mouse ptx3 elisa kits  (Boster Bio)

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

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