egcg  (MedChemExpress)


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    Structured Review

    MedChemExpress egcg
    Cotreatment with <t>EGCG</t> and <t>BAY11-7082</t> significantly inhibits NF-κB signaling. (A-D) Western blot analysis of total NF-κB and phosphorylated NF-κB p65 in A549 and H1299 whole cell lysates after treatment with 20 µM EGCG; 0.625, 1.25, or 2.5 μM BAY 11-7082; or the combination thereof for 48 h. (E) A549 and H1299 cells were cotransfected with SV40 and SV40 for dual luciferase reporter assays. (F) qRT-PCR analysis of NF-κB expression levels. (G-H) qRT-PCR analysis of C-MYC, Cyclin D1, Bcl-2, Bcl-xL, COX-2, TNF-α, TWIST1, and MMP2 mRNA expression in A549 and H1299 cells after treatment with 20 µM EGCG; 0.625, 1.25, or 2.5 μM BAY11-7082; or the combination thereof for 48 h. Data are shown as the mean ± S.D. (n=3). * P
    Egcg, supplied by MedChemExpress, 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/egcg/product/MedChemExpress
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    egcg - by Bioz Stars, 2022-05
    94/100 stars

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    1) Product Images from "Synergistic inhibition of lung cancer cells by EGCG and NF-κB inhibitor BAY11-7082"

    Article Title: Synergistic inhibition of lung cancer cells by EGCG and NF-κB inhibitor BAY11-7082

    Journal: Journal of Cancer

    doi: 10.7150/jca.34285

    Cotreatment with EGCG and BAY11-7082 significantly inhibits NF-κB signaling. (A-D) Western blot analysis of total NF-κB and phosphorylated NF-κB p65 in A549 and H1299 whole cell lysates after treatment with 20 µM EGCG; 0.625, 1.25, or 2.5 μM BAY 11-7082; or the combination thereof for 48 h. (E) A549 and H1299 cells were cotransfected with SV40 and SV40 for dual luciferase reporter assays. (F) qRT-PCR analysis of NF-κB expression levels. (G-H) qRT-PCR analysis of C-MYC, Cyclin D1, Bcl-2, Bcl-xL, COX-2, TNF-α, TWIST1, and MMP2 mRNA expression in A549 and H1299 cells after treatment with 20 µM EGCG; 0.625, 1.25, or 2.5 μM BAY11-7082; or the combination thereof for 48 h. Data are shown as the mean ± S.D. (n=3). * P
    Figure Legend Snippet: Cotreatment with EGCG and BAY11-7082 significantly inhibits NF-κB signaling. (A-D) Western blot analysis of total NF-κB and phosphorylated NF-κB p65 in A549 and H1299 whole cell lysates after treatment with 20 µM EGCG; 0.625, 1.25, or 2.5 μM BAY 11-7082; or the combination thereof for 48 h. (E) A549 and H1299 cells were cotransfected with SV40 and SV40 for dual luciferase reporter assays. (F) qRT-PCR analysis of NF-κB expression levels. (G-H) qRT-PCR analysis of C-MYC, Cyclin D1, Bcl-2, Bcl-xL, COX-2, TNF-α, TWIST1, and MMP2 mRNA expression in A549 and H1299 cells after treatment with 20 µM EGCG; 0.625, 1.25, or 2.5 μM BAY11-7082; or the combination thereof for 48 h. Data are shown as the mean ± S.D. (n=3). * P

    Techniques Used: Western Blot, Luciferase, Quantitative RT-PCR, Expressing

    Cotreatment with BAY11-7082 (10mg/kg) enhances the antitumor effects of EGCG (20mg/kg) in an A549 xenograft model. (A) No significant body weight loss was observed during the treatment period in mice. (B) Representative images of tumors from each group at the termination of the experiment. (C-D) Graph showing the tumor weights from the different groups. Cotreatment with EGCG and BAY11-7082 resulted in a significant decrease in tumor weight. (E-F) Graph showing the tumor volumes in each group, which was assessed by caliper measurements and calculated according to the formula length*width*width*0.5. Data are expressed as the mean ± S.E.M., n=6. (G-J) Immunohistochemistry staining (Ki67 and P-NF-kB) of tumor tissues. (G-H) Representative images of IHC staining for Ki67 (G) and P-NF-κB (H) of tumor tissues, ×40 for (G-H). (I-J) Quantitative analysis of the Ki67 (I) and P-NF-κB (J). * P
    Figure Legend Snippet: Cotreatment with BAY11-7082 (10mg/kg) enhances the antitumor effects of EGCG (20mg/kg) in an A549 xenograft model. (A) No significant body weight loss was observed during the treatment period in mice. (B) Representative images of tumors from each group at the termination of the experiment. (C-D) Graph showing the tumor weights from the different groups. Cotreatment with EGCG and BAY11-7082 resulted in a significant decrease in tumor weight. (E-F) Graph showing the tumor volumes in each group, which was assessed by caliper measurements and calculated according to the formula length*width*width*0.5. Data are expressed as the mean ± S.E.M., n=6. (G-J) Immunohistochemistry staining (Ki67 and P-NF-kB) of tumor tissues. (G-H) Representative images of IHC staining for Ki67 (G) and P-NF-κB (H) of tumor tissues, ×40 for (G-H). (I-J) Quantitative analysis of the Ki67 (I) and P-NF-κB (J). * P

    Techniques Used: Mouse Assay, Immunohistochemistry, Staining

    Cell growth is more effectively inhibited by cotreatment with EGCG and BAY11-7082 than by either agent alone. Growth inhibition curves A549 (A) and H1299 (B) cells exposed to various concentrations of BAY11-7082 for 48 and 72 h, as determined using an MTT assay. Each value is expressed as the mean ± SD (n=3). (C-D) A549 cells were treated with 20 µM EGCG; 1.25, 2.5, 5 µM BAY 11-7082; or the combination thereof for 48 and 72 h. Growth inhibition was significantly potentiated upon cotreatment with EGCG and BAY11-7082. (E-F) H1299 cells were treated with 20 µM EGCG; 0.625, 1.25, 2.5 µM BAY 117082; or the combination thereof for 48 or 72 h. (G-H) CI versus affected cell-fraction (fa) curves for both 48 and 72 h cotreatment with BAY-117082 and EGCG in A549 and H1299 cells. (I-L) The combined effects of EGCG and BAY11-7082 on colony formation in A549 and H1299 cells. Representative photographs of the clonogenic assay are presented in panels I-J. * P
    Figure Legend Snippet: Cell growth is more effectively inhibited by cotreatment with EGCG and BAY11-7082 than by either agent alone. Growth inhibition curves A549 (A) and H1299 (B) cells exposed to various concentrations of BAY11-7082 for 48 and 72 h, as determined using an MTT assay. Each value is expressed as the mean ± SD (n=3). (C-D) A549 cells were treated with 20 µM EGCG; 1.25, 2.5, 5 µM BAY 11-7082; or the combination thereof for 48 and 72 h. Growth inhibition was significantly potentiated upon cotreatment with EGCG and BAY11-7082. (E-F) H1299 cells were treated with 20 µM EGCG; 0.625, 1.25, 2.5 µM BAY 117082; or the combination thereof for 48 or 72 h. (G-H) CI versus affected cell-fraction (fa) curves for both 48 and 72 h cotreatment with BAY-117082 and EGCG in A549 and H1299 cells. (I-L) The combined effects of EGCG and BAY11-7082 on colony formation in A549 and H1299 cells. Representative photographs of the clonogenic assay are presented in panels I-J. * P

    Techniques Used: Inhibition, MTT Assay, Clonogenic Assay

    Combined treatment with EGCG and BAY11-7082 induces apoptosis in A549 and H1299 cells. (A-B) Flow cytometry images. (C-D) Quantitative analysis of the percentage of apoptotic cells after EGCG and BAY11-7082 treatment for 48 h. The percentage of total apoptotic cells was defined as the sum of both early and late apoptotic cells. (E-F) Representative Western blotting images of proteins collected from treated A549 and H1299 cells. (G-H) Statistical analysis of C3, CC3, C9, CC9, Bcl-2 and β-actin protein expression in A549 and H1299 cells after treatment. * P
    Figure Legend Snippet: Combined treatment with EGCG and BAY11-7082 induces apoptosis in A549 and H1299 cells. (A-B) Flow cytometry images. (C-D) Quantitative analysis of the percentage of apoptotic cells after EGCG and BAY11-7082 treatment for 48 h. The percentage of total apoptotic cells was defined as the sum of both early and late apoptotic cells. (E-F) Representative Western blotting images of proteins collected from treated A549 and H1299 cells. (G-H) Statistical analysis of C3, CC3, C9, CC9, Bcl-2 and β-actin protein expression in A549 and H1299 cells after treatment. * P

    Techniques Used: Flow Cytometry, Western Blot, Expressing

    The combination treatment of EGCG and BAY11-7082 inhibits the migration and invasion of lung cancer cells. Representative images of the wounded cell monolayers of A549 (A) and H1299 (C) cells, ×10 for (A, C). (B, D) Quantitative analysis of migration inhibition induced by 24 h treatment with EGCG and BAY-117082. Data are expressed as the percent open wound area compared to untreated cultures. Representative images of the stained A549 (E) and H1299 (F) cells, ×20 for (E-F). (G-H) Quantitative analysis of the anti-invasion activity of EGCG and BAY11-7082. Data are presented as the mean ± S.D. (n=3). * P
    Figure Legend Snippet: The combination treatment of EGCG and BAY11-7082 inhibits the migration and invasion of lung cancer cells. Representative images of the wounded cell monolayers of A549 (A) and H1299 (C) cells, ×10 for (A, C). (B, D) Quantitative analysis of migration inhibition induced by 24 h treatment with EGCG and BAY-117082. Data are expressed as the percent open wound area compared to untreated cultures. Representative images of the stained A549 (E) and H1299 (F) cells, ×20 for (E-F). (G-H) Quantitative analysis of the anti-invasion activity of EGCG and BAY11-7082. Data are presented as the mean ± S.D. (n=3). * P

    Techniques Used: Migration, Inhibition, Staining, Activity Assay

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    MedChemExpress epigallocatechin gallate egcg
    E-GNPs exhibit selective and superior anticancer activity. 5 × 10 3 noncancerous cells (HaCaT, MCF-10A, HPNE, and RWPE1) and cancerous cells (A375SM, MDA-MB-231, MIA PaCa, and PC3) were seeded in 96-well plates and treated with different concentrations of E-GNPs, <t>epigallocatechin</t> gallate (EGCG), C-GNPs, or citrate for 96 h, and cell viability was determined by WST-1 assay. Data represent the mean of triplicates ± SD.
    Epigallocatechin Gallate Egcg, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 1 article reviews
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    E-GNPs exhibit selective and superior anticancer activity. 5 × 10 3 noncancerous cells (HaCaT, MCF-10A, HPNE, and RWPE1) and cancerous cells (A375SM, MDA-MB-231, MIA PaCa, and PC3) were seeded in 96-well plates and treated with different concentrations of E-GNPs, epigallocatechin gallate (EGCG), C-GNPs, or citrate for 96 h, and cell viability was determined by WST-1 assay. Data represent the mean of triplicates ± SD.

    Journal: Nanomaterials

    Article Title: Epigallocatechin Gallate-Gold Nanoparticles Exhibit Superior Antitumor Activity Compared to Conventional Gold Nanoparticles: Potential Synergistic Interactions

    doi: 10.3390/nano9030396

    Figure Lengend Snippet: E-GNPs exhibit selective and superior anticancer activity. 5 × 10 3 noncancerous cells (HaCaT, MCF-10A, HPNE, and RWPE1) and cancerous cells (A375SM, MDA-MB-231, MIA PaCa, and PC3) were seeded in 96-well plates and treated with different concentrations of E-GNPs, epigallocatechin gallate (EGCG), C-GNPs, or citrate for 96 h, and cell viability was determined by WST-1 assay. Data represent the mean of triplicates ± SD.

    Article Snippet: PE Annexin V apoptosis detection kit was from BD Bioscience (San Diego, CA, USA); gold (III) chloride trihydrate (HAuCl4 ·3H2 O), trisodium citrate (TSC), and citrate assay kit were from Sigma-Aldrich (St. Louis, MO, USA); nuclear extract kit was from Active Motif (Carlsbad, CA, USA); epigallocatechin gallate (EGCG) was from Medchemexpress LLC (Monmouth Junction, NJ, USA); anti-cleaved caspase 7, -cleaved caspase 3 (rabbit polyclonal), anti-BCL2, -BCL-xL, -Bax, -NF-κB/p65 (rabbit monoclonal) were from Cell Signaling Technology (Danvers, MA, USA); anti-laminin receptor antibody (MLuC5, mouse monoclonal) was from Invitrogen (Carlsbad, CA, USA); anti-rabbit and anti-mouse horseradish peroxidase (HRP)-conjugated secondary antibodies were from Santa Cruz Biotechnology (Santa Cruz, CA, USA); β-actin (mouse monoclonal) antibody was from Sigma–Aldrich; ECL plus detection kit was from Thermo Scientific (Logan, UT, USA); pGL4.32 [luc2P/NF-B-RE/Hygro] and pRL-TK plasmids were from Promega (Madison, WI, USA); TRIzol reagent and reverse-transcribed with high capacity cDNA reverse transcription kit were from Invitrogen and Applied Biosystems (Carlsbad, CA, USA); SYBR green master mix was from Applied Biosystems (Carlsbad, CA, USA); tris-buffered saline (TBS) and Tween 20 were from Boston Bioproducts (Ashland, MA, USA).

    Techniques: Activity Assay, Multiple Displacement Amplification, WST-1 Assay

    Cotreatment with EGCG and BAY11-7082 significantly inhibits NF-κB signaling. (A-D) Western blot analysis of total NF-κB and phosphorylated NF-κB p65 in A549 and H1299 whole cell lysates after treatment with 20 µM EGCG; 0.625, 1.25, or 2.5 μM BAY 11-7082; or the combination thereof for 48 h. (E) A549 and H1299 cells were cotransfected with SV40 and SV40 for dual luciferase reporter assays. (F) qRT-PCR analysis of NF-κB expression levels. (G-H) qRT-PCR analysis of C-MYC, Cyclin D1, Bcl-2, Bcl-xL, COX-2, TNF-α, TWIST1, and MMP2 mRNA expression in A549 and H1299 cells after treatment with 20 µM EGCG; 0.625, 1.25, or 2.5 μM BAY11-7082; or the combination thereof for 48 h. Data are shown as the mean ± S.D. (n=3). * P

    Journal: Journal of Cancer

    Article Title: Synergistic inhibition of lung cancer cells by EGCG and NF-κB inhibitor BAY11-7082

    doi: 10.7150/jca.34285

    Figure Lengend Snippet: Cotreatment with EGCG and BAY11-7082 significantly inhibits NF-κB signaling. (A-D) Western blot analysis of total NF-κB and phosphorylated NF-κB p65 in A549 and H1299 whole cell lysates after treatment with 20 µM EGCG; 0.625, 1.25, or 2.5 μM BAY 11-7082; or the combination thereof for 48 h. (E) A549 and H1299 cells were cotransfected with SV40 and SV40 for dual luciferase reporter assays. (F) qRT-PCR analysis of NF-κB expression levels. (G-H) qRT-PCR analysis of C-MYC, Cyclin D1, Bcl-2, Bcl-xL, COX-2, TNF-α, TWIST1, and MMP2 mRNA expression in A549 and H1299 cells after treatment with 20 µM EGCG; 0.625, 1.25, or 2.5 μM BAY11-7082; or the combination thereof for 48 h. Data are shown as the mean ± S.D. (n=3). * P

    Article Snippet: NF-κB inhibitor (BAY11-7082) and EGCG were provided by MCE, USA.

    Techniques: Western Blot, Luciferase, Quantitative RT-PCR, Expressing

    Cotreatment with BAY11-7082 (10mg/kg) enhances the antitumor effects of EGCG (20mg/kg) in an A549 xenograft model. (A) No significant body weight loss was observed during the treatment period in mice. (B) Representative images of tumors from each group at the termination of the experiment. (C-D) Graph showing the tumor weights from the different groups. Cotreatment with EGCG and BAY11-7082 resulted in a significant decrease in tumor weight. (E-F) Graph showing the tumor volumes in each group, which was assessed by caliper measurements and calculated according to the formula length*width*width*0.5. Data are expressed as the mean ± S.E.M., n=6. (G-J) Immunohistochemistry staining (Ki67 and P-NF-kB) of tumor tissues. (G-H) Representative images of IHC staining for Ki67 (G) and P-NF-κB (H) of tumor tissues, ×40 for (G-H). (I-J) Quantitative analysis of the Ki67 (I) and P-NF-κB (J). * P

    Journal: Journal of Cancer

    Article Title: Synergistic inhibition of lung cancer cells by EGCG and NF-κB inhibitor BAY11-7082

    doi: 10.7150/jca.34285

    Figure Lengend Snippet: Cotreatment with BAY11-7082 (10mg/kg) enhances the antitumor effects of EGCG (20mg/kg) in an A549 xenograft model. (A) No significant body weight loss was observed during the treatment period in mice. (B) Representative images of tumors from each group at the termination of the experiment. (C-D) Graph showing the tumor weights from the different groups. Cotreatment with EGCG and BAY11-7082 resulted in a significant decrease in tumor weight. (E-F) Graph showing the tumor volumes in each group, which was assessed by caliper measurements and calculated according to the formula length*width*width*0.5. Data are expressed as the mean ± S.E.M., n=6. (G-J) Immunohistochemistry staining (Ki67 and P-NF-kB) of tumor tissues. (G-H) Representative images of IHC staining for Ki67 (G) and P-NF-κB (H) of tumor tissues, ×40 for (G-H). (I-J) Quantitative analysis of the Ki67 (I) and P-NF-κB (J). * P

    Article Snippet: NF-κB inhibitor (BAY11-7082) and EGCG were provided by MCE, USA.

    Techniques: Mouse Assay, Immunohistochemistry, Staining

    Cell growth is more effectively inhibited by cotreatment with EGCG and BAY11-7082 than by either agent alone. Growth inhibition curves A549 (A) and H1299 (B) cells exposed to various concentrations of BAY11-7082 for 48 and 72 h, as determined using an MTT assay. Each value is expressed as the mean ± SD (n=3). (C-D) A549 cells were treated with 20 µM EGCG; 1.25, 2.5, 5 µM BAY 11-7082; or the combination thereof for 48 and 72 h. Growth inhibition was significantly potentiated upon cotreatment with EGCG and BAY11-7082. (E-F) H1299 cells were treated with 20 µM EGCG; 0.625, 1.25, 2.5 µM BAY 117082; or the combination thereof for 48 or 72 h. (G-H) CI versus affected cell-fraction (fa) curves for both 48 and 72 h cotreatment with BAY-117082 and EGCG in A549 and H1299 cells. (I-L) The combined effects of EGCG and BAY11-7082 on colony formation in A549 and H1299 cells. Representative photographs of the clonogenic assay are presented in panels I-J. * P

    Journal: Journal of Cancer

    Article Title: Synergistic inhibition of lung cancer cells by EGCG and NF-κB inhibitor BAY11-7082

    doi: 10.7150/jca.34285

    Figure Lengend Snippet: Cell growth is more effectively inhibited by cotreatment with EGCG and BAY11-7082 than by either agent alone. Growth inhibition curves A549 (A) and H1299 (B) cells exposed to various concentrations of BAY11-7082 for 48 and 72 h, as determined using an MTT assay. Each value is expressed as the mean ± SD (n=3). (C-D) A549 cells were treated with 20 µM EGCG; 1.25, 2.5, 5 µM BAY 11-7082; or the combination thereof for 48 and 72 h. Growth inhibition was significantly potentiated upon cotreatment with EGCG and BAY11-7082. (E-F) H1299 cells were treated with 20 µM EGCG; 0.625, 1.25, 2.5 µM BAY 117082; or the combination thereof for 48 or 72 h. (G-H) CI versus affected cell-fraction (fa) curves for both 48 and 72 h cotreatment with BAY-117082 and EGCG in A549 and H1299 cells. (I-L) The combined effects of EGCG and BAY11-7082 on colony formation in A549 and H1299 cells. Representative photographs of the clonogenic assay are presented in panels I-J. * P

    Article Snippet: NF-κB inhibitor (BAY11-7082) and EGCG were provided by MCE, USA.

    Techniques: Inhibition, MTT Assay, Clonogenic Assay

    Combined treatment with EGCG and BAY11-7082 induces apoptosis in A549 and H1299 cells. (A-B) Flow cytometry images. (C-D) Quantitative analysis of the percentage of apoptotic cells after EGCG and BAY11-7082 treatment for 48 h. The percentage of total apoptotic cells was defined as the sum of both early and late apoptotic cells. (E-F) Representative Western blotting images of proteins collected from treated A549 and H1299 cells. (G-H) Statistical analysis of C3, CC3, C9, CC9, Bcl-2 and β-actin protein expression in A549 and H1299 cells after treatment. * P

    Journal: Journal of Cancer

    Article Title: Synergistic inhibition of lung cancer cells by EGCG and NF-κB inhibitor BAY11-7082

    doi: 10.7150/jca.34285

    Figure Lengend Snippet: Combined treatment with EGCG and BAY11-7082 induces apoptosis in A549 and H1299 cells. (A-B) Flow cytometry images. (C-D) Quantitative analysis of the percentage of apoptotic cells after EGCG and BAY11-7082 treatment for 48 h. The percentage of total apoptotic cells was defined as the sum of both early and late apoptotic cells. (E-F) Representative Western blotting images of proteins collected from treated A549 and H1299 cells. (G-H) Statistical analysis of C3, CC3, C9, CC9, Bcl-2 and β-actin protein expression in A549 and H1299 cells after treatment. * P

    Article Snippet: NF-κB inhibitor (BAY11-7082) and EGCG were provided by MCE, USA.

    Techniques: Flow Cytometry, Western Blot, Expressing

    The combination treatment of EGCG and BAY11-7082 inhibits the migration and invasion of lung cancer cells. Representative images of the wounded cell monolayers of A549 (A) and H1299 (C) cells, ×10 for (A, C). (B, D) Quantitative analysis of migration inhibition induced by 24 h treatment with EGCG and BAY-117082. Data are expressed as the percent open wound area compared to untreated cultures. Representative images of the stained A549 (E) and H1299 (F) cells, ×20 for (E-F). (G-H) Quantitative analysis of the anti-invasion activity of EGCG and BAY11-7082. Data are presented as the mean ± S.D. (n=3). * P

    Journal: Journal of Cancer

    Article Title: Synergistic inhibition of lung cancer cells by EGCG and NF-κB inhibitor BAY11-7082

    doi: 10.7150/jca.34285

    Figure Lengend Snippet: The combination treatment of EGCG and BAY11-7082 inhibits the migration and invasion of lung cancer cells. Representative images of the wounded cell monolayers of A549 (A) and H1299 (C) cells, ×10 for (A, C). (B, D) Quantitative analysis of migration inhibition induced by 24 h treatment with EGCG and BAY-117082. Data are expressed as the percent open wound area compared to untreated cultures. Representative images of the stained A549 (E) and H1299 (F) cells, ×20 for (E-F). (G-H) Quantitative analysis of the anti-invasion activity of EGCG and BAY11-7082. Data are presented as the mean ± S.D. (n=3). * P

    Article Snippet: NF-κB inhibitor (BAY11-7082) and EGCG were provided by MCE, USA.

    Techniques: Migration, Inhibition, Staining, Activity Assay