values in LINC01508 inhibition OV2008 cells. (B) qPCR inspects a higher LINC01508 expression, and the CCK-8 assay measures the cell viability. IC 50 values in LINC01508 overexpression C13K cells. (C and D) Colony formation assays were conducted to determine the cell proliferation ability for transfected OC cells. (E and F) GAPDH, Cyr61, ERCC1, and p-AKT protein levels were determined by Western blot. All experiments are repeated in triplicated, and data are shown as mean±SE. lncRNA, long non-coding RNAs; OC, ovarian cancer; qPCR, quantitative real-time polymerase chain reaction; CCK-8, cell counting kit-8; IC 50 , half maximal inhibitory concentration; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; Cyr61, cysteine-rich angiogenic inducer 61; ERCC1, excision repair cross complementing‐group 1; p-AKT, phospho-AKT; SE, standard error. * p<0.05; † p<0.01.
    Figure Legend Snippet: The cell function analysis are all chemically synthesized interference lncRNA and eukaryotic plasmid-mediated lncRNA transient transfection. These have limited gene silencing and overexpression efficiency and show that the correlation between LNC01508 and OC cisplatin resistance is not highly significant. Furthermore, the effect of eukaryotic plasmid-mediated lncRNA overexpression is better than the chemical synthesis of lncRNA. This suggests a stable transfection in vitro to provide knockout and overexpression effects. (A) qPCR detects a lower LINC01508 expression, and the CCK-8 assay measures the cell viability. IC 50 values in LINC01508 inhibition OV2008 cells. (B) qPCR inspects a higher LINC01508 expression, and the CCK-8 assay measures the cell viability. IC 50 values in LINC01508 overexpression C13K cells. (C and D) Colony formation assays were conducted to determine the cell proliferation ability for transfected OC cells. (E and F) GAPDH, Cyr61, ERCC1, and p-AKT protein levels were determined by Western blot. All experiments are repeated in triplicated, and data are shown as mean±SE. lncRNA, long non-coding RNAs; OC, ovarian cancer; qPCR, quantitative real-time polymerase chain reaction; CCK-8, cell counting kit-8; IC 50 , half maximal inhibitory concentration; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; Cyr61, cysteine-rich angiogenic inducer 61; ERCC1, excision repair cross complementing‐group 1; p-AKT, phospho-AKT; SE, standard error. * p<0.05; † p<0.01.

    Techniques Used: Cell Function Assay, Synthesized, Plasmid Preparation, Transfection, Over Expression, Stable Transfection, In Vitro, Knock-Out, Expressing, CCK-8 Assay, Inhibition, Western Blot, Real-time Polymerase Chain Reaction, Cell Counting, Concentration Assay

    (A) Western blot analyses of YAP and p-YAP protein expression in OC cells. (B and C) Cell survival rate and colony formation pictures of C13K cells after treatment of verteporfin and different doses of cisplatin. Data were shown as mean±SE of 3 experiments. (D) Cyr61 protein is marked by green fluorescence. Cyr61 protein was mainly localized in the cytoplasm. Nuclear staining with DAPI is shown in blue (magnification ×400). Representative images from 3 independent experiments are shown. OC, ovarian cancer; YAP, yes-associated protein 1; p-YAP, phospho-YAP; SE, standard error; Cyr61, cysteine-rich angiogenic inducer 61; DAPI, diamidino-2-phenylindole; DMSO, dimethyl sulfoxide. * p<0.05; † p<0.01, compared with DMSO group.
    Figure Legend Snippet: (A) Western blot analyses of YAP and p-YAP protein expression in OC cells. (B and C) Cell survival rate and colony formation pictures of C13K cells after treatment of verteporfin and different doses of cisplatin. Data were shown as mean±SE of 3 experiments. (D) Cyr61 protein is marked by green fluorescence. Cyr61 protein was mainly localized in the cytoplasm. Nuclear staining with DAPI is shown in blue (magnification ×400). Representative images from 3 independent experiments are shown. OC, ovarian cancer; YAP, yes-associated protein 1; p-YAP, phospho-YAP; SE, standard error; Cyr61, cysteine-rich angiogenic inducer 61; DAPI, diamidino-2-phenylindole; DMSO, dimethyl sulfoxide. * p<0.05; † p<0.01, compared with DMSO group.

    Techniques Used: Western Blot, Expressing, Fluorescence, Staining

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    Cell Signaling Technology Inc anti cyr61
    Anti Cyr61, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Cell Signaling Technology Inc cyr61
    YAP confers resistance to cisplatin in ovarian cancer cells. Notes: ( A ) Cells were treated with different concentrations (0–50 μmol/L) of cisplatin for 48 hours. Cell viability was assessed using the CCK-8 assay. Data represent the mean and standard deviation values from three independent experiments (** P <0.01). ( B ) The 50% maximal inhibitory concentration (IC 50 ) values of cisplatin in the cisplatin-sensitive parent cell line OV2008 and its resistant clone C13K were calculated. Each value represents the mean ± standard deviation values from three independent experiments (** P <0.01). ( C ) The messenger RNA levels of YAP, <t>Cyr61,</t> CTGF, and CCND1 in the cells were examined using a real-time polymerase chain-reaction kit. Data represent the mean and standard deviation values from three independent experiments (** P <0.01). ( D ) Cell lysates were collected for Western blot analyses of the protein levels of YAP, Cyr61, CTGF, and CCND1.
    Cyr61, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc anti human cyr61 monoclonal antibody 093g9
    The level of <t>Cyr61</t> in the HCT-8/L-OHP and HCT116/L-OHP cell lines. (A) and (D) The mRNA level of Cyr61 was determined by RT-PCR. (B) and (E) The protein level of Cyr61 was determined by western blotting. (C) and (F) The concentration of Cyr61 in the cell supernatant was measured by ELISA. The data are expressed as the mean ± SEM values (n=3). *P < 0.05, **P < 0.01.
    Anti Human Cyr61 Monoclonal Antibody 093g9, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc angiogenic inducer 61 cyr61
    The cell function analysis are all chemically synthesized interference lncRNA and eukaryotic plasmid-mediated lncRNA transient transfection. These have limited gene silencing and overexpression efficiency and show that the correlation between LNC01508 and OC cisplatin resistance is not highly significant. Furthermore, the effect of eukaryotic plasmid-mediated lncRNA overexpression is better than the chemical synthesis of lncRNA. This suggests a stable transfection in vitro to provide knockout and overexpression effects. (A) qPCR detects a lower LINC01508 expression, and the CCK-8 assay measures the cell viability. IC 50 values in LINC01508 inhibition OV2008 cells. (B) qPCR inspects a higher LINC01508 expression, and the CCK-8 assay measures the cell viability. IC 50 values in LINC01508 overexpression C13K cells. (C and D) Colony formation assays were conducted to determine the cell proliferation ability for transfected OC cells. (E and F) GAPDH, <t>Cyr61,</t> ERCC1, and p-AKT protein levels were determined by Western blot. All experiments are repeated in triplicated, and data are shown as mean±SE. lncRNA, long non-coding RNAs; OC, ovarian cancer; qPCR, quantitative real-time polymerase chain reaction; CCK-8, cell counting kit-8; IC 50 , half maximal inhibitory concentration; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; Cyr61, cysteine-rich angiogenic inducer 61; ERCC1, excision repair cross complementing‐group 1; p-AKT, phospho-AKT; SE, standard error. * p<0.05; † p<0.01.
    Angiogenic Inducer 61 Cyr61, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    YAP confers resistance to cisplatin in ovarian cancer cells. Notes: ( A ) Cells were treated with different concentrations (0–50 μmol/L) of cisplatin for 48 hours. Cell viability was assessed using the CCK-8 assay. Data represent the mean and standard deviation values from three independent experiments (** P <0.01). ( B ) The 50% maximal inhibitory concentration (IC 50 ) values of cisplatin in the cisplatin-sensitive parent cell line OV2008 and its resistant clone C13K were calculated. Each value represents the mean ± standard deviation values from three independent experiments (** P <0.01). ( C ) The messenger RNA levels of YAP, Cyr61, CTGF, and CCND1 in the cells were examined using a real-time polymerase chain-reaction kit. Data represent the mean and standard deviation values from three independent experiments (** P <0.01). ( D ) Cell lysates were collected for Western blot analyses of the protein levels of YAP, Cyr61, CTGF, and CCND1.

    Journal: OncoTargets and therapy

    Article Title: YAP induces cisplatin resistance through activation of autophagy in human ovarian carcinoma cells

    doi: 10.2147/OTT.S102837

    Figure Lengend Snippet: YAP confers resistance to cisplatin in ovarian cancer cells. Notes: ( A ) Cells were treated with different concentrations (0–50 μmol/L) of cisplatin for 48 hours. Cell viability was assessed using the CCK-8 assay. Data represent the mean and standard deviation values from three independent experiments (** P <0.01). ( B ) The 50% maximal inhibitory concentration (IC 50 ) values of cisplatin in the cisplatin-sensitive parent cell line OV2008 and its resistant clone C13K were calculated. Each value represents the mean ± standard deviation values from three independent experiments (** P <0.01). ( C ) The messenger RNA levels of YAP, Cyr61, CTGF, and CCND1 in the cells were examined using a real-time polymerase chain-reaction kit. Data represent the mean and standard deviation values from three independent experiments (** P <0.01). ( D ) Cell lysates were collected for Western blot analyses of the protein levels of YAP, Cyr61, CTGF, and CCND1.

    Article Snippet: The primary antibodies used were as follows: YAP (sc-15407; Santa Cruz Biotechnology), Cyr61 (sc-13100; Santa Cruz Biotechnology), CTGF (sc-101586; Santa Cruz Biotechnology), CCND1 (sc-20044; Santa Cruz Biotechnology), LC3B and Beclin1 (3868S and 3738, respectively; Cell Signaling Technology), cleaved PARP and caspase 3 (9541 and 9661, respectively; Cell Signaling Technology), and Atg-3 and -5 (3415 and 2630, respectively; Cell Signaling Technology).

    Techniques: CCK-8 Assay, Standard Deviation, Concentration Assay, Real-time Polymerase Chain Reaction, Western Blot

    Effects of YAP knockdown on cisplatin sensitivity in resistant C13K cells via impairment of autophagy. Notes: After C13K cells were transfected with YAP small interfering RNA (siRNA) and control siRNA (37.5 nM) for 48 hours, they were treated with 50 μmol/L cisplatin for 48 hours. ( A ) Cell lysates were collected for Western blot analysis of the protein expression of YAP, Cyr61, CTGF, and CCND1. ( B ) Cell viability was determined using a CCK-8 assay. Data represent the mean and standard deviation values from three independent experiments (** P <0.01). ( C ) The fluorescence intensity of rhodamine 123 in the cells was measured by fluorescence-activated cell sorting. Data shown represent the mean ± standard error values from three independent experiments (** P <0.01 vs the control siRNA group). ( D ) Cells were subjected to annexin V–propidium iodide staining. The apoptosis ratio represents the ratio of the number of cells in early stage apoptosis to that in advanced-stage apoptosis. Quantification of apoptotic cells: mean ± standard deviation values represent those from three independent experiments (** P <0.01). ( E ) Western blot analysis of the expression of cleaved caspase 3 and PARP and the autophagy-related proteins Atg-3 and Atg-5 in the control siRNA and YAP siRNA C13K cells. ( F ) Electron transmission microscopy for the detection of autophagosomes in the control siRNA and YAP siRNA C13K cells; the black arrows indicate the autophagic vacuoles (magnification 10,000×). Scale bars 2 μm.

    Journal: OncoTargets and therapy

    Article Title: YAP induces cisplatin resistance through activation of autophagy in human ovarian carcinoma cells

    doi: 10.2147/OTT.S102837

    Figure Lengend Snippet: Effects of YAP knockdown on cisplatin sensitivity in resistant C13K cells via impairment of autophagy. Notes: After C13K cells were transfected with YAP small interfering RNA (siRNA) and control siRNA (37.5 nM) for 48 hours, they were treated with 50 μmol/L cisplatin for 48 hours. ( A ) Cell lysates were collected for Western blot analysis of the protein expression of YAP, Cyr61, CTGF, and CCND1. ( B ) Cell viability was determined using a CCK-8 assay. Data represent the mean and standard deviation values from three independent experiments (** P <0.01). ( C ) The fluorescence intensity of rhodamine 123 in the cells was measured by fluorescence-activated cell sorting. Data shown represent the mean ± standard error values from three independent experiments (** P <0.01 vs the control siRNA group). ( D ) Cells were subjected to annexin V–propidium iodide staining. The apoptosis ratio represents the ratio of the number of cells in early stage apoptosis to that in advanced-stage apoptosis. Quantification of apoptotic cells: mean ± standard deviation values represent those from three independent experiments (** P <0.01). ( E ) Western blot analysis of the expression of cleaved caspase 3 and PARP and the autophagy-related proteins Atg-3 and Atg-5 in the control siRNA and YAP siRNA C13K cells. ( F ) Electron transmission microscopy for the detection of autophagosomes in the control siRNA and YAP siRNA C13K cells; the black arrows indicate the autophagic vacuoles (magnification 10,000×). Scale bars 2 μm.

    Article Snippet: The primary antibodies used were as follows: YAP (sc-15407; Santa Cruz Biotechnology), Cyr61 (sc-13100; Santa Cruz Biotechnology), CTGF (sc-101586; Santa Cruz Biotechnology), CCND1 (sc-20044; Santa Cruz Biotechnology), LC3B and Beclin1 (3868S and 3738, respectively; Cell Signaling Technology), cleaved PARP and caspase 3 (9541 and 9661, respectively; Cell Signaling Technology), and Atg-3 and -5 (3415 and 2630, respectively; Cell Signaling Technology).

    Techniques: Transfection, Small Interfering RNA, Western Blot, Expressing, CCK-8 Assay, Standard Deviation, Fluorescence, FACS, Staining, Transmission Assay, Microscopy

    The level of Cyr61 in the HCT-8/L-OHP and HCT116/L-OHP cell lines. (A) and (D) The mRNA level of Cyr61 was determined by RT-PCR. (B) and (E) The protein level of Cyr61 was determined by western blotting. (C) and (F) The concentration of Cyr61 in the cell supernatant was measured by ELISA. The data are expressed as the mean ± SEM values (n=3). *P < 0.05, **P < 0.01.

    Journal: Journal of Cancer

    Article Title: Cyr61 mediates oxaliplatin resistance in colorectal cancer cells by regulating Bcl-xL expression

    doi: 10.7150/jca.48891

    Figure Lengend Snippet: The level of Cyr61 in the HCT-8/L-OHP and HCT116/L-OHP cell lines. (A) and (D) The mRNA level of Cyr61 was determined by RT-PCR. (B) and (E) The protein level of Cyr61 was determined by western blotting. (C) and (F) The concentration of Cyr61 in the cell supernatant was measured by ELISA. The data are expressed as the mean ± SEM values (n=3). *P < 0.05, **P < 0.01.

    Article Snippet: Anti-human Cyr61 monoclonal antibody (093G9) (A gift of professor Ningli Li in Shanghai Jiao Tong University School of Medicine, Shanghai, China), anti-GAPDH and anti-Bcl-xL (Cell Signaling Technology, Inc., Beverly, MA) were used in this study.

    Techniques: Reverse Transcription Polymerase Chain Reaction, Western Blot, Concentration Assay, Enzyme-linked Immunosorbent Assay

    Cyr61 knockdown reduces the resistance of L-OHP-resistant CRC cells. (A) and (D) Lentiviral vectors expressing shCyr61 were transduced into HCT-8/L-OHP cells and HCT116/L-OHP cells to knock down Cyr61 expression, and the concentration of Cyr61 in the cell supernatant was detected by ELISA. (B) and (E) shCyr61 and shNC cells from HCT-8/L-OHP cells and HCT116/L-OHP cells were treated with increasing doses of L-OHP for 72 h and subjected to a CCK8 assay; the IC50 of L-OHP in the cells was then calculated using GraphPad Prism 5.0. (C) and (F) HCT-8 and HCT116 cells were preincubated with exogenous Cyr61 (1 µg/ml) for 24 h and were then treated with increasing doses of L-OHP. After incubation for 72 hours and analysis with a CCK8 assay, the IC50 of L-OHP in the cells was calculated using GraphPad Prism 5.0. The data are expressed as the mean ± SEM values (n=3). *P < 0.05, **P < 0.01.

    Journal: Journal of Cancer

    Article Title: Cyr61 mediates oxaliplatin resistance in colorectal cancer cells by regulating Bcl-xL expression

    doi: 10.7150/jca.48891

    Figure Lengend Snippet: Cyr61 knockdown reduces the resistance of L-OHP-resistant CRC cells. (A) and (D) Lentiviral vectors expressing shCyr61 were transduced into HCT-8/L-OHP cells and HCT116/L-OHP cells to knock down Cyr61 expression, and the concentration of Cyr61 in the cell supernatant was detected by ELISA. (B) and (E) shCyr61 and shNC cells from HCT-8/L-OHP cells and HCT116/L-OHP cells were treated with increasing doses of L-OHP for 72 h and subjected to a CCK8 assay; the IC50 of L-OHP in the cells was then calculated using GraphPad Prism 5.0. (C) and (F) HCT-8 and HCT116 cells were preincubated with exogenous Cyr61 (1 µg/ml) for 24 h and were then treated with increasing doses of L-OHP. After incubation for 72 hours and analysis with a CCK8 assay, the IC50 of L-OHP in the cells was calculated using GraphPad Prism 5.0. The data are expressed as the mean ± SEM values (n=3). *P < 0.05, **P < 0.01.

    Article Snippet: Anti-human Cyr61 monoclonal antibody (093G9) (A gift of professor Ningli Li in Shanghai Jiao Tong University School of Medicine, Shanghai, China), anti-GAPDH and anti-Bcl-xL (Cell Signaling Technology, Inc., Beverly, MA) were used in this study.

    Techniques: Expressing, Concentration Assay, Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Incubation

    Cyr61 knockdown enhances L-OHP-induced apoptosis in L-OHP-resistant CRC cells . (A) HCT-8/L-OHP-shCyr61 and HCT-8/L-OHP-shNC cells were treated with L-OHP (50 µg/ml) for 72 h, and apoptosis was assessed with a BD FACSCanto II cytometer. (B) HCT116/L-OHP-shCyr61 and HCT116/L-OHP-shNC cells were treated with L-OHP (30 µg/ml) for 72 h, and the percentages of apoptotic cells were determined with a BD FACSCanto II cytometer. The data are expressed as the mean ± SEM values (n=3). *P < 0.05, **P < 0.01.

    Journal: Journal of Cancer

    Article Title: Cyr61 mediates oxaliplatin resistance in colorectal cancer cells by regulating Bcl-xL expression

    doi: 10.7150/jca.48891

    Figure Lengend Snippet: Cyr61 knockdown enhances L-OHP-induced apoptosis in L-OHP-resistant CRC cells . (A) HCT-8/L-OHP-shCyr61 and HCT-8/L-OHP-shNC cells were treated with L-OHP (50 µg/ml) for 72 h, and apoptosis was assessed with a BD FACSCanto II cytometer. (B) HCT116/L-OHP-shCyr61 and HCT116/L-OHP-shNC cells were treated with L-OHP (30 µg/ml) for 72 h, and the percentages of apoptotic cells were determined with a BD FACSCanto II cytometer. The data are expressed as the mean ± SEM values (n=3). *P < 0.05, **P < 0.01.

    Article Snippet: Anti-human Cyr61 monoclonal antibody (093G9) (A gift of professor Ningli Li in Shanghai Jiao Tong University School of Medicine, Shanghai, China), anti-GAPDH and anti-Bcl-xL (Cell Signaling Technology, Inc., Beverly, MA) were used in this study.

    Techniques: Cytometry

    Bcl-xL is involved in the effect of Cyr61 on drug resistance. (A) Left panel: Bcl-2, Bcl-xL, XIAP and Survivin mRNA levels in HCT-8/L-OHP and parental HCT-8 cells were determined by real-time PCR; Right panel: Bcl-xL protein levels in HCT-8/L-OHP and parental HCT-8 cells were determined by western blotting. (B) HCT-8/L-OHP-shCyr61 and HCT-8/L-OHP-shNC cells were treated with L-OHP (50 µg/ml) for 72 h, and the protein level of Bcl-xL was detected by western blotting. (C) HCT-8-Cyr61 and HCT-8-NC cells were cultured for 72 h, and the concentration of Cyr61 in the cell supernatant was determined by ELISA. (D) HCT8-Cyr61 and HCT8-NC cells were treated with L-OHP (10 µg/ml) for 72 h, and the protein level of Bcl-xL was determined by western blotting. (E) HCT-8-Cyr61 and HCT-8-NC cells were treated with L-OHP (10 µg/ml), A1155463 (5 µM) (a specific Bcl-xL inhibitor), or L-OHP + A1155463 for 72 h, and apoptosis was analyzed by flow cytometry. (F) Left panel: HCT-8-Cyr61 and HCT-8-NC cells were treated with increasing doses of L-OHP or increasing doses of L-OHP+ A1155463 (5 µM) for 72 h and were then analyzed with a CCK8 assay The IC50 of L-OHP in HCT-8-Cyr61 and HCT-8-NC cells was calculated using GraphPad Prism 5.0. (G) HCT116/L-OHP-shCyr61 and HCT116/L-OHP-shNC cells were treated with L-OHP (30 µg/ml) for 72 h, and the protein level of Bcl-xL was determined by western blotting. (H) HCT116-Cyr61 and HCT116-NC cells were cultured for 72 h, and the concentration of Cyr61 in the cell supernatant was determined by ELISA. (I) HCT116-Cyr61 and HCT116-NC cells were treated with L-OHP (10 µg/ml) for 72 h, and the protein level of Bcl-xL was determined by western blotting. (J) HCT116-Cyr61 and HCT116-NC cells were treated with increasing doses of L-OHP or increasing doses of L-OHP+ A1155463 (5 µM) for 72 h and were then analyzed with a CCK8 assay. Then, the IC50 of L-OHP in HCT116-Cyr61 and HCT116-NC cells was calculated using GraphPad Prism 5.0. The data are expressed as the mean ± SEM values (n=3). *P < 0.05, **P < 0.01.

    Journal: Journal of Cancer

    Article Title: Cyr61 mediates oxaliplatin resistance in colorectal cancer cells by regulating Bcl-xL expression

    doi: 10.7150/jca.48891

    Figure Lengend Snippet: Bcl-xL is involved in the effect of Cyr61 on drug resistance. (A) Left panel: Bcl-2, Bcl-xL, XIAP and Survivin mRNA levels in HCT-8/L-OHP and parental HCT-8 cells were determined by real-time PCR; Right panel: Bcl-xL protein levels in HCT-8/L-OHP and parental HCT-8 cells were determined by western blotting. (B) HCT-8/L-OHP-shCyr61 and HCT-8/L-OHP-shNC cells were treated with L-OHP (50 µg/ml) for 72 h, and the protein level of Bcl-xL was detected by western blotting. (C) HCT-8-Cyr61 and HCT-8-NC cells were cultured for 72 h, and the concentration of Cyr61 in the cell supernatant was determined by ELISA. (D) HCT8-Cyr61 and HCT8-NC cells were treated with L-OHP (10 µg/ml) for 72 h, and the protein level of Bcl-xL was determined by western blotting. (E) HCT-8-Cyr61 and HCT-8-NC cells were treated with L-OHP (10 µg/ml), A1155463 (5 µM) (a specific Bcl-xL inhibitor), or L-OHP + A1155463 for 72 h, and apoptosis was analyzed by flow cytometry. (F) Left panel: HCT-8-Cyr61 and HCT-8-NC cells were treated with increasing doses of L-OHP or increasing doses of L-OHP+ A1155463 (5 µM) for 72 h and were then analyzed with a CCK8 assay The IC50 of L-OHP in HCT-8-Cyr61 and HCT-8-NC cells was calculated using GraphPad Prism 5.0. (G) HCT116/L-OHP-shCyr61 and HCT116/L-OHP-shNC cells were treated with L-OHP (30 µg/ml) for 72 h, and the protein level of Bcl-xL was determined by western blotting. (H) HCT116-Cyr61 and HCT116-NC cells were cultured for 72 h, and the concentration of Cyr61 in the cell supernatant was determined by ELISA. (I) HCT116-Cyr61 and HCT116-NC cells were treated with L-OHP (10 µg/ml) for 72 h, and the protein level of Bcl-xL was determined by western blotting. (J) HCT116-Cyr61 and HCT116-NC cells were treated with increasing doses of L-OHP or increasing doses of L-OHP+ A1155463 (5 µM) for 72 h and were then analyzed with a CCK8 assay. Then, the IC50 of L-OHP in HCT116-Cyr61 and HCT116-NC cells was calculated using GraphPad Prism 5.0. The data are expressed as the mean ± SEM values (n=3). *P < 0.05, **P < 0.01.

    Article Snippet: Anti-human Cyr61 monoclonal antibody (093G9) (A gift of professor Ningli Li in Shanghai Jiao Tong University School of Medicine, Shanghai, China), anti-GAPDH and anti-Bcl-xL (Cell Signaling Technology, Inc., Beverly, MA) were used in this study.

    Techniques: Real-time Polymerase Chain Reaction, Western Blot, Cell Culture, Concentration Assay, Enzyme-linked Immunosorbent Assay, Flow Cytometry, CCK-8 Assay

    The cell function analysis are all chemically synthesized interference lncRNA and eukaryotic plasmid-mediated lncRNA transient transfection. These have limited gene silencing and overexpression efficiency and show that the correlation between LNC01508 and OC cisplatin resistance is not highly significant. Furthermore, the effect of eukaryotic plasmid-mediated lncRNA overexpression is better than the chemical synthesis of lncRNA. This suggests a stable transfection in vitro to provide knockout and overexpression effects. (A) qPCR detects a lower LINC01508 expression, and the CCK-8 assay measures the cell viability. IC 50 values in LINC01508 inhibition OV2008 cells. (B) qPCR inspects a higher LINC01508 expression, and the CCK-8 assay measures the cell viability. IC 50 values in LINC01508 overexpression C13K cells. (C and D) Colony formation assays were conducted to determine the cell proliferation ability for transfected OC cells. (E and F) GAPDH, Cyr61, ERCC1, and p-AKT protein levels were determined by Western blot. All experiments are repeated in triplicated, and data are shown as mean±SE. lncRNA, long non-coding RNAs; OC, ovarian cancer; qPCR, quantitative real-time polymerase chain reaction; CCK-8, cell counting kit-8; IC 50 , half maximal inhibitory concentration; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; Cyr61, cysteine-rich angiogenic inducer 61; ERCC1, excision repair cross complementing‐group 1; p-AKT, phospho-AKT; SE, standard error. * p<0.05; † p<0.01.

    Journal: Journal of Gynecologic Oncology

    Article Title: Downregulation of LINC01508 contributes to cisplatin resistance in ovarian cancer via the regulation of the Hippo-YAP pathway

    doi: 10.3802/jgo.2021.32.e77

    Figure Lengend Snippet: The cell function analysis are all chemically synthesized interference lncRNA and eukaryotic plasmid-mediated lncRNA transient transfection. These have limited gene silencing and overexpression efficiency and show that the correlation between LNC01508 and OC cisplatin resistance is not highly significant. Furthermore, the effect of eukaryotic plasmid-mediated lncRNA overexpression is better than the chemical synthesis of lncRNA. This suggests a stable transfection in vitro to provide knockout and overexpression effects. (A) qPCR detects a lower LINC01508 expression, and the CCK-8 assay measures the cell viability. IC 50 values in LINC01508 inhibition OV2008 cells. (B) qPCR inspects a higher LINC01508 expression, and the CCK-8 assay measures the cell viability. IC 50 values in LINC01508 overexpression C13K cells. (C and D) Colony formation assays were conducted to determine the cell proliferation ability for transfected OC cells. (E and F) GAPDH, Cyr61, ERCC1, and p-AKT protein levels were determined by Western blot. All experiments are repeated in triplicated, and data are shown as mean±SE. lncRNA, long non-coding RNAs; OC, ovarian cancer; qPCR, quantitative real-time polymerase chain reaction; CCK-8, cell counting kit-8; IC 50 , half maximal inhibitory concentration; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; Cyr61, cysteine-rich angiogenic inducer 61; ERCC1, excision repair cross complementing‐group 1; p-AKT, phospho-AKT; SE, standard error. * p<0.05; † p<0.01.

    Article Snippet: The primary antibodies used were as follows: yes-associated protein (YAP) and cysteine-rich angiogenic inducer 61 (Cyr61) (sc-15407 and sc-13100, respectively; Santa Cruz Biotechnology, Dallas, TX, USA), GAPDH and phospho-AKT (p-AKT) (sc-166574 and sc-135650, respectively; Santa Cruz Biotechnology), phospho-YAP (p-YAP) and excision repair cross complementing‐group 1 (ERCC1) (4911 and 3885s, respectively; Cell Signaling Technology).

    Techniques: Cell Function Assay, Synthesized, Plasmid Preparation, Transfection, Over Expression, Stable Transfection, In Vitro, Knock-Out, Expressing, CCK-8 Assay, Inhibition, Western Blot, Real-time Polymerase Chain Reaction, Cell Counting, Concentration Assay

    (A) Western blot analyses of YAP and p-YAP protein expression in OC cells. (B and C) Cell survival rate and colony formation pictures of C13K cells after treatment of verteporfin and different doses of cisplatin. Data were shown as mean±SE of 3 experiments. (D) Cyr61 protein is marked by green fluorescence. Cyr61 protein was mainly localized in the cytoplasm. Nuclear staining with DAPI is shown in blue (magnification ×400). Representative images from 3 independent experiments are shown. OC, ovarian cancer; YAP, yes-associated protein 1; p-YAP, phospho-YAP; SE, standard error; Cyr61, cysteine-rich angiogenic inducer 61; DAPI, diamidino-2-phenylindole; DMSO, dimethyl sulfoxide. * p<0.05; † p<0.01, compared with DMSO group.

    Journal: Journal of Gynecologic Oncology

    Article Title: Downregulation of LINC01508 contributes to cisplatin resistance in ovarian cancer via the regulation of the Hippo-YAP pathway

    doi: 10.3802/jgo.2021.32.e77

    Figure Lengend Snippet: (A) Western blot analyses of YAP and p-YAP protein expression in OC cells. (B and C) Cell survival rate and colony formation pictures of C13K cells after treatment of verteporfin and different doses of cisplatin. Data were shown as mean±SE of 3 experiments. (D) Cyr61 protein is marked by green fluorescence. Cyr61 protein was mainly localized in the cytoplasm. Nuclear staining with DAPI is shown in blue (magnification ×400). Representative images from 3 independent experiments are shown. OC, ovarian cancer; YAP, yes-associated protein 1; p-YAP, phospho-YAP; SE, standard error; Cyr61, cysteine-rich angiogenic inducer 61; DAPI, diamidino-2-phenylindole; DMSO, dimethyl sulfoxide. * p<0.05; † p<0.01, compared with DMSO group.

    Article Snippet: The primary antibodies used were as follows: yes-associated protein (YAP) and cysteine-rich angiogenic inducer 61 (Cyr61) (sc-15407 and sc-13100, respectively; Santa Cruz Biotechnology, Dallas, TX, USA), GAPDH and phospho-AKT (p-AKT) (sc-166574 and sc-135650, respectively; Santa Cruz Biotechnology), phospho-YAP (p-YAP) and excision repair cross complementing‐group 1 (ERCC1) (4911 and 3885s, respectively; Cell Signaling Technology).

    Techniques: Western Blot, Expressing, Fluorescence, Staining