Review

recombinant human ptx3 rhptx3 (Boster Bio)

Boster Bio is a verified supplier

Boster Bio manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Boster Bio recombinant human ptx3 rhptx3

dePTX3 suppresses the growth and migration of human lung cancer cells. (A) CCK-8 assay was used to analyze the viability of A549 and SPCA1 cells. Cells were treated with or without <t>rhPTX3</t> (100 ng/ml) or dePTX3 (rhPTX3; 100 ng/ml + PNGase F; 500 U/ml) for 0-72 h. Data were presented as a percentage of viable cells. (B) Lung cancer cells treated with TM (0.01, 0.05, 0.5 and 1 µ g/ml) for 48 h. (C) Immunofluorescent staining of <t>PTX3</t> (red color) and N-glycan levels (green color) in A549 and SPCA1 cells analyzed following treatment with TM (0.5 µ g/ml) for 48 h. (D) SDS-PAGE gel (12%) stained with CBB and lectinblot against PHA to analyze N-glycans in lung cancer cells following treatment with TM for 48 h and PNGase F (500 U/ml) for 2 h of incubation. (E) Western blot analysis of dePTX3 in A549 and SPCA1 cells following treatment with TM or rhPTX3 + PNGase F. The lanes are labeled as follows: lane 1, glycosylated PTX3; lane 2, deglycosylated PTX3 by TM; lane 3, deglycosylated PTX3 by PNGase F. (F) Representative images of wound healing of A549 and SPCA1 cells analyzed after treatment with rhPTX3, dePTX3 and TM (0.5 µ g/ml), followed by measurement of relative wound width (48 h average wound width divided by 0 h wound width). (G) Microscopic images and graphs of transwell migration assay of A549 and SPCA1 cells following treatment with rhPTX3, dePTX3 and TM. Bar graph values represent the means ± SEM of 3 independent experiments. * P<0.05 and ** P<0.01.

Recombinant Human Ptx3 Rhptx3, 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
https://www.bioz.com/result/recombinant human ptx3 rhptx3/product/Boster Bio
Average 90 stars, based on 1 article reviews

recombinant human ptx3 rhptx3 - by Bioz Stars, 2026-03

90/100 stars

Images

1) Product Images from "Tunicamycin enhances the suppressive effects of cisplatin on lung cancer growth through PTX3 glycosylation via AKT/NF-κB signaling pathway"

Article Title: Tunicamycin enhances the suppressive effects of cisplatin on lung cancer growth through PTX3 glycosylation via AKT/NF-κB signaling pathway

Journal: International Journal of Oncology

doi: 10.3892/ijo.2018.4650

Figure Legend Snippet: dePTX3 suppresses the growth and migration of human lung cancer cells. (A) CCK-8 assay was used to analyze the viability of A549 and SPCA1 cells. Cells were treated with or without rhPTX3 (100 ng/ml) or dePTX3 (rhPTX3; 100 ng/ml + PNGase F; 500 U/ml) for 0-72 h. Data were presented as a percentage of viable cells. (B) Lung cancer cells treated with TM (0.01, 0.05, 0.5 and 1 µ g/ml) for 48 h. (C) Immunofluorescent staining of PTX3 (red color) and N-glycan levels (green color) in A549 and SPCA1 cells analyzed following treatment with TM (0.5 µ g/ml) for 48 h. (D) SDS-PAGE gel (12%) stained with CBB and lectinblot against PHA to analyze N-glycans in lung cancer cells following treatment with TM for 48 h and PNGase F (500 U/ml) for 2 h of incubation. (E) Western blot analysis of dePTX3 in A549 and SPCA1 cells following treatment with TM or rhPTX3 + PNGase F. The lanes are labeled as follows: lane 1, glycosylated PTX3; lane 2, deglycosylated PTX3 by TM; lane 3, deglycosylated PTX3 by PNGase F. (F) Representative images of wound healing of A549 and SPCA1 cells analyzed after treatment with rhPTX3, dePTX3 and TM (0.5 µ g/ml), followed by measurement of relative wound width (48 h average wound width divided by 0 h wound width). (G) Microscopic images and graphs of transwell migration assay of A549 and SPCA1 cells following treatment with rhPTX3, dePTX3 and TM. Bar graph values represent the means ± SEM of 3 independent experiments. * P<0.05 and ** P<0.01.

Techniques Used: Migration, CCK-8 Assay, Staining, Glycoproteomics, SDS Page, Incubation, Western Blot, Labeling, Transwell Migration Assay

PTX3 expression in human lung cancer samples and cell lines. (A) Immunohistochemical staining of PTX3 in paired human lung cancer tissue (P1, P2, P3) and normal lung tissue (N1, N2, N3) of the same patient (magnification, ×10). (B) PTX3 level in serum from lung cancer patients and normal healthy individuals by ELISA; * P<0.05. (C) PTX3 level in the supernatant collected from A549, SPCA1 and H1299 cells was examined by ELISA. (D) Immunofluorescent staining of PTX3 protein (red color) in A549, SPCA1 and H1299 lung cancer cells. DAPI (blue color) was used to stain the nuclei. (E) mRNA expression level of PTX3 detected by qPCR in A549, SPCA1 and H1299 cells. (F) PTX3 expression level in A549, SPCA1 and H1299 cells detected by western blot analysis. GAPDH was used as an internal control.

Figure Legend Snippet: PTX3 expression in human lung cancer samples and cell lines. (A) Immunohistochemical staining of PTX3 in paired human lung cancer tissue (P1, P2, P3) and normal lung tissue (N1, N2, N3) of the same patient (magnification, ×10). (B) PTX3 level in serum from lung cancer patients and normal healthy individuals by ELISA; * P<0.05. (C) PTX3 level in the supernatant collected from A549, SPCA1 and H1299 cells was examined by ELISA. (D) Immunofluorescent staining of PTX3 protein (red color) in A549, SPCA1 and H1299 lung cancer cells. DAPI (blue color) was used to stain the nuclei. (E) mRNA expression level of PTX3 detected by qPCR in A549, SPCA1 and H1299 cells. (F) PTX3 expression level in A549, SPCA1 and H1299 cells detected by western blot analysis. GAPDH was used as an internal control.

Techniques Used: Expressing, Immunohistochemical staining, Staining, Enzyme-linked Immunosorbent Assay, Western Blot, Control

PTX3 deglycosylation enhances the sensitivity of lung cancer cells to Cisplatin treatment. (A) suPTX3 level was detected by ELISA in the supernatant of A549 and SPCA1 cells following treatment with Cis (20 µ M) for 48 h. (B) Immunofluorescent staining of PTX3 (red color) in A549 and SPCA1 cells following treatment with Cis for 48 h. DAPI (blue color) was used to stain the nuclei. (C) Bar graph of A549 and SPCA1 cell viability analyzed following treatment with Cis and deglycosylated PTX3 (dePTX3). Each bar represents the average of 3 independent experiments. Data are expressed as a percentage of viable cells. (D) Western blot analysis of PCNA and AKT phosphorylation following treatment with Cis or dePTX3, and combined treatment for 48 h. (E) Western blot analysis for PTX3 expression in the cell lysate from control, mock and mutated PTX3 (mPTX3) in A549 and SPCA1 cells. (F) Western blot analysis of Cis, mPTX3 or Cis combined with mPTX3 and combined treatment for 48 h. The level of PCNA expression and AKT phosphorylation were examined by western blot analysis. GAPDH was used as an internal control. * P<0.05 and ** P<0.01.

Figure Legend Snippet: PTX3 deglycosylation enhances the sensitivity of lung cancer cells to Cisplatin treatment. (A) suPTX3 level was detected by ELISA in the supernatant of A549 and SPCA1 cells following treatment with Cis (20 µ M) for 48 h. (B) Immunofluorescent staining of PTX3 (red color) in A549 and SPCA1 cells following treatment with Cis for 48 h. DAPI (blue color) was used to stain the nuclei. (C) Bar graph of A549 and SPCA1 cell viability analyzed following treatment with Cis and deglycosylated PTX3 (dePTX3). Each bar represents the average of 3 independent experiments. Data are expressed as a percentage of viable cells. (D) Western blot analysis of PCNA and AKT phosphorylation following treatment with Cis or dePTX3, and combined treatment for 48 h. (E) Western blot analysis for PTX3 expression in the cell lysate from control, mock and mutated PTX3 (mPTX3) in A549 and SPCA1 cells. (F) Western blot analysis of Cis, mPTX3 or Cis combined with mPTX3 and combined treatment for 48 h. The level of PCNA expression and AKT phosphorylation were examined by western blot analysis. GAPDH was used as an internal control. * P<0.05 and ** P<0.01.

Techniques Used: Enzyme-linked Immunosorbent Assay, Staining, Western Blot, Phospho-proteomics, Expressing, Control

TM increases the sensitivity of lung cancer cells to cisplatin-induced apoptosis through deactivating AKT/NF-κB signaling pathway. (A) CCK-8 assay used to analyze the viability of A549 and SPCA1 cells treated with GDC0941 (4 µ M), IKK-16 (10 µ M), MEK162 (20 µ M) or rhPTX3 (100 ng/ml) for 48 h. (B) Western blot analysis of Bcl2 expression in A549 and SPCA1 cells, incubated with rhPTX3 (100 ng/ml) with or without NF-κB inhibitor IKK-16 (10 µ M). (C) A549 and SPCA1 cells were treated with TM (0.5 µ g/ml) + Cis (20 µ M) together or in combination. Western blot analysis of AKT, IKK, p65 phosphorylation in cytoplasmic and nuclear extracts of A549 and SPCA1 cells treated with TM, Cis or in combination. PARP was used as an internal control. (D) A549 and SPCA1 cells were double-stained with Annexin V-FITC/PI and analyzed by flow cytometry after 24 h of treatment with TM (0.5 µ g/ml), Cis (20 µ M) or combined treatment. The histogram showed the average percentage of total apoptotic cells in both A549 and SPCA1 cells. (E) Bcl2, Bax and cleaved PARP expression detected by western blot analysis following treatment with TM, Cis or in combination for 48 h. GAPDH was used as an internal control. Data represented the mean values ± SEM. * P<0.05 and ** P<0.01.

Figure Legend Snippet: TM increases the sensitivity of lung cancer cells to cisplatin-induced apoptosis through deactivating AKT/NF-κB signaling pathway. (A) CCK-8 assay used to analyze the viability of A549 and SPCA1 cells treated with GDC0941 (4 µ M), IKK-16 (10 µ M), MEK162 (20 µ M) or rhPTX3 (100 ng/ml) for 48 h. (B) Western blot analysis of Bcl2 expression in A549 and SPCA1 cells, incubated with rhPTX3 (100 ng/ml) with or without NF-κB inhibitor IKK-16 (10 µ M). (C) A549 and SPCA1 cells were treated with TM (0.5 µ g/ml) + Cis (20 µ M) together or in combination. Western blot analysis of AKT, IKK, p65 phosphorylation in cytoplasmic and nuclear extracts of A549 and SPCA1 cells treated with TM, Cis or in combination. PARP was used as an internal control. (D) A549 and SPCA1 cells were double-stained with Annexin V-FITC/PI and analyzed by flow cytometry after 24 h of treatment with TM (0.5 µ g/ml), Cis (20 µ M) or combined treatment. The histogram showed the average percentage of total apoptotic cells in both A549 and SPCA1 cells. (E) Bcl2, Bax and cleaved PARP expression detected by western blot analysis following treatment with TM, Cis or in combination for 48 h. GAPDH was used as an internal control. Data represented the mean values ± SEM. * P<0.05 and ** P<0.01.

Techniques Used: CCK-8 Assay, Western Blot, Expressing, Incubation, Phospho-proteomics, Control, Staining, Flow Cytometry

Image Search Results

Journal: International Journal of Oncology

Article Title: Tunicamycin enhances the suppressive effects of cisplatin on lung cancer growth through PTX3 glycosylation via AKT/NF-κB signaling pathway

doi: 10.3892/ijo.2018.4650

Figure Lengend Snippet: dePTX3 suppresses the growth and migration of human lung cancer cells. (A) CCK-8 assay was used to analyze the viability of A549 and SPCA1 cells. Cells were treated with or without rhPTX3 (100 ng/ml) or dePTX3 (rhPTX3; 100 ng/ml + PNGase F; 500 U/ml) for 0-72 h. Data were presented as a percentage of viable cells. (B) Lung cancer cells treated with TM (0.01, 0.05, 0.5 and 1 µ g/ml) for 48 h. (C) Immunofluorescent staining of PTX3 (red color) and N-glycan levels (green color) in A549 and SPCA1 cells analyzed following treatment with TM (0.5 µ g/ml) for 48 h. (D) SDS-PAGE gel (12%) stained with CBB and lectinblot against PHA to analyze N-glycans in lung cancer cells following treatment with TM for 48 h and PNGase F (500 U/ml) for 2 h of incubation. (E) Western blot analysis of dePTX3 in A549 and SPCA1 cells following treatment with TM or rhPTX3 + PNGase F. The lanes are labeled as follows: lane 1, glycosylated PTX3; lane 2, deglycosylated PTX3 by TM; lane 3, deglycosylated PTX3 by PNGase F. (F) Representative images of wound healing of A549 and SPCA1 cells analyzed after treatment with rhPTX3, dePTX3 and TM (0.5 µ g/ml), followed by measurement of relative wound width (48 h average wound width divided by 0 h wound width). (G) Microscopic images and graphs of transwell migration assay of A549 and SPCA1 cells following treatment with rhPTX3, dePTX3 and TM. Bar graph values represent the means ± SEM of 3 independent experiments. * P<0.05 and ** P<0.01.

Article Snippet: Cell Counting kit-8 (CCK-8) was obtained from Beyotime Biotechnology (Shanghai, China); recombinant human PTX3 (rhPTX3) (#PROTP26022; Boster Biological Technology Co., Ltd., Fremont, CA); NF-κB inhibitor (IKK-16), PI3K inhibitor (GDC0941), MEK1/2 inhibitor, (MEK162) were purchased from Selleck Chemicals (Shanghai, China).

Techniques: Migration, CCK-8 Assay, Staining, Glycoproteomics, SDS Page, Incubation, Western Blot, Labeling, Transwell Migration Assay

Journal: International Journal of Oncology

Article Title: Tunicamycin enhances the suppressive effects of cisplatin on lung cancer growth through PTX3 glycosylation via AKT/NF-κB signaling pathway

doi: 10.3892/ijo.2018.4650

Figure Lengend Snippet: PTX3 expression in human lung cancer samples and cell lines. (A) Immunohistochemical staining of PTX3 in paired human lung cancer tissue (P1, P2, P3) and normal lung tissue (N1, N2, N3) of the same patient (magnification, ×10). (B) PTX3 level in serum from lung cancer patients and normal healthy individuals by ELISA; * P<0.05. (C) PTX3 level in the supernatant collected from A549, SPCA1 and H1299 cells was examined by ELISA. (D) Immunofluorescent staining of PTX3 protein (red color) in A549, SPCA1 and H1299 lung cancer cells. DAPI (blue color) was used to stain the nuclei. (E) mRNA expression level of PTX3 detected by qPCR in A549, SPCA1 and H1299 cells. (F) PTX3 expression level in A549, SPCA1 and H1299 cells detected by western blot analysis. GAPDH was used as an internal control.

Techniques: Expressing, Immunohistochemical staining, Staining, Enzyme-linked Immunosorbent Assay, Western Blot, Control

Journal: International Journal of Oncology

Article Title: Tunicamycin enhances the suppressive effects of cisplatin on lung cancer growth through PTX3 glycosylation via AKT/NF-κB signaling pathway

doi: 10.3892/ijo.2018.4650

Figure Lengend Snippet: PTX3 deglycosylation enhances the sensitivity of lung cancer cells to Cisplatin treatment. (A) suPTX3 level was detected by ELISA in the supernatant of A549 and SPCA1 cells following treatment with Cis (20 µ M) for 48 h. (B) Immunofluorescent staining of PTX3 (red color) in A549 and SPCA1 cells following treatment with Cis for 48 h. DAPI (blue color) was used to stain the nuclei. (C) Bar graph of A549 and SPCA1 cell viability analyzed following treatment with Cis and deglycosylated PTX3 (dePTX3). Each bar represents the average of 3 independent experiments. Data are expressed as a percentage of viable cells. (D) Western blot analysis of PCNA and AKT phosphorylation following treatment with Cis or dePTX3, and combined treatment for 48 h. (E) Western blot analysis for PTX3 expression in the cell lysate from control, mock and mutated PTX3 (mPTX3) in A549 and SPCA1 cells. (F) Western blot analysis of Cis, mPTX3 or Cis combined with mPTX3 and combined treatment for 48 h. The level of PCNA expression and AKT phosphorylation were examined by western blot analysis. GAPDH was used as an internal control. * P<0.05 and ** P<0.01.

Techniques: Enzyme-linked Immunosorbent Assay, Staining, Western Blot, Phospho-proteomics, Expressing, Control

Journal: International Journal of Oncology

Article Title: Tunicamycin enhances the suppressive effects of cisplatin on lung cancer growth through PTX3 glycosylation via AKT/NF-κB signaling pathway

doi: 10.3892/ijo.2018.4650

Figure Lengend Snippet: TM increases the sensitivity of lung cancer cells to cisplatin-induced apoptosis through deactivating AKT/NF-κB signaling pathway. (A) CCK-8 assay used to analyze the viability of A549 and SPCA1 cells treated with GDC0941 (4 µ M), IKK-16 (10 µ M), MEK162 (20 µ M) or rhPTX3 (100 ng/ml) for 48 h. (B) Western blot analysis of Bcl2 expression in A549 and SPCA1 cells, incubated with rhPTX3 (100 ng/ml) with or without NF-κB inhibitor IKK-16 (10 µ M). (C) A549 and SPCA1 cells were treated with TM (0.5 µ g/ml) + Cis (20 µ M) together or in combination. Western blot analysis of AKT, IKK, p65 phosphorylation in cytoplasmic and nuclear extracts of A549 and SPCA1 cells treated with TM, Cis or in combination. PARP was used as an internal control. (D) A549 and SPCA1 cells were double-stained with Annexin V-FITC/PI and analyzed by flow cytometry after 24 h of treatment with TM (0.5 µ g/ml), Cis (20 µ M) or combined treatment. The histogram showed the average percentage of total apoptotic cells in both A549 and SPCA1 cells. (E) Bcl2, Bax and cleaved PARP expression detected by western blot analysis following treatment with TM, Cis or in combination for 48 h. GAPDH was used as an internal control. Data represented the mean values ± SEM. * P<0.05 and ** P<0.01.

Techniques: CCK-8 Assay, Western Blot, Expressing, Incubation, Phospho-proteomics, Control, Staining, Flow Cytometry

Review

Structured Review

Images

1) Product Images from "Tunicamycin enhances the suppressive effects of cisplatin on lung cancer growth through PTX3 glycosylation via AKT/NF-κB signaling pathway"

Similar Products

Image Search Results