mouse ptx3 elisa kits  (Boster Bio)


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    Boster Bio mouse ptx3 elisa kits
    BmK AGAP suppresses the expression of <t>PTX3</t> in breast cancer cells. (A) IC50 values of rBmK AGAP for MCF-7 and MDA-MB-231 cells. The cells were treated with different concentrations of rBmKAGAP for 24 h; cell viability was measured by MTT assay. (B) rhPTX3 promotes breast cancer cell survival. MCF-7 and MDA-MB-231 cells were treated with different concentration of rhPTX3 and the effect of PTX3 on cells viability examined by cell viability assay. (C) siRNA inhibition of PTX3 and/or rBmK AGAP treatment suppresses cell viability of breast cancer cells. MCF-7 and MDA-MB-231 cells were treated with rBmK AGAP or siPTX3 or both, and their effect on cell viability was examined by MTT assay. (D) rBmK AGAP suppresses PTX3 secretion. MCF-7 and MDA-MB-231 cells were treated with different concentrations of rBmK AGAP for 48 h. SecretedPTX3 in supernatant samples were measured using <t>ELISA.</t> (E) Relative gene expression of PTX3 following rBmK AGAP treatment. Cells were treated with different concentrations of rBmK AGAP for 48 h, and the expression of PTX3 and GAPDH (internal control) were analyzed by qPCR. (F) PTX3 protein expression following rBmK AGAP treatment of MDA-MB-231 and MCF-7 cells. rBmK AGAP treated cells were lysed and subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against PTX3. (G) PTX3 assessment by immunofluorescence. rBmK AGAP treated cells were stained with anti-PTX3 antibodies (red) and DAPI (blue) and observed under a fluorescence microscopy (bar = 50 μm; magnification, 400x). rBmK AGAP suppresses PTX3 expression in a time-dependent manner. MDA-MB-231 and MCF-7 cells were treated with rBmK AGAP (30 μM) for 0, 24, and 48 h and the gene (H) and protein (I) expression levels of PTX3 was examined by qPCR and western blot, respectively. GAPDH served as internal control. (J) rBmK AGAP (30 μM) or Jingzhaotoxin-III (100 μM) suppresses the expression of Nav 1.5, p65/NF-κB, TNF-α, and PTX3 in MCF-7 and MDA-MB-231 cells as analyzed by western blotting. GAPDH was used as an internal control. The data was statistically significant at * P
    Mouse Ptx3 Elisa Kits, supplied by Boster Bio, 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/mouse ptx3 elisa kits/product/Boster Bio
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    mouse ptx3 elisa kits - by Bioz Stars, 2022-07
    91/100 stars

    Images

    1) Product Images from "Scorpion Venom Analgesic Peptide, BmK AGAP Inhibits Stemness, and Epithelial-Mesenchymal Transition by Down-Regulating PTX3 in Breast Cancer"

    Article Title: Scorpion Venom Analgesic Peptide, BmK AGAP Inhibits Stemness, and Epithelial-Mesenchymal Transition by Down-Regulating PTX3 in Breast Cancer

    Journal: Frontiers in Oncology

    doi: 10.3389/fonc.2019.00021

    BmK AGAP suppresses the expression of PTX3 in breast cancer cells. (A) IC50 values of rBmK AGAP for MCF-7 and MDA-MB-231 cells. The cells were treated with different concentrations of rBmKAGAP for 24 h; cell viability was measured by MTT assay. (B) rhPTX3 promotes breast cancer cell survival. MCF-7 and MDA-MB-231 cells were treated with different concentration of rhPTX3 and the effect of PTX3 on cells viability examined by cell viability assay. (C) siRNA inhibition of PTX3 and/or rBmK AGAP treatment suppresses cell viability of breast cancer cells. MCF-7 and MDA-MB-231 cells were treated with rBmK AGAP or siPTX3 or both, and their effect on cell viability was examined by MTT assay. (D) rBmK AGAP suppresses PTX3 secretion. MCF-7 and MDA-MB-231 cells were treated with different concentrations of rBmK AGAP for 48 h. SecretedPTX3 in supernatant samples were measured using ELISA. (E) Relative gene expression of PTX3 following rBmK AGAP treatment. Cells were treated with different concentrations of rBmK AGAP for 48 h, and the expression of PTX3 and GAPDH (internal control) were analyzed by qPCR. (F) PTX3 protein expression following rBmK AGAP treatment of MDA-MB-231 and MCF-7 cells. rBmK AGAP treated cells were lysed and subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against PTX3. (G) PTX3 assessment by immunofluorescence. rBmK AGAP treated cells were stained with anti-PTX3 antibodies (red) and DAPI (blue) and observed under a fluorescence microscopy (bar = 50 μm; magnification, 400x). rBmK AGAP suppresses PTX3 expression in a time-dependent manner. MDA-MB-231 and MCF-7 cells were treated with rBmK AGAP (30 μM) for 0, 24, and 48 h and the gene (H) and protein (I) expression levels of PTX3 was examined by qPCR and western blot, respectively. GAPDH served as internal control. (J) rBmK AGAP (30 μM) or Jingzhaotoxin-III (100 μM) suppresses the expression of Nav 1.5, p65/NF-κB, TNF-α, and PTX3 in MCF-7 and MDA-MB-231 cells as analyzed by western blotting. GAPDH was used as an internal control. The data was statistically significant at * P
    Figure Legend Snippet: BmK AGAP suppresses the expression of PTX3 in breast cancer cells. (A) IC50 values of rBmK AGAP for MCF-7 and MDA-MB-231 cells. The cells were treated with different concentrations of rBmKAGAP for 24 h; cell viability was measured by MTT assay. (B) rhPTX3 promotes breast cancer cell survival. MCF-7 and MDA-MB-231 cells were treated with different concentration of rhPTX3 and the effect of PTX3 on cells viability examined by cell viability assay. (C) siRNA inhibition of PTX3 and/or rBmK AGAP treatment suppresses cell viability of breast cancer cells. MCF-7 and MDA-MB-231 cells were treated with rBmK AGAP or siPTX3 or both, and their effect on cell viability was examined by MTT assay. (D) rBmK AGAP suppresses PTX3 secretion. MCF-7 and MDA-MB-231 cells were treated with different concentrations of rBmK AGAP for 48 h. SecretedPTX3 in supernatant samples were measured using ELISA. (E) Relative gene expression of PTX3 following rBmK AGAP treatment. Cells were treated with different concentrations of rBmK AGAP for 48 h, and the expression of PTX3 and GAPDH (internal control) were analyzed by qPCR. (F) PTX3 protein expression following rBmK AGAP treatment of MDA-MB-231 and MCF-7 cells. rBmK AGAP treated cells were lysed and subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against PTX3. (G) PTX3 assessment by immunofluorescence. rBmK AGAP treated cells were stained with anti-PTX3 antibodies (red) and DAPI (blue) and observed under a fluorescence microscopy (bar = 50 μm; magnification, 400x). rBmK AGAP suppresses PTX3 expression in a time-dependent manner. MDA-MB-231 and MCF-7 cells were treated with rBmK AGAP (30 μM) for 0, 24, and 48 h and the gene (H) and protein (I) expression levels of PTX3 was examined by qPCR and western blot, respectively. GAPDH served as internal control. (J) rBmK AGAP (30 μM) or Jingzhaotoxin-III (100 μM) suppresses the expression of Nav 1.5, p65/NF-κB, TNF-α, and PTX3 in MCF-7 and MDA-MB-231 cells as analyzed by western blotting. GAPDH was used as an internal control. The data was statistically significant at * P

    Techniques Used: Expressing, Multiple Displacement Amplification, MTT Assay, Concentration Assay, Viability Assay, Inhibition, Enzyme-linked Immunosorbent Assay, Real-time Polymerase Chain Reaction, SDS Page, Western Blot, Immunofluorescence, Staining, Fluorescence, Microscopy

    2) Product Images from "Scorpion Venom Analgesic Peptide, BmK AGAP Inhibits Stemness, and Epithelial-Mesenchymal Transition by Down-Regulating PTX3 in Breast Cancer"

    Article Title: Scorpion Venom Analgesic Peptide, BmK AGAP Inhibits Stemness, and Epithelial-Mesenchymal Transition by Down-Regulating PTX3 in Breast Cancer

    Journal: Frontiers in Oncology

    doi: 10.3389/fonc.2019.00021

    BmK AGAP suppresses the expression of PTX3 in breast cancer cells. (A) IC50 values of rBmK AGAP for MCF-7 and MDA-MB-231 cells. The cells were treated with different concentrations of rBmKAGAP for 24 h; cell viability was measured by MTT assay. (B) rhPTX3 promotes breast cancer cell survival. MCF-7 and MDA-MB-231 cells were treated with different concentration of rhPTX3 and the effect of PTX3 on cells viability examined by cell viability assay. (C) siRNA inhibition of PTX3 and/or rBmK AGAP treatment suppresses cell viability of breast cancer cells. MCF-7 and MDA-MB-231 cells were treated with rBmK AGAP or siPTX3 or both, and their effect on cell viability was examined by MTT assay. (D) rBmK AGAP suppresses PTX3 secretion. MCF-7 and MDA-MB-231 cells were treated with different concentrations of rBmK AGAP for 48 h. SecretedPTX3 in supernatant samples were measured using ELISA. (E) Relative gene expression of PTX3 following rBmK AGAP treatment. Cells were treated with different concentrations of rBmK AGAP for 48 h, and the expression of PTX3 and GAPDH (internal control) were analyzed by qPCR. (F) PTX3 protein expression following rBmK AGAP treatment of MDA-MB-231 and MCF-7 cells. rBmK AGAP treated cells were lysed and subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against PTX3. (G) PTX3 assessment by immunofluorescence. rBmK AGAP treated cells were stained with anti-PTX3 antibodies (red) and DAPI (blue) and observed under a fluorescence microscopy (bar = 50 μm; magnification, 400x). rBmK AGAP suppresses PTX3 expression in a time-dependent manner. MDA-MB-231 and MCF-7 cells were treated with rBmK AGAP (30 μM) for 0, 24, and 48 h and the gene (H) and protein (I) expression levels of PTX3 was examined by qPCR and western blot, respectively. GAPDH served as internal control. (J) rBmK AGAP (30 μM) or Jingzhaotoxin-III (100 μM) suppresses the expression of Nav 1.5, p65/NF-κB, TNF-α, and PTX3 in MCF-7 and MDA-MB-231 cells as analyzed by western blotting. GAPDH was used as an internal control. The data was statistically significant at * P
    Figure Legend Snippet: BmK AGAP suppresses the expression of PTX3 in breast cancer cells. (A) IC50 values of rBmK AGAP for MCF-7 and MDA-MB-231 cells. The cells were treated with different concentrations of rBmKAGAP for 24 h; cell viability was measured by MTT assay. (B) rhPTX3 promotes breast cancer cell survival. MCF-7 and MDA-MB-231 cells were treated with different concentration of rhPTX3 and the effect of PTX3 on cells viability examined by cell viability assay. (C) siRNA inhibition of PTX3 and/or rBmK AGAP treatment suppresses cell viability of breast cancer cells. MCF-7 and MDA-MB-231 cells were treated with rBmK AGAP or siPTX3 or both, and their effect on cell viability was examined by MTT assay. (D) rBmK AGAP suppresses PTX3 secretion. MCF-7 and MDA-MB-231 cells were treated with different concentrations of rBmK AGAP for 48 h. SecretedPTX3 in supernatant samples were measured using ELISA. (E) Relative gene expression of PTX3 following rBmK AGAP treatment. Cells were treated with different concentrations of rBmK AGAP for 48 h, and the expression of PTX3 and GAPDH (internal control) were analyzed by qPCR. (F) PTX3 protein expression following rBmK AGAP treatment of MDA-MB-231 and MCF-7 cells. rBmK AGAP treated cells were lysed and subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against PTX3. (G) PTX3 assessment by immunofluorescence. rBmK AGAP treated cells were stained with anti-PTX3 antibodies (red) and DAPI (blue) and observed under a fluorescence microscopy (bar = 50 μm; magnification, 400x). rBmK AGAP suppresses PTX3 expression in a time-dependent manner. MDA-MB-231 and MCF-7 cells were treated with rBmK AGAP (30 μM) for 0, 24, and 48 h and the gene (H) and protein (I) expression levels of PTX3 was examined by qPCR and western blot, respectively. GAPDH served as internal control. (J) rBmK AGAP (30 μM) or Jingzhaotoxin-III (100 μM) suppresses the expression of Nav 1.5, p65/NF-κB, TNF-α, and PTX3 in MCF-7 and MDA-MB-231 cells as analyzed by western blotting. GAPDH was used as an internal control. The data was statistically significant at * P

    Techniques Used: Expressing, Multiple Displacement Amplification, MTT Assay, Concentration Assay, Viability Assay, Inhibition, Enzyme-linked Immunosorbent Assay, Real-time Polymerase Chain Reaction, SDS Page, Western Blot, Immunofluorescence, Staining, Fluorescence, Microscopy

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    Boster Bio mouse ptx3 elisa kits
    BmK AGAP suppresses the expression of <t>PTX3</t> in breast cancer cells. (A) IC50 values of rBmK AGAP for MCF-7 and MDA-MB-231 cells. The cells were treated with different concentrations of rBmKAGAP for 24 h; cell viability was measured by MTT assay. (B) rhPTX3 promotes breast cancer cell survival. MCF-7 and MDA-MB-231 cells were treated with different concentration of rhPTX3 and the effect of PTX3 on cells viability examined by cell viability assay. (C) siRNA inhibition of PTX3 and/or rBmK AGAP treatment suppresses cell viability of breast cancer cells. MCF-7 and MDA-MB-231 cells were treated with rBmK AGAP or siPTX3 or both, and their effect on cell viability was examined by MTT assay. (D) rBmK AGAP suppresses PTX3 secretion. MCF-7 and MDA-MB-231 cells were treated with different concentrations of rBmK AGAP for 48 h. SecretedPTX3 in supernatant samples were measured using <t>ELISA.</t> (E) Relative gene expression of PTX3 following rBmK AGAP treatment. Cells were treated with different concentrations of rBmK AGAP for 48 h, and the expression of PTX3 and GAPDH (internal control) were analyzed by qPCR. (F) PTX3 protein expression following rBmK AGAP treatment of MDA-MB-231 and MCF-7 cells. rBmK AGAP treated cells were lysed and subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against PTX3. (G) PTX3 assessment by immunofluorescence. rBmK AGAP treated cells were stained with anti-PTX3 antibodies (red) and DAPI (blue) and observed under a fluorescence microscopy (bar = 50 μm; magnification, 400x). rBmK AGAP suppresses PTX3 expression in a time-dependent manner. MDA-MB-231 and MCF-7 cells were treated with rBmK AGAP (30 μM) for 0, 24, and 48 h and the gene (H) and protein (I) expression levels of PTX3 was examined by qPCR and western blot, respectively. GAPDH served as internal control. (J) rBmK AGAP (30 μM) or Jingzhaotoxin-III (100 μM) suppresses the expression of Nav 1.5, p65/NF-κB, TNF-α, and PTX3 in MCF-7 and MDA-MB-231 cells as analyzed by western blotting. GAPDH was used as an internal control. The data was statistically significant at * P
    Mouse Ptx3 Elisa Kits, supplied by Boster Bio, 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/mouse ptx3 elisa kits/product/Boster Bio
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    mouse ptx3 elisa kits - by Bioz Stars, 2022-07
    91/100 stars
      Buy from Supplier

    94
    Boster Bio ptx3 kit
    BmK AGAP suppresses the expression of <t>PTX3</t> in breast cancer cells. (A) IC50 values of rBmK AGAP for MCF-7 and MDA-MB-231 cells. The cells were treated with different concentrations of rBmKAGAP for 24 h; cell viability was measured by MTT assay. (B) rhPTX3 promotes breast cancer cell survival. MCF-7 and MDA-MB-231 cells were treated with different concentration of rhPTX3 and the effect of PTX3 on cells viability examined by cell viability assay. (C) siRNA inhibition of PTX3 and/or rBmK AGAP treatment suppresses cell viability of breast cancer cells. MCF-7 and MDA-MB-231 cells were treated with rBmK AGAP or siPTX3 or both, and their effect on cell viability was examined by MTT assay. (D) rBmK AGAP suppresses PTX3 secretion. MCF-7 and MDA-MB-231 cells were treated with different concentrations of rBmK AGAP for 48 h. SecretedPTX3 in supernatant samples were measured using <t>ELISA.</t> (E) Relative gene expression of PTX3 following rBmK AGAP treatment. Cells were treated with different concentrations of rBmK AGAP for 48 h, and the expression of PTX3 and GAPDH (internal control) were analyzed by qPCR. (F) PTX3 protein expression following rBmK AGAP treatment of MDA-MB-231 and MCF-7 cells. rBmK AGAP treated cells were lysed and subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against PTX3. (G) PTX3 assessment by immunofluorescence. rBmK AGAP treated cells were stained with anti-PTX3 antibodies (red) and DAPI (blue) and observed under a fluorescence microscopy (bar = 50 μm; magnification, 400x). rBmK AGAP suppresses PTX3 expression in a time-dependent manner. MDA-MB-231 and MCF-7 cells were treated with rBmK AGAP (30 μM) for 0, 24, and 48 h and the gene (H) and protein (I) expression levels of PTX3 was examined by qPCR and western blot, respectively. GAPDH served as internal control. (J) rBmK AGAP (30 μM) or Jingzhaotoxin-III (100 μM) suppresses the expression of Nav 1.5, p65/NF-κB, TNF-α, and PTX3 in MCF-7 and MDA-MB-231 cells as analyzed by western blotting. GAPDH was used as an internal control. The data was statistically significant at * P
    Ptx3 Kit, supplied by Boster Bio, 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/ptx3 kit/product/Boster Bio
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    ptx3 kit - by Bioz Stars, 2022-07
    94/100 stars
      Buy from Supplier

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    BmK AGAP suppresses the expression of PTX3 in breast cancer cells. (A) IC50 values of rBmK AGAP for MCF-7 and MDA-MB-231 cells. The cells were treated with different concentrations of rBmKAGAP for 24 h; cell viability was measured by MTT assay. (B) rhPTX3 promotes breast cancer cell survival. MCF-7 and MDA-MB-231 cells were treated with different concentration of rhPTX3 and the effect of PTX3 on cells viability examined by cell viability assay. (C) siRNA inhibition of PTX3 and/or rBmK AGAP treatment suppresses cell viability of breast cancer cells. MCF-7 and MDA-MB-231 cells were treated with rBmK AGAP or siPTX3 or both, and their effect on cell viability was examined by MTT assay. (D) rBmK AGAP suppresses PTX3 secretion. MCF-7 and MDA-MB-231 cells were treated with different concentrations of rBmK AGAP for 48 h. SecretedPTX3 in supernatant samples were measured using ELISA. (E) Relative gene expression of PTX3 following rBmK AGAP treatment. Cells were treated with different concentrations of rBmK AGAP for 48 h, and the expression of PTX3 and GAPDH (internal control) were analyzed by qPCR. (F) PTX3 protein expression following rBmK AGAP treatment of MDA-MB-231 and MCF-7 cells. rBmK AGAP treated cells were lysed and subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against PTX3. (G) PTX3 assessment by immunofluorescence. rBmK AGAP treated cells were stained with anti-PTX3 antibodies (red) and DAPI (blue) and observed under a fluorescence microscopy (bar = 50 μm; magnification, 400x). rBmK AGAP suppresses PTX3 expression in a time-dependent manner. MDA-MB-231 and MCF-7 cells were treated with rBmK AGAP (30 μM) for 0, 24, and 48 h and the gene (H) and protein (I) expression levels of PTX3 was examined by qPCR and western blot, respectively. GAPDH served as internal control. (J) rBmK AGAP (30 μM) or Jingzhaotoxin-III (100 μM) suppresses the expression of Nav 1.5, p65/NF-κB, TNF-α, and PTX3 in MCF-7 and MDA-MB-231 cells as analyzed by western blotting. GAPDH was used as an internal control. The data was statistically significant at * P

    Journal: Frontiers in Oncology

    Article Title: Scorpion Venom Analgesic Peptide, BmK AGAP Inhibits Stemness, and Epithelial-Mesenchymal Transition by Down-Regulating PTX3 in Breast Cancer

    doi: 10.3389/fonc.2019.00021

    Figure Lengend Snippet: BmK AGAP suppresses the expression of PTX3 in breast cancer cells. (A) IC50 values of rBmK AGAP for MCF-7 and MDA-MB-231 cells. The cells were treated with different concentrations of rBmKAGAP for 24 h; cell viability was measured by MTT assay. (B) rhPTX3 promotes breast cancer cell survival. MCF-7 and MDA-MB-231 cells were treated with different concentration of rhPTX3 and the effect of PTX3 on cells viability examined by cell viability assay. (C) siRNA inhibition of PTX3 and/or rBmK AGAP treatment suppresses cell viability of breast cancer cells. MCF-7 and MDA-MB-231 cells were treated with rBmK AGAP or siPTX3 or both, and their effect on cell viability was examined by MTT assay. (D) rBmK AGAP suppresses PTX3 secretion. MCF-7 and MDA-MB-231 cells were treated with different concentrations of rBmK AGAP for 48 h. SecretedPTX3 in supernatant samples were measured using ELISA. (E) Relative gene expression of PTX3 following rBmK AGAP treatment. Cells were treated with different concentrations of rBmK AGAP for 48 h, and the expression of PTX3 and GAPDH (internal control) were analyzed by qPCR. (F) PTX3 protein expression following rBmK AGAP treatment of MDA-MB-231 and MCF-7 cells. rBmK AGAP treated cells were lysed and subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against PTX3. (G) PTX3 assessment by immunofluorescence. rBmK AGAP treated cells were stained with anti-PTX3 antibodies (red) and DAPI (blue) and observed under a fluorescence microscopy (bar = 50 μm; magnification, 400x). rBmK AGAP suppresses PTX3 expression in a time-dependent manner. MDA-MB-231 and MCF-7 cells were treated with rBmK AGAP (30 μM) for 0, 24, and 48 h and the gene (H) and protein (I) expression levels of PTX3 was examined by qPCR and western blot, respectively. GAPDH served as internal control. (J) rBmK AGAP (30 μM) or Jingzhaotoxin-III (100 μM) suppresses the expression of Nav 1.5, p65/NF-κB, TNF-α, and PTX3 in MCF-7 and MDA-MB-231 cells as analyzed by western blotting. GAPDH was used as an internal control. The data was statistically significant at * P

    Article Snippet: Human and mouse PTX3 ELISA kits (Boster Biological Technology, China); IKK-16, and Jingzhaotoxin-III (Tocris Bioscience, USA), rhPTX3 and siPTX3 (Guangzhou Ribobio, China) and Dimethyl sulfoxide (Beyotime Biotechnology, China).

    Techniques: Expressing, Multiple Displacement Amplification, MTT Assay, Concentration Assay, Viability Assay, Inhibition, Enzyme-linked Immunosorbent Assay, Real-time Polymerase Chain Reaction, SDS Page, Western Blot, Immunofluorescence, Staining, Fluorescence, Microscopy

    BmK AGAP suppresses the expression of PTX3 in breast cancer cells. (A) IC50 values of rBmK AGAP for MCF-7 and MDA-MB-231 cells. The cells were treated with different concentrations of rBmKAGAP for 24 h; cell viability was measured by MTT assay. (B) rhPTX3 promotes breast cancer cell survival. MCF-7 and MDA-MB-231 cells were treated with different concentration of rhPTX3 and the effect of PTX3 on cells viability examined by cell viability assay. (C) siRNA inhibition of PTX3 and/or rBmK AGAP treatment suppresses cell viability of breast cancer cells. MCF-7 and MDA-MB-231 cells were treated with rBmK AGAP or siPTX3 or both, and their effect on cell viability was examined by MTT assay. (D) rBmK AGAP suppresses PTX3 secretion. MCF-7 and MDA-MB-231 cells were treated with different concentrations of rBmK AGAP for 48 h. SecretedPTX3 in supernatant samples were measured using ELISA. (E) Relative gene expression of PTX3 following rBmK AGAP treatment. Cells were treated with different concentrations of rBmK AGAP for 48 h, and the expression of PTX3 and GAPDH (internal control) were analyzed by qPCR. (F) PTX3 protein expression following rBmK AGAP treatment of MDA-MB-231 and MCF-7 cells. rBmK AGAP treated cells were lysed and subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against PTX3. (G) PTX3 assessment by immunofluorescence. rBmK AGAP treated cells were stained with anti-PTX3 antibodies (red) and DAPI (blue) and observed under a fluorescence microscopy (bar = 50 μm; magnification, 400x). rBmK AGAP suppresses PTX3 expression in a time-dependent manner. MDA-MB-231 and MCF-7 cells were treated with rBmK AGAP (30 μM) for 0, 24, and 48 h and the gene (H) and protein (I) expression levels of PTX3 was examined by qPCR and western blot, respectively. GAPDH served as internal control. (J) rBmK AGAP (30 μM) or Jingzhaotoxin-III (100 μM) suppresses the expression of Nav 1.5, p65/NF-κB, TNF-α, and PTX3 in MCF-7 and MDA-MB-231 cells as analyzed by western blotting. GAPDH was used as an internal control. The data was statistically significant at * P

    Journal: Frontiers in Oncology

    Article Title: Scorpion Venom Analgesic Peptide, BmK AGAP Inhibits Stemness, and Epithelial-Mesenchymal Transition by Down-Regulating PTX3 in Breast Cancer

    doi: 10.3389/fonc.2019.00021

    Figure Lengend Snippet: BmK AGAP suppresses the expression of PTX3 in breast cancer cells. (A) IC50 values of rBmK AGAP for MCF-7 and MDA-MB-231 cells. The cells were treated with different concentrations of rBmKAGAP for 24 h; cell viability was measured by MTT assay. (B) rhPTX3 promotes breast cancer cell survival. MCF-7 and MDA-MB-231 cells were treated with different concentration of rhPTX3 and the effect of PTX3 on cells viability examined by cell viability assay. (C) siRNA inhibition of PTX3 and/or rBmK AGAP treatment suppresses cell viability of breast cancer cells. MCF-7 and MDA-MB-231 cells were treated with rBmK AGAP or siPTX3 or both, and their effect on cell viability was examined by MTT assay. (D) rBmK AGAP suppresses PTX3 secretion. MCF-7 and MDA-MB-231 cells were treated with different concentrations of rBmK AGAP for 48 h. SecretedPTX3 in supernatant samples were measured using ELISA. (E) Relative gene expression of PTX3 following rBmK AGAP treatment. Cells were treated with different concentrations of rBmK AGAP for 48 h, and the expression of PTX3 and GAPDH (internal control) were analyzed by qPCR. (F) PTX3 protein expression following rBmK AGAP treatment of MDA-MB-231 and MCF-7 cells. rBmK AGAP treated cells were lysed and subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against PTX3. (G) PTX3 assessment by immunofluorescence. rBmK AGAP treated cells were stained with anti-PTX3 antibodies (red) and DAPI (blue) and observed under a fluorescence microscopy (bar = 50 μm; magnification, 400x). rBmK AGAP suppresses PTX3 expression in a time-dependent manner. MDA-MB-231 and MCF-7 cells were treated with rBmK AGAP (30 μM) for 0, 24, and 48 h and the gene (H) and protein (I) expression levels of PTX3 was examined by qPCR and western blot, respectively. GAPDH served as internal control. (J) rBmK AGAP (30 μM) or Jingzhaotoxin-III (100 μM) suppresses the expression of Nav 1.5, p65/NF-κB, TNF-α, and PTX3 in MCF-7 and MDA-MB-231 cells as analyzed by western blotting. GAPDH was used as an internal control. The data was statistically significant at * P

    Article Snippet: Human and mouse PTX3 ELISA kits (Boster Biological Technology, China); IKK-16, and Jingzhaotoxin-III (Tocris Bioscience, USA), rhPTX3 and siPTX3 (Guangzhou Ribobio, China) and Dimethyl sulfoxide (Beyotime Biotechnology, China).

    Techniques: Expressing, Multiple Displacement Amplification, MTT Assay, Concentration Assay, Viability Assay, Inhibition, Enzyme-linked Immunosorbent Assay, Real-time Polymerase Chain Reaction, SDS Page, Western Blot, Immunofluorescence, Staining, Fluorescence, Microscopy