triptorelin  (Millipore)

 
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    Name:
    Triptorelin Related Compound C
    Description:
    This product is provided as delivered and specified by the issuing Pharmacopoeia All information provided in support of this product including SDS and any product information leaflets have been developed and issued under the Authority of the issuing Pharmacopoeia For further information and support please go to the website of the issuing Pharmacopoeia
    Catalog Number:
    1696142
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    Structured Review

    Millipore triptorelin
    The level of p-ERK1/2 is influenced by integration of signaling from multiple cell surface receptors, blocking the response to activated GnRH receptor . A. <t>Triptorelin</t> did not affect levels of p-ERK1/2 in serum-starved MCF-7-30 or MDA-MB-231-34 cells. B. Treatment of stably transfected cells with 100 nM Triptorelin transiently elevated levels of phosphorylated ERK1/2 (p-ERK1/2) in serum-starved MCF-7-30-7hygro14 cells but not in the presence of serum. Bar graphs indicate effect of no serum vs with serum on ERK response in MCF7hygro14, statistically significant for no serum, p
    This product is provided as delivered and specified by the issuing Pharmacopoeia All information provided in support of this product including SDS and any product information leaflets have been developed and issued under the Authority of the issuing Pharmacopoeia For further information and support please go to the website of the issuing Pharmacopoeia
    https://www.bioz.com/result/triptorelin/product/Millipore
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    triptorelin - by Bioz Stars, 2021-07
    91/100 stars

    Images

    1) Product Images from "GnRH receptor activation competes at a low level with growth signaling in stably transfected human breast cell lines"

    Article Title: GnRH receptor activation competes at a low level with growth signaling in stably transfected human breast cell lines

    Journal: BMC Cancer

    doi: 10.1186/1471-2407-11-476

    The level of p-ERK1/2 is influenced by integration of signaling from multiple cell surface receptors, blocking the response to activated GnRH receptor . A. Triptorelin did not affect levels of p-ERK1/2 in serum-starved MCF-7-30 or MDA-MB-231-34 cells. B. Treatment of stably transfected cells with 100 nM Triptorelin transiently elevated levels of phosphorylated ERK1/2 (p-ERK1/2) in serum-starved MCF-7-30-7hygro14 cells but not in the presence of serum. Bar graphs indicate effect of no serum vs with serum on ERK response in MCF7hygro14, statistically significant for no serum, p
    Figure Legend Snippet: The level of p-ERK1/2 is influenced by integration of signaling from multiple cell surface receptors, blocking the response to activated GnRH receptor . A. Triptorelin did not affect levels of p-ERK1/2 in serum-starved MCF-7-30 or MDA-MB-231-34 cells. B. Treatment of stably transfected cells with 100 nM Triptorelin transiently elevated levels of phosphorylated ERK1/2 (p-ERK1/2) in serum-starved MCF-7-30-7hygro14 cells but not in the presence of serum. Bar graphs indicate effect of no serum vs with serum on ERK response in MCF7hygro14, statistically significant for no serum, p

    Techniques Used: Blocking Assay, Multiple Displacement Amplification, Stable Transfection, Transfection

    Dynamics of GnRH receptor activation following treatment with Triptorelin . Treatment of stably transfected cells with GnRH elicited high levels of 3 H- inositol phosphate (IP) production (A-C). Removal of GnRH and LiCl revealed the dynamics of 3 H- inositol phosphate turnover in different cell types (D,E). The decrease in levels of 3 H- inositol phosphates was slower in SVCT-2 cells. Statistically different values (p
    Figure Legend Snippet: Dynamics of GnRH receptor activation following treatment with Triptorelin . Treatment of stably transfected cells with GnRH elicited high levels of 3 H- inositol phosphate (IP) production (A-C). Removal of GnRH and LiCl revealed the dynamics of 3 H- inositol phosphate turnover in different cell types (D,E). The decrease in levels of 3 H- inositol phosphates was slower in SVCT-2 cells. Statistically different values (p

    Techniques Used: Activation Assay, Stable Transfection, Transfection

    The effect of Triptorelin on growth of cells stably transfected with GnRH . A. Growth of SVCT-2 after 4 days was marginally inhibited (10-18%) by treatment with Triptorelin. However, cell growth was effectively inhibited by IGF-IR inhibitor II and co-treatment with Triptorelin exerted a small additive effect (B). EGFR/ErbB2 inhibitor reduced SVCT-2 cell growth, but co-treatment with Triptorelin had no effect (C). Growth of MCF-7-30-7hygro14 cells was not affected by treatment with 100 nM Triptorelin (D), unlike HEK293 [SCL60] cells (E) after 4 days. Growth and survival were inhibited by IGF-IR inhibitor II but co-treatment with Triptorelin had no effect (F). Transient exposure to 15 μM IGF-IR inhibitor II for up to 2 hours resulted in less than 10% growth-inhibition after 4 days, longer exposures resulted in more extensive growth-inhibition (G). Growth of MCF-7-30-7hygro14 cells was inhibited by EGFR/ErbB2 inhibitor but not affected by treatment with 7 μM PI3Kγ inhibitor and co-treatment with 100 nM Triptorelin exerted no significant growth-inhibition (H and I). Growth of ZR75-1-12 (J) and MDA-MB-231-34 (K) was unaffected by treatment with 100 nM Triptorelin. * p
    Figure Legend Snippet: The effect of Triptorelin on growth of cells stably transfected with GnRH . A. Growth of SVCT-2 after 4 days was marginally inhibited (10-18%) by treatment with Triptorelin. However, cell growth was effectively inhibited by IGF-IR inhibitor II and co-treatment with Triptorelin exerted a small additive effect (B). EGFR/ErbB2 inhibitor reduced SVCT-2 cell growth, but co-treatment with Triptorelin had no effect (C). Growth of MCF-7-30-7hygro14 cells was not affected by treatment with 100 nM Triptorelin (D), unlike HEK293 [SCL60] cells (E) after 4 days. Growth and survival were inhibited by IGF-IR inhibitor II but co-treatment with Triptorelin had no effect (F). Transient exposure to 15 μM IGF-IR inhibitor II for up to 2 hours resulted in less than 10% growth-inhibition after 4 days, longer exposures resulted in more extensive growth-inhibition (G). Growth of MCF-7-30-7hygro14 cells was inhibited by EGFR/ErbB2 inhibitor but not affected by treatment with 7 μM PI3Kγ inhibitor and co-treatment with 100 nM Triptorelin exerted no significant growth-inhibition (H and I). Growth of ZR75-1-12 (J) and MDA-MB-231-34 (K) was unaffected by treatment with 100 nM Triptorelin. * p

    Techniques Used: Stable Transfection, Transfection, Inhibition, Multiple Displacement Amplification

    Related Articles

    other:

    Article Title: GnRH regulates the expression of its receptor accessory protein SET in pituitary gonadotropes
    Article Snippet: GnRH agonist ([D-Trp6 ]GnRH, triptorelin), poly-L-lysine, GF109203X and proteasome inhibitor MG132 were purchased from Sigma-Aldrich Chemie (Saint-Quentin Fallavier, France).

    Article Title: GnRH regulates the expression of its receptor accessory protein SET in pituitary gonadotropes
    Article Snippet: Materials and antibodies GnRH agonist ([D-Trp6 ]GnRH, triptorelin), poly-L-lysine, GF109203X and proteasome inhibitor MG132 were purchased from Sigma-Aldrich Chemie (Saint-Quentin Fallavier, France).

    In Vitro:

    Article Title: Comparison of mechanisms of action of luteinizing hormone-releasing hormone (LHRH) antagonist cetrorelix and LHRH agonist triptorelin on the gene expression of pituitary LHRH receptors in rats
    Article Snippet: Aliquots of this suspension (3 mg/0.2 ml) were injected i.m., giving an estimated a daily release of about 100 μg of cetrorelix for 30 days. .. For in vitro experiments, cetrorelix, triptorelin, and the synthetic LHRH decapeptide were dissolved in medium 199 (Sigma). .. Adult female Sprague–Dawley rats (Charles River Breeding Laboratories) were used in the experiments.

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    Millipore compound c
    Ginsenoside Mc1 inhibited hydrogen peroxide (H 2 O 2 )–mediated reactive oxygen species (ROS) production by increasing the expression of antioxidant proteins in H9c2 cells. (A) Cells were stimulated with various doses (0, 10, 25, or 50 μg/mL) of ginsenoside Mc1 for 30 min. (B) H9c2 cells were incubated with ginsenoside Mc1 (50 μg/mL) for the indicated times (0, 15, 30, or 60 min). The extent of AMPK phosphorylation was determined by Western blotting. (C) Cells were incubated with several doses (0, 25, or 50 μg/mL) of ginsenoside Mc1 for 24 h. (D) H9c2 cells were stimulated with ginsenoside Mc1 (50 μg/mL) or ginsenoside Mc1 plus <t>compound</t> C (2 or 5 μM) for 24 h. Catalase and SOD2 levels were determined by Western blotting. (E) Cells were pretreated with ginsenoside Mc1 (25 or 50 μg/mL) for 24 h and then stimulated with H 2 O 2 (600 μM) for 2 h. (F) H9c2 cells were preincubated with ginsenoside Mc1 (50 μg/mL) or ginsenoside Mc1 plus compound C (2 or 5 μM) for 24 h and then stimulated with H 2 O 2 (600 μM) for 2 h. The stimulated cells were stained with dihydroethidium (DHE) solution to assess the prevalence of intracellular ROS. The mean ± standard deviation was obtained from 3 separate experiments [*, p
    Compound C, supplied by Millipore, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Millipore ampk inhibitors
    AMP-activated protein kinase <t>(AMPK)</t> is involved in resistin-induced matrix metalloproteinase (MMP-2) expression and cell migration JJ012 and SW1353 cells were pre-treated with Ara A (0.5 mM) and compound C (10 μM) for 30 min or pre-transfected with control, AMPKα1, or AMPKα2 siRNA for 24 h, and subsequently stimulated with resistin (3 ng/ml) for 24 h. In vitro migration, MMP-2 protein expression (JJ012 cells), and MMP-2 mRNA expression were measured by (A) Transwell assays, (B) enzyme-linked immunosorbent assay (ELISA), and (C) real-time quantitative polymerase chain reaction (RT-qPCR), respectively. Next, the JJ012 and SW1353 cells were pre-treated with SB203580 (10 μM) for 30 min or pre-transfected with control or <t>p38</t> siRNA for 24 h, and subsequently stimulated with resistin (3 ng/ml) for 24 h. In vitro migration, MMP-2 protein expression (JJ012 cells), and MMP-2 mRNA expression were measured by (D) Transwell assays, (E) ELISA, and (F) RT-qPCR, respectively. (G) The JJ012 cells were incubated with resistin for the indicated time intervals, and the p-AMPK and p38 expression were examined by western blot. (H) The JJ012 cells were pre-treated for 30 min with Ara A and compound C, or SB203580 followed by stimulation with resistin. The p-p38 and p-AMPK expression were measured by western blot. The results are expressed as mean ± SEM. *, P
    Ampk Inhibitors, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Millipore triptorelin
    The level of p-ERK1/2 is influenced by integration of signaling from multiple cell surface receptors, blocking the response to activated GnRH receptor . A. <t>Triptorelin</t> did not affect levels of p-ERK1/2 in serum-starved MCF-7-30 or MDA-MB-231-34 cells. B. Treatment of stably transfected cells with 100 nM Triptorelin transiently elevated levels of phosphorylated ERK1/2 (p-ERK1/2) in serum-starved MCF-7-30-7hygro14 cells but not in the presence of serum. Bar graphs indicate effect of no serum vs with serum on ERK response in MCF7hygro14, statistically significant for no serum, p
    Triptorelin, supplied by Millipore, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/triptorelin/product/Millipore
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    triptorelin - by Bioz Stars, 2021-07
    91/100 stars
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    N/A
    This product is provided as delivered and specified by the issuing Pharmacopoeia All information provided in support of this product including SDS and any product information leaflets have been developed
      Buy from Supplier

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    Ginsenoside Mc1 inhibited hydrogen peroxide (H 2 O 2 )–mediated reactive oxygen species (ROS) production by increasing the expression of antioxidant proteins in H9c2 cells. (A) Cells were stimulated with various doses (0, 10, 25, or 50 μg/mL) of ginsenoside Mc1 for 30 min. (B) H9c2 cells were incubated with ginsenoside Mc1 (50 μg/mL) for the indicated times (0, 15, 30, or 60 min). The extent of AMPK phosphorylation was determined by Western blotting. (C) Cells were incubated with several doses (0, 25, or 50 μg/mL) of ginsenoside Mc1 for 24 h. (D) H9c2 cells were stimulated with ginsenoside Mc1 (50 μg/mL) or ginsenoside Mc1 plus compound C (2 or 5 μM) for 24 h. Catalase and SOD2 levels were determined by Western blotting. (E) Cells were pretreated with ginsenoside Mc1 (25 or 50 μg/mL) for 24 h and then stimulated with H 2 O 2 (600 μM) for 2 h. (F) H9c2 cells were preincubated with ginsenoside Mc1 (50 μg/mL) or ginsenoside Mc1 plus compound C (2 or 5 μM) for 24 h and then stimulated with H 2 O 2 (600 μM) for 2 h. The stimulated cells were stained with dihydroethidium (DHE) solution to assess the prevalence of intracellular ROS. The mean ± standard deviation was obtained from 3 separate experiments [*, p

    Journal: Journal of Ginseng Research

    Article Title: Ginsenoside compound-Mc1 attenuates oxidative stress and apoptosis in cardiomyocytes through an AMP-activated protein kinase–dependent mechanism

    doi: 10.1016/j.jgr.2019.08.006

    Figure Lengend Snippet: Ginsenoside Mc1 inhibited hydrogen peroxide (H 2 O 2 )–mediated reactive oxygen species (ROS) production by increasing the expression of antioxidant proteins in H9c2 cells. (A) Cells were stimulated with various doses (0, 10, 25, or 50 μg/mL) of ginsenoside Mc1 for 30 min. (B) H9c2 cells were incubated with ginsenoside Mc1 (50 μg/mL) for the indicated times (0, 15, 30, or 60 min). The extent of AMPK phosphorylation was determined by Western blotting. (C) Cells were incubated with several doses (0, 25, or 50 μg/mL) of ginsenoside Mc1 for 24 h. (D) H9c2 cells were stimulated with ginsenoside Mc1 (50 μg/mL) or ginsenoside Mc1 plus compound C (2 or 5 μM) for 24 h. Catalase and SOD2 levels were determined by Western blotting. (E) Cells were pretreated with ginsenoside Mc1 (25 or 50 μg/mL) for 24 h and then stimulated with H 2 O 2 (600 μM) for 2 h. (F) H9c2 cells were preincubated with ginsenoside Mc1 (50 μg/mL) or ginsenoside Mc1 plus compound C (2 or 5 μM) for 24 h and then stimulated with H 2 O 2 (600 μM) for 2 h. The stimulated cells were stained with dihydroethidium (DHE) solution to assess the prevalence of intracellular ROS. The mean ± standard deviation was obtained from 3 separate experiments [*, p

    Article Snippet: Ginsenoside Mc1, compound C (AMPK inhibitor; Sigma-Aldrich), and N-acetylcysteine (NAC; Cayman Chemical, MI, USA) were dissolved in dimethyl sulfoxide (Sigma-Aldrich).

    Techniques: Expressing, Incubation, Western Blot, Staining, Standard Deviation

    Ginsenoside Mc1 exhibited a protective effect after the treatment of H9c2 cells with hydrogen peroxide (H 2 O 2 ). (A and B) Cells were preincubated with ginsenoside Mc1 (25 or 50 μg/mL) or ginsenoside Mc1 plus compound C (2 μM) for 24 h and then stimulated with H 2 O 2 (600 μM) for 2 h. Bax and Bcl2 levels were determined by Western blotting. (C and D) H9c2 cells were pretreated with ginsenoside Mc1 or ginsenoside Mc1 plus compound C for 24 h and then stimulated with H 2 O 2 for 4 h. Cell viability was measured using an EZ-CYTOX kit. The mean ± standard deviation was obtained from 3 separate experiments [*, p

    Journal: Journal of Ginseng Research

    Article Title: Ginsenoside compound-Mc1 attenuates oxidative stress and apoptosis in cardiomyocytes through an AMP-activated protein kinase–dependent mechanism

    doi: 10.1016/j.jgr.2019.08.006

    Figure Lengend Snippet: Ginsenoside Mc1 exhibited a protective effect after the treatment of H9c2 cells with hydrogen peroxide (H 2 O 2 ). (A and B) Cells were preincubated with ginsenoside Mc1 (25 or 50 μg/mL) or ginsenoside Mc1 plus compound C (2 μM) for 24 h and then stimulated with H 2 O 2 (600 μM) for 2 h. Bax and Bcl2 levels were determined by Western blotting. (C and D) H9c2 cells were pretreated with ginsenoside Mc1 or ginsenoside Mc1 plus compound C for 24 h and then stimulated with H 2 O 2 for 4 h. Cell viability was measured using an EZ-CYTOX kit. The mean ± standard deviation was obtained from 3 separate experiments [*, p

    Article Snippet: Ginsenoside Mc1, compound C (AMPK inhibitor; Sigma-Aldrich), and N-acetylcysteine (NAC; Cayman Chemical, MI, USA) were dissolved in dimethyl sulfoxide (Sigma-Aldrich).

    Techniques: Western Blot, Standard Deviation

    Ginsenoside Mc1 inhibited hydrogen peroxide (H 2 O 2 )– induced apoptotic events in H9c2 cells. (A) Cells were preincubated with ginsenoside Mc1 (50 μg/mL) or ginsenoside Mc1 plus compound C (2 μM) for 24 h and then stimulated with H 2 O 2 (600 μM) for 2 h. The shape of the nucleus was determined by Hoechst staining. White arrows indicate DNA-damaged cells. (B) H9c2 cells were pretreated with ginsenoside Mc1 or ginsenoside Mc1 plus compound C for 24 h and then stimulated with H 2 O 2 for 4 h. The rate of apoptosis was determined using annexin V/propidium iodide (PI) double staining and flow cytometry. The mean ± standard deviation was obtained from 3 separate experiments [***, p

    Journal: Journal of Ginseng Research

    Article Title: Ginsenoside compound-Mc1 attenuates oxidative stress and apoptosis in cardiomyocytes through an AMP-activated protein kinase–dependent mechanism

    doi: 10.1016/j.jgr.2019.08.006

    Figure Lengend Snippet: Ginsenoside Mc1 inhibited hydrogen peroxide (H 2 O 2 )– induced apoptotic events in H9c2 cells. (A) Cells were preincubated with ginsenoside Mc1 (50 μg/mL) or ginsenoside Mc1 plus compound C (2 μM) for 24 h and then stimulated with H 2 O 2 (600 μM) for 2 h. The shape of the nucleus was determined by Hoechst staining. White arrows indicate DNA-damaged cells. (B) H9c2 cells were pretreated with ginsenoside Mc1 or ginsenoside Mc1 plus compound C for 24 h and then stimulated with H 2 O 2 for 4 h. The rate of apoptosis was determined using annexin V/propidium iodide (PI) double staining and flow cytometry. The mean ± standard deviation was obtained from 3 separate experiments [***, p

    Article Snippet: Ginsenoside Mc1, compound C (AMPK inhibitor; Sigma-Aldrich), and N-acetylcysteine (NAC; Cayman Chemical, MI, USA) were dissolved in dimethyl sulfoxide (Sigma-Aldrich).

    Techniques: Staining, Double Staining, Flow Cytometry, Standard Deviation

    Schematic diagram of the experiment with LPS-tolerance induction (LPS/LPS) in macrophages and LPS injection in mice are shown (upper part). Supernatant cytokines of LPS-tolerant FcgRIIB–/– macrophages and wild-type (FcgRIIB+/+) with or without compound C (AMPK inhibitor) (A–C) , semi-quantitative expression of mitochondrial DNA content (mtDNA) relative to β2 microglobulin (β2M) gene by qRT-PCR (D) , and luminescence intensity of cellular ATP production (E) are demonstrated (independent triplicate experiments were performed). Serum cytokine from FcgRIIB–/– and wild-type mice after LPS-tolerance induction with placebo control or compound C treatment (F–H) are shown ( n = 6–7/group). BMDMs, bone marrow-derived macrophages.

    Journal: Frontiers in Immunology

    Article Title: Dysregulation of Lipid Metabolism in Macrophages Is Responsible for Severe Endotoxin Tolerance in FcgRIIB-Deficient Lupus Mice

    doi: 10.3389/fimmu.2020.00959

    Figure Lengend Snippet: Schematic diagram of the experiment with LPS-tolerance induction (LPS/LPS) in macrophages and LPS injection in mice are shown (upper part). Supernatant cytokines of LPS-tolerant FcgRIIB–/– macrophages and wild-type (FcgRIIB+/+) with or without compound C (AMPK inhibitor) (A–C) , semi-quantitative expression of mitochondrial DNA content (mtDNA) relative to β2 microglobulin (β2M) gene by qRT-PCR (D) , and luminescence intensity of cellular ATP production (E) are demonstrated (independent triplicate experiments were performed). Serum cytokine from FcgRIIB–/– and wild-type mice after LPS-tolerance induction with placebo control or compound C treatment (F–H) are shown ( n = 6–7/group). BMDMs, bone marrow-derived macrophages.

    Article Snippet: AICAR (50, 100, or 200 μM) or Compound C (5 μM) (Sigma-Aldrich) was incubated in macrophages together with the second dose of LPS in sequential LPS protocol (100/100) before supernatant cytokine determination.

    Techniques: Injection, Mouse Assay, Expressing, Quantitative RT-PCR, Derivative Assay

    AMP-activated protein kinase (AMPK) is involved in resistin-induced matrix metalloproteinase (MMP-2) expression and cell migration JJ012 and SW1353 cells were pre-treated with Ara A (0.5 mM) and compound C (10 μM) for 30 min or pre-transfected with control, AMPKα1, or AMPKα2 siRNA for 24 h, and subsequently stimulated with resistin (3 ng/ml) for 24 h. In vitro migration, MMP-2 protein expression (JJ012 cells), and MMP-2 mRNA expression were measured by (A) Transwell assays, (B) enzyme-linked immunosorbent assay (ELISA), and (C) real-time quantitative polymerase chain reaction (RT-qPCR), respectively. Next, the JJ012 and SW1353 cells were pre-treated with SB203580 (10 μM) for 30 min or pre-transfected with control or p38 siRNA for 24 h, and subsequently stimulated with resistin (3 ng/ml) for 24 h. In vitro migration, MMP-2 protein expression (JJ012 cells), and MMP-2 mRNA expression were measured by (D) Transwell assays, (E) ELISA, and (F) RT-qPCR, respectively. (G) The JJ012 cells were incubated with resistin for the indicated time intervals, and the p-AMPK and p38 expression were examined by western blot. (H) The JJ012 cells were pre-treated for 30 min with Ara A and compound C, or SB203580 followed by stimulation with resistin. The p-p38 and p-AMPK expression were measured by western blot. The results are expressed as mean ± SEM. *, P

    Journal: Oncotarget

    Article Title: Resistin promotes tumor metastasis by down-regulation of miR-519d through the AMPK/p38 signaling pathway in human chondrosarcoma cells

    doi:

    Figure Lengend Snippet: AMP-activated protein kinase (AMPK) is involved in resistin-induced matrix metalloproteinase (MMP-2) expression and cell migration JJ012 and SW1353 cells were pre-treated with Ara A (0.5 mM) and compound C (10 μM) for 30 min or pre-transfected with control, AMPKα1, or AMPKα2 siRNA for 24 h, and subsequently stimulated with resistin (3 ng/ml) for 24 h. In vitro migration, MMP-2 protein expression (JJ012 cells), and MMP-2 mRNA expression were measured by (A) Transwell assays, (B) enzyme-linked immunosorbent assay (ELISA), and (C) real-time quantitative polymerase chain reaction (RT-qPCR), respectively. Next, the JJ012 and SW1353 cells were pre-treated with SB203580 (10 μM) for 30 min or pre-transfected with control or p38 siRNA for 24 h, and subsequently stimulated with resistin (3 ng/ml) for 24 h. In vitro migration, MMP-2 protein expression (JJ012 cells), and MMP-2 mRNA expression were measured by (D) Transwell assays, (E) ELISA, and (F) RT-qPCR, respectively. (G) The JJ012 cells were incubated with resistin for the indicated time intervals, and the p-AMPK and p38 expression were examined by western blot. (H) The JJ012 cells were pre-treated for 30 min with Ara A and compound C, or SB203580 followed by stimulation with resistin. The p-p38 and p-AMPK expression were measured by western blot. The results are expressed as mean ± SEM. *, P

    Article Snippet: AMPK inhibitors (Ara A and compound C), p38 inhibitor (SB203580), MMP-2 inhibitor, and human MMP-2 ELISA kits were purchased from Calbiochem (San Diego, CA).

    Techniques: Expressing, Migration, Acetylene Reduction Assay, Transfection, In Vitro, Enzyme-linked Immunosorbent Assay, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Incubation, Western Blot

    Resistin promotes cell migration and matrix metalloproteinase (MMP-2) expression by down-regulating microRNA (miR)-519d expression (A) The JJ012 and SW1353 cells were transfected with miR-519d mimic or inhibitor for 24 h, and cell migration ability was examined by Transwell assay. (B) The JJ012 cells were transfected with an miR-519d mimic or inhibitor for 24 h, and MMP-2 expression was examined by western blot (upper panel), and enzyme-linked immunosorbent assay (lower panel). (C) The JJ012 and SW1353 cells were incubated with resistin (0.3–3 ng/ml) for 24 h, and miR-519d expression was detected by real-time quantitative polymerase chain reaction. (D) Sequences of miR-519d and the potential miR-519d binding site at the MMP-2 3′ untranslated region (3′ UTR; WT-MMP-2 3′ UTR). Also shown are the nucleotides mutated in the MMP-2 3′UTR mutant (MUT-MMP2 3′ UTR). (E) The JJ012 and SW1353 cells were transfected with a wild-type or mutant MMP-2 3′ UTR luciferase plasmid for 24 h followed by stimulation with resistin (0.3-3 ng/ml) for 24 h, and the relative luciferase activity was measured. The JJ012 cells were pre-treated with AMPK and p38 inhibitors for 30 min or pre-transfected with specific siRNAs for 24 h followed by stimulation with resistin (3 ng/ml) for 24 h; and the (F, G) miR-519d expression and (H) MMP-2 3′ UTR activity were examined. The results are expressed as mean ± SEM. *, P

    Journal: Oncotarget

    Article Title: Resistin promotes tumor metastasis by down-regulation of miR-519d through the AMPK/p38 signaling pathway in human chondrosarcoma cells

    doi:

    Figure Lengend Snippet: Resistin promotes cell migration and matrix metalloproteinase (MMP-2) expression by down-regulating microRNA (miR)-519d expression (A) The JJ012 and SW1353 cells were transfected with miR-519d mimic or inhibitor for 24 h, and cell migration ability was examined by Transwell assay. (B) The JJ012 cells were transfected with an miR-519d mimic or inhibitor for 24 h, and MMP-2 expression was examined by western blot (upper panel), and enzyme-linked immunosorbent assay (lower panel). (C) The JJ012 and SW1353 cells were incubated with resistin (0.3–3 ng/ml) for 24 h, and miR-519d expression was detected by real-time quantitative polymerase chain reaction. (D) Sequences of miR-519d and the potential miR-519d binding site at the MMP-2 3′ untranslated region (3′ UTR; WT-MMP-2 3′ UTR). Also shown are the nucleotides mutated in the MMP-2 3′UTR mutant (MUT-MMP2 3′ UTR). (E) The JJ012 and SW1353 cells were transfected with a wild-type or mutant MMP-2 3′ UTR luciferase plasmid for 24 h followed by stimulation with resistin (0.3-3 ng/ml) for 24 h, and the relative luciferase activity was measured. The JJ012 cells were pre-treated with AMPK and p38 inhibitors for 30 min or pre-transfected with specific siRNAs for 24 h followed by stimulation with resistin (3 ng/ml) for 24 h; and the (F, G) miR-519d expression and (H) MMP-2 3′ UTR activity were examined. The results are expressed as mean ± SEM. *, P

    Article Snippet: AMPK inhibitors (Ara A and compound C), p38 inhibitor (SB203580), MMP-2 inhibitor, and human MMP-2 ELISA kits were purchased from Calbiochem (San Diego, CA).

    Techniques: Migration, Expressing, Transfection, Transwell Assay, Western Blot, Enzyme-linked Immunosorbent Assay, Incubation, Real-time Polymerase Chain Reaction, Binding Assay, Mutagenesis, Luciferase, Plasmid Preparation, Activity Assay

    The level of p-ERK1/2 is influenced by integration of signaling from multiple cell surface receptors, blocking the response to activated GnRH receptor . A. Triptorelin did not affect levels of p-ERK1/2 in serum-starved MCF-7-30 or MDA-MB-231-34 cells. B. Treatment of stably transfected cells with 100 nM Triptorelin transiently elevated levels of phosphorylated ERK1/2 (p-ERK1/2) in serum-starved MCF-7-30-7hygro14 cells but not in the presence of serum. Bar graphs indicate effect of no serum vs with serum on ERK response in MCF7hygro14, statistically significant for no serum, p

    Journal: BMC Cancer

    Article Title: GnRH receptor activation competes at a low level with growth signaling in stably transfected human breast cell lines

    doi: 10.1186/1471-2407-11-476

    Figure Lengend Snippet: The level of p-ERK1/2 is influenced by integration of signaling from multiple cell surface receptors, blocking the response to activated GnRH receptor . A. Triptorelin did not affect levels of p-ERK1/2 in serum-starved MCF-7-30 or MDA-MB-231-34 cells. B. Treatment of stably transfected cells with 100 nM Triptorelin transiently elevated levels of phosphorylated ERK1/2 (p-ERK1/2) in serum-starved MCF-7-30-7hygro14 cells but not in the presence of serum. Bar graphs indicate effect of no serum vs with serum on ERK response in MCF7hygro14, statistically significant for no serum, p

    Article Snippet: Cells were treated with a dose range of Triptorelin or vehicle (20% propylene glycol, Sigma, UK).

    Techniques: Blocking Assay, Multiple Displacement Amplification, Stable Transfection, Transfection

    Dynamics of GnRH receptor activation following treatment with Triptorelin . Treatment of stably transfected cells with GnRH elicited high levels of 3 H- inositol phosphate (IP) production (A-C). Removal of GnRH and LiCl revealed the dynamics of 3 H- inositol phosphate turnover in different cell types (D,E). The decrease in levels of 3 H- inositol phosphates was slower in SVCT-2 cells. Statistically different values (p

    Journal: BMC Cancer

    Article Title: GnRH receptor activation competes at a low level with growth signaling in stably transfected human breast cell lines

    doi: 10.1186/1471-2407-11-476

    Figure Lengend Snippet: Dynamics of GnRH receptor activation following treatment with Triptorelin . Treatment of stably transfected cells with GnRH elicited high levels of 3 H- inositol phosphate (IP) production (A-C). Removal of GnRH and LiCl revealed the dynamics of 3 H- inositol phosphate turnover in different cell types (D,E). The decrease in levels of 3 H- inositol phosphates was slower in SVCT-2 cells. Statistically different values (p

    Article Snippet: Cells were treated with a dose range of Triptorelin or vehicle (20% propylene glycol, Sigma, UK).

    Techniques: Activation Assay, Stable Transfection, Transfection

    The effect of Triptorelin on growth of cells stably transfected with GnRH . A. Growth of SVCT-2 after 4 days was marginally inhibited (10-18%) by treatment with Triptorelin. However, cell growth was effectively inhibited by IGF-IR inhibitor II and co-treatment with Triptorelin exerted a small additive effect (B). EGFR/ErbB2 inhibitor reduced SVCT-2 cell growth, but co-treatment with Triptorelin had no effect (C). Growth of MCF-7-30-7hygro14 cells was not affected by treatment with 100 nM Triptorelin (D), unlike HEK293 [SCL60] cells (E) after 4 days. Growth and survival were inhibited by IGF-IR inhibitor II but co-treatment with Triptorelin had no effect (F). Transient exposure to 15 μM IGF-IR inhibitor II for up to 2 hours resulted in less than 10% growth-inhibition after 4 days, longer exposures resulted in more extensive growth-inhibition (G). Growth of MCF-7-30-7hygro14 cells was inhibited by EGFR/ErbB2 inhibitor but not affected by treatment with 7 μM PI3Kγ inhibitor and co-treatment with 100 nM Triptorelin exerted no significant growth-inhibition (H and I). Growth of ZR75-1-12 (J) and MDA-MB-231-34 (K) was unaffected by treatment with 100 nM Triptorelin. * p

    Journal: BMC Cancer

    Article Title: GnRH receptor activation competes at a low level with growth signaling in stably transfected human breast cell lines

    doi: 10.1186/1471-2407-11-476

    Figure Lengend Snippet: The effect of Triptorelin on growth of cells stably transfected with GnRH . A. Growth of SVCT-2 after 4 days was marginally inhibited (10-18%) by treatment with Triptorelin. However, cell growth was effectively inhibited by IGF-IR inhibitor II and co-treatment with Triptorelin exerted a small additive effect (B). EGFR/ErbB2 inhibitor reduced SVCT-2 cell growth, but co-treatment with Triptorelin had no effect (C). Growth of MCF-7-30-7hygro14 cells was not affected by treatment with 100 nM Triptorelin (D), unlike HEK293 [SCL60] cells (E) after 4 days. Growth and survival were inhibited by IGF-IR inhibitor II but co-treatment with Triptorelin had no effect (F). Transient exposure to 15 μM IGF-IR inhibitor II for up to 2 hours resulted in less than 10% growth-inhibition after 4 days, longer exposures resulted in more extensive growth-inhibition (G). Growth of MCF-7-30-7hygro14 cells was inhibited by EGFR/ErbB2 inhibitor but not affected by treatment with 7 μM PI3Kγ inhibitor and co-treatment with 100 nM Triptorelin exerted no significant growth-inhibition (H and I). Growth of ZR75-1-12 (J) and MDA-MB-231-34 (K) was unaffected by treatment with 100 nM Triptorelin. * p

    Article Snippet: Cells were treated with a dose range of Triptorelin or vehicle (20% propylene glycol, Sigma, UK).

    Techniques: Stable Transfection, Transfection, Inhibition, Multiple Displacement Amplification