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human ptx3 elisa kit  (Boster Bio)
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Boster Bio human ptx3 elisa kit
<t>PTX3</t> expression in breast cancer cells and tissues. (A) Assessment of PTX3 gene expression relative to GAPDH in MCF-10A, MDA-MB-231, BT549, and MCF-7 cells by qPCR. (B) <t>PTX3</t> <t>protein</t> expression in MCF-10A, MDA-MB-231, BT549, and MCF-7 cells. Total protein from cell lysates was subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against PTX3. GAPDH was used as loading control. (C) Representative micrographs of PTX3 expression in MCF-10A, MDA-MB-231, BT549, and MCF-7 cells. The cells were stained with anti-PTX3 antibodies (red) and DAPI (blue) and observed under a fluorescence microscope (bar = 50 μm; magnification, 400x). (D) PTX3 expression in human breast cancer tissues (patient 1, first-grade tumor, molecular subtype HER2; patient 2, second-grade tumor, molecular subtype BLBC; and patient 3, third-grade tumor, molecular subtype BLBC) examined by immunohistochemical staining. (Scale bars = 100 μm; magnification, 200x). (E) PTX3 expression in human breast cancer tissues and normal breast tissue. Tissues were homogenized and equal amount of proteins were subjected to SDS-PAGE and analyzed by western blotting with antibodies against PTX3. GAPDH was used as an internal control. The data are reported as mean ± SEM of three independent experiments. * Indicates statistical significance, P < 0.05; ** P < 0.01.
Human Ptx3 Elisa Kit, supplied by Boster Bio, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human ptx3 elisa kit - by Bioz Stars, 2026-08
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PTX3 expression in breast cancer cells and tissues. (A) Assessment of PTX3 gene expression relative to GAPDH in MCF-10A, MDA-MB-231, BT549, and MCF-7 cells by qPCR. (B) PTX3 protein expression in MCF-10A, MDA-MB-231, BT549, and MCF-7 cells. Total protein from cell lysates was subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against PTX3. GAPDH was used as loading control. (C) Representative micrographs of PTX3 expression in MCF-10A, MDA-MB-231, BT549, and MCF-7 cells. The cells were stained with anti-PTX3 antibodies (red) and DAPI (blue) and observed under a fluorescence microscope (bar = 50 μm; magnification, 400x). (D) PTX3 expression in human breast cancer tissues (patient 1, first-grade tumor, molecular subtype HER2; patient 2, second-grade tumor, molecular subtype BLBC; and patient 3, third-grade tumor, molecular subtype BLBC) examined by immunohistochemical staining. (Scale bars = 100 μm; magnification, 200x). (E) PTX3 expression in human breast cancer tissues and normal breast tissue. Tissues were homogenized and equal amount of proteins were subjected to SDS-PAGE and analyzed by western blotting with antibodies against PTX3. GAPDH was used as an internal control. The data are reported as mean ± SEM of three independent experiments. * Indicates statistical significance, P < 0.05; ** P < 0.01.

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: PTX3 expression in breast cancer cells and tissues. (A) Assessment of PTX3 gene expression relative to GAPDH in MCF-10A, MDA-MB-231, BT549, and MCF-7 cells by qPCR. (B) PTX3 protein expression in MCF-10A, MDA-MB-231, BT549, and MCF-7 cells. Total protein from cell lysates was subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against PTX3. GAPDH was used as loading control. (C) Representative micrographs of PTX3 expression in MCF-10A, MDA-MB-231, BT549, and MCF-7 cells. The cells were stained with anti-PTX3 antibodies (red) and DAPI (blue) and observed under a fluorescence microscope (bar = 50 μm; magnification, 400x). (D) PTX3 expression in human breast cancer tissues (patient 1, first-grade tumor, molecular subtype HER2; patient 2, second-grade tumor, molecular subtype BLBC; and patient 3, third-grade tumor, molecular subtype BLBC) examined by immunohistochemical staining. (Scale bars = 100 μm; magnification, 200x). (E) PTX3 expression in human breast cancer tissues and normal breast tissue. Tissues were homogenized and equal amount of proteins were subjected to SDS-PAGE and analyzed by western blotting with antibodies against PTX3. GAPDH was used as an internal control. The data are reported as mean ± SEM of three independent experiments. * Indicates statistical significance, P < 0.05; ** P < 0.01.

Article Snippet: Human PTX3 ELISA Kit (Boster Biological Technology, China) was used to measure PTX3 secretion in supernatant samples from MCF-7 and MDA-MB-231 cells as described elsewhere ( ).

Techniques: Expressing, Gene Expression, SDS Page, Western Blot, Control, Staining, Fluorescence, Microscopy, Immunohistochemical staining

PTX3 expression in breast cancer cells is associated with stem-like features and epithelial-mesenchymal transition. (A) Tumorsphere formation of MCF-7 and MDA-MB-231 cells. MCF-7 and MDA-MB-231 cells were treated with siPTX3 or rhPTX3 for 14 days, and tumor spheres expansion were analyzed at 40x magnification under a microscope (bar = 50 μm; magnification, 400x). (B) PTX3 promotes cell migration and invasion in breast cancer. MCF-7 and MDA-MB-231 cells were treated with either siPTX3 or rhPTX3. The migration and invasion abilities of the cells were examined by migration and invasion assay (Transwell assay). (C,D) Effect of PTX3 on stem-like features and epithelial-mesenchymal transition markers. siPTX3 or rhPTX3-treated MDA-MB-231 and MCF-7 cells were lysed and subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against PTX3, Oct4, Sox2, E-cadherin, N-cadherin, and Snail. GAPDH was used as an internal control. The data was statistically significant at * P < 0.05; ** P < 0.01; and *** P < 0.001 as compared to control. Data are represented as mean ± SEM of three independent experiments.

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: PTX3 expression in breast cancer cells is associated with stem-like features and epithelial-mesenchymal transition. (A) Tumorsphere formation of MCF-7 and MDA-MB-231 cells. MCF-7 and MDA-MB-231 cells were treated with siPTX3 or rhPTX3 for 14 days, and tumor spheres expansion were analyzed at 40x magnification under a microscope (bar = 50 μm; magnification, 400x). (B) PTX3 promotes cell migration and invasion in breast cancer. MCF-7 and MDA-MB-231 cells were treated with either siPTX3 or rhPTX3. The migration and invasion abilities of the cells were examined by migration and invasion assay (Transwell assay). (C,D) Effect of PTX3 on stem-like features and epithelial-mesenchymal transition markers. siPTX3 or rhPTX3-treated MDA-MB-231 and MCF-7 cells were lysed and subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against PTX3, Oct4, Sox2, E-cadherin, N-cadherin, and Snail. GAPDH was used as an internal control. The data was statistically significant at * P < 0.05; ** P < 0.01; and *** P < 0.001 as compared to control. Data are represented as mean ± SEM of three independent experiments.

Article Snippet: Human PTX3 ELISA Kit (Boster Biological Technology, China) was used to measure PTX3 secretion in supernatant samples from MCF-7 and MDA-MB-231 cells as described elsewhere ( ).

Techniques: Expressing, Microscopy, Migration, Invasion Assay, Transwell Assay, SDS Page, Western Blot, Control

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 < 0.05; ** P < 0.01; and *** P < 0.001 as compared to untreated cells. The data represent the mean ± SEM of three independent experiments.

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 < 0.05; ** P < 0.01; and *** P < 0.001 as compared to untreated cells. The data represent the mean ± SEM of three independent experiments.

Article Snippet: Human PTX3 ELISA Kit (Boster Biological Technology, China) was used to measure PTX3 secretion in supernatant samples from MCF-7 and MDA-MB-231 cells as described elsewhere ( ).

Techniques: Expressing, MTT Assay, Concentration Assay, Viability Assay, Inhibition, Enzyme-linked Immunosorbent Assay, Gene Expression, Control, SDS Page, Western Blot, Immunofluorescence, Staining, Fluorescence, Microscopy

Nav 1.5 is involved in BmK AGAP mediated down-regulation of PTX3 via NF-κB and Wnt/β-catenin signaling pathway. (A) rBmK AGAP or IKK-16 impairs NF-κB pathway, TNF-α, and PTX3. MCF-7 and MDA-MB-231 cells were treated with either rBmK AGAP (30 μM) or IKK-16 (5 μM) for 48 h. The cells were lysed and subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against IKKα, p-p65/NF-κB, TNF-α, and PTX3. The data indicated decreased expression of IKKα, p-p65/NF-κB, TNF-α, and PTX3. (B) Inhibition of Nav 1.5 or IKKα suppresses PTX3, NF-κB activation, and TNF-α. Jingzhaotoxin-III or IKK-16 was used to treat MCF-7 and MDA-MB-231 cells for 48 h. The cells were then lysed and subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against Nav 1.5, IKKα, TNF-α, PTX3, and p-p65/NF-κB. The data showed decreased expression of Nav 1.5, IKKα, TNF-α, PTX3, and p-p65/NF-κB following the inhibition of Nav 1.5 or NF-κB. (C) rBmK AGAP suppresses NF-κB activation, PTX3, and TNF-α in breast cancer. MCF-7 and MDA-MB-231 cells were treated with different concentrations of rBmK AGAP for 48 h. Cells were lysed and subjected to SDS-PAGE and analyzed by western blotting with antibodies against p65/NF-κB, TNF-α, IKKα, IκBα, p-p65/NF-κB, and PTX3. (D) Impaired β-catenin pathway suppresses NF-κB and PTX3 expression. MCF-7 and MDA-MB-231 cells treated with siβ-catenin were lysed and subjected to SDS-PAGE and analyzed by western blotting with antibodies against β-catenin, PTX3, and p65/NF-κB. (E) rBmK AGAP suppresses β-catenin pathway. MCF-7 and MDA-MB-231 cells were treated with different concentrations of rBmK AGAP for 48 h. Cells were then lysed and subjected to SDS-PAGE and analyzed by western blotting with antibodies against β-catenin, GSK3-β, Snail 1, and pGSK3-β. GAPDH and PARP were used as internal controls. The data was statistically significant at P < 0.05 compared to untreated cells. The data correspond to the mean ± SEM of three independent experiments.

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: Nav 1.5 is involved in BmK AGAP mediated down-regulation of PTX3 via NF-κB and Wnt/β-catenin signaling pathway. (A) rBmK AGAP or IKK-16 impairs NF-κB pathway, TNF-α, and PTX3. MCF-7 and MDA-MB-231 cells were treated with either rBmK AGAP (30 μM) or IKK-16 (5 μM) for 48 h. The cells were lysed and subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against IKKα, p-p65/NF-κB, TNF-α, and PTX3. The data indicated decreased expression of IKKα, p-p65/NF-κB, TNF-α, and PTX3. (B) Inhibition of Nav 1.5 or IKKα suppresses PTX3, NF-κB activation, and TNF-α. Jingzhaotoxin-III or IKK-16 was used to treat MCF-7 and MDA-MB-231 cells for 48 h. The cells were then lysed and subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against Nav 1.5, IKKα, TNF-α, PTX3, and p-p65/NF-κB. The data showed decreased expression of Nav 1.5, IKKα, TNF-α, PTX3, and p-p65/NF-κB following the inhibition of Nav 1.5 or NF-κB. (C) rBmK AGAP suppresses NF-κB activation, PTX3, and TNF-α in breast cancer. MCF-7 and MDA-MB-231 cells were treated with different concentrations of rBmK AGAP for 48 h. Cells were lysed and subjected to SDS-PAGE and analyzed by western blotting with antibodies against p65/NF-κB, TNF-α, IKKα, IκBα, p-p65/NF-κB, and PTX3. (D) Impaired β-catenin pathway suppresses NF-κB and PTX3 expression. MCF-7 and MDA-MB-231 cells treated with siβ-catenin were lysed and subjected to SDS-PAGE and analyzed by western blotting with antibodies against β-catenin, PTX3, and p65/NF-κB. (E) rBmK AGAP suppresses β-catenin pathway. MCF-7 and MDA-MB-231 cells were treated with different concentrations of rBmK AGAP for 48 h. Cells were then lysed and subjected to SDS-PAGE and analyzed by western blotting with antibodies against β-catenin, GSK3-β, Snail 1, and pGSK3-β. GAPDH and PARP were used as internal controls. The data was statistically significant at P < 0.05 compared to untreated cells. The data correspond to the mean ± SEM of three independent experiments.

Article Snippet: Human PTX3 ELISA Kit (Boster Biological Technology, China) was used to measure PTX3 secretion in supernatant samples from MCF-7 and MDA-MB-231 cells as described elsewhere ( ).

Techniques: SDS Page, Western Blot, Expressing, Inhibition, Activation Assay

BmK AGAP inhibits the growth of breast xenograft tumors, stem-like features and epithelial-mesenchymal transition in a mouse model. (A) Weight changes in rBmK AGAP-treated and untreated tumor model mice. BALB/c nude mice were treated with rBmK AGAP or saline and the changes in body weight of mice bearing xenograft tumors were examined for 20 days. (B) Tumor volume of tumors from rBmK AGAP-treated and untreated tumor model mice. Xenograft tumor volume were calculated from measuring the length, height and width of tumors using digital caliper following rBmK AGAP treatment. (C) Image of excised xenograft tumors from the different treatment groups after 20 days of tumor implantation. (D) Quantitative analysis of excised tumor weight. Tumors excised from tumor-bearing mice sacrificed after day 20 were weighed on a digital weighting apparatus. (E) Immunohistochemical assessment of stemness, EMT, and inflammation markers in excised tumor tissues. Xenograft tumor tissues were stained with antibodies against Nav 1.5, PTX3, Oct4, Sox2, E-cadherin, N-cadherin, and p65/NF-κB and examined by immunohistochemical staining (Scale bars = 100 μm; magnification, 200x). (F) Protein expression assessment of PTX3, stemness, EMT, Wnt/β-catenin pathway and NF-κB, in excised tumors. Xenograft tumor tissues from rBmK AGAP-treated and untreated mice were lyse. Equal amount of protein samples were subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against Nav 1.5, PTX3, Oct4, Sox2, E-cadherin, N-cadherin, pGSK3-β, GSK3-β, p65/NF-κB, and β-catenin. GAPDH was used as an internal control. The data was statistically significant at * P < 0.05; ** P < 0.01; and *** P < 0.001 as compared to untreated group. The data represent mean ± SD of three independent experiments.

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 inhibits the growth of breast xenograft tumors, stem-like features and epithelial-mesenchymal transition in a mouse model. (A) Weight changes in rBmK AGAP-treated and untreated tumor model mice. BALB/c nude mice were treated with rBmK AGAP or saline and the changes in body weight of mice bearing xenograft tumors were examined for 20 days. (B) Tumor volume of tumors from rBmK AGAP-treated and untreated tumor model mice. Xenograft tumor volume were calculated from measuring the length, height and width of tumors using digital caliper following rBmK AGAP treatment. (C) Image of excised xenograft tumors from the different treatment groups after 20 days of tumor implantation. (D) Quantitative analysis of excised tumor weight. Tumors excised from tumor-bearing mice sacrificed after day 20 were weighed on a digital weighting apparatus. (E) Immunohistochemical assessment of stemness, EMT, and inflammation markers in excised tumor tissues. Xenograft tumor tissues were stained with antibodies against Nav 1.5, PTX3, Oct4, Sox2, E-cadherin, N-cadherin, and p65/NF-κB and examined by immunohistochemical staining (Scale bars = 100 μm; magnification, 200x). (F) Protein expression assessment of PTX3, stemness, EMT, Wnt/β-catenin pathway and NF-κB, in excised tumors. Xenograft tumor tissues from rBmK AGAP-treated and untreated mice were lyse. Equal amount of protein samples were subjected to 12% SDS-PAGE and analyzed by western blotting with antibodies against Nav 1.5, PTX3, Oct4, Sox2, E-cadherin, N-cadherin, pGSK3-β, GSK3-β, p65/NF-κB, and β-catenin. GAPDH was used as an internal control. The data was statistically significant at * P < 0.05; ** P < 0.01; and *** P < 0.001 as compared to untreated group. The data represent mean ± SD of three independent experiments.

Article Snippet: Human PTX3 ELISA Kit (Boster Biological Technology, China) was used to measure PTX3 secretion in supernatant samples from MCF-7 and MDA-MB-231 cells as described elsewhere ( ).

Techniques: Saline, Tumor Implantation, Immunohistochemical staining, Staining, Expressing, SDS Page, Western Blot, Control