Structured Review

Supelco β elemene
<t>β-elemene</t> reverse the resistance of HCT116p53 –/– cells to 5-Fu by inducing pro-death autophagy. (A) HCT116p53 +/+ and HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the protein expression of LC3B, Beclin-1, and Active caspase-3 were examined by Western blot; (B) HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the autophagy flow was observed by immunofluorescence, red arrow indicates autolysosomes; (C) HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the occurrence of autophagy was observed by transmission electron microscope; (D) HCT116p53 –/– cells were treated with 5-Fu + β-elemene, 5-Fu + β-elemene + Bafilomycin A1, the cell viability was examined by CCK8. (*** p
β Elemene, supplied by Supelco, used in various techniques. Bioz Stars score: 89/100, based on 0 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/β elemene/product/Supelco
Average 89 stars, based on 1 article reviews
Price from $9.99 to $1999.99
β elemene - by Bioz Stars, 2020-09
89/100 stars

Images

1) Product Images from "β-Elemene Reverses the Resistance of p53-Deficient Colorectal Cancer Cells to 5-Fluorouracil by Inducing Pro-death Autophagy and Cyclin D3-Dependent Cycle Arrest"

Article Title: β-Elemene Reverses the Resistance of p53-Deficient Colorectal Cancer Cells to 5-Fluorouracil by Inducing Pro-death Autophagy and Cyclin D3-Dependent Cycle Arrest

Journal: Frontiers in Bioengineering and Biotechnology

doi: 10.3389/fbioe.2020.00378

β-elemene reverse the resistance of HCT116p53 –/– cells to 5-Fu by inducing pro-death autophagy. (A) HCT116p53 +/+ and HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the protein expression of LC3B, Beclin-1, and Active caspase-3 were examined by Western blot; (B) HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the autophagy flow was observed by immunofluorescence, red arrow indicates autolysosomes; (C) HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the occurrence of autophagy was observed by transmission electron microscope; (D) HCT116p53 –/– cells were treated with 5-Fu + β-elemene, 5-Fu + β-elemene + Bafilomycin A1, the cell viability was examined by CCK8. (*** p
Figure Legend Snippet: β-elemene reverse the resistance of HCT116p53 –/– cells to 5-Fu by inducing pro-death autophagy. (A) HCT116p53 +/+ and HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the protein expression of LC3B, Beclin-1, and Active caspase-3 were examined by Western blot; (B) HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the autophagy flow was observed by immunofluorescence, red arrow indicates autolysosomes; (C) HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the occurrence of autophagy was observed by transmission electron microscope; (D) HCT116p53 –/– cells were treated with 5-Fu + β-elemene, 5-Fu + β-elemene + Bafilomycin A1, the cell viability was examined by CCK8. (*** p

Techniques Used: Expressing, Western Blot, Immunofluorescence, Transmission Assay, Microscopy

5-Fu and β-elemene inhibits proliferation of colorectal cancer cells. (A) HCT116p53 +/+ and HCT116p53 –/– cells were treated with different concentrations of 5-Fu for 24 h, or treated with β-elemene for 24, 48, and 72 h, the cell viability was examined by CCK8; (B) the cell proliferation was detected by a clone formation assays; (C) the apoptosis rate of cells was examined by flow cytometry. ( ∗ p
Figure Legend Snippet: 5-Fu and β-elemene inhibits proliferation of colorectal cancer cells. (A) HCT116p53 +/+ and HCT116p53 –/– cells were treated with different concentrations of 5-Fu for 24 h, or treated with β-elemene for 24, 48, and 72 h, the cell viability was examined by CCK8; (B) the cell proliferation was detected by a clone formation assays; (C) the apoptosis rate of cells was examined by flow cytometry. ( ∗ p

Techniques Used: Flow Cytometry

β-elemene reverse the resistance of HCT116p53 –/– cells to 5-Fu by inducing Cyclin D3- dependent cycle arrest. (A) HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the expression of cell cycle-related proteins were examined by Western blot; (B) HCT116p53 –/– cells were treated with 5-Fu + β-elemene, Cyclin-D3, 5-Fu + β-elemene + Cyclin D3, the protein expression of Cyclin D3 and CDK6 were examined by Western blot; (C) Overexpression Cyclin D3 of HCT116p53 –/– cells and treated with 5-Fu, β-elemene, 5-Fu + β-elemene, the cell viability was examined by CCK8. (** p
Figure Legend Snippet: β-elemene reverse the resistance of HCT116p53 –/– cells to 5-Fu by inducing Cyclin D3- dependent cycle arrest. (A) HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the expression of cell cycle-related proteins were examined by Western blot; (B) HCT116p53 –/– cells were treated with 5-Fu + β-elemene, Cyclin-D3, 5-Fu + β-elemene + Cyclin D3, the protein expression of Cyclin D3 and CDK6 were examined by Western blot; (C) Overexpression Cyclin D3 of HCT116p53 –/– cells and treated with 5-Fu, β-elemene, 5-Fu + β-elemene, the cell viability was examined by CCK8. (** p

Techniques Used: Expressing, Western Blot, Over Expression

Effect of β-elemene combined with 5-Fu on tumorigenicity of HCT116p53 –/– cells in vivo. (A) The tumor tissue; (B) Tumor volume curve. (* p
Figure Legend Snippet: Effect of β-elemene combined with 5-Fu on tumorigenicity of HCT116p53 –/– cells in vivo. (A) The tumor tissue; (B) Tumor volume curve. (* p

Techniques Used: In Vivo

2) Product Images from "β-Elemene Reverses the Resistance of p53-Deficient Colorectal Cancer Cells to 5-Fluorouracil by Inducing Pro-death Autophagy and Cyclin D3-Dependent Cycle Arrest"

Article Title: β-Elemene Reverses the Resistance of p53-Deficient Colorectal Cancer Cells to 5-Fluorouracil by Inducing Pro-death Autophagy and Cyclin D3-Dependent Cycle Arrest

Journal: Frontiers in Bioengineering and Biotechnology

doi: 10.3389/fbioe.2020.00378

β-elemene reverse the resistance of HCT116p53 –/– cells to 5-Fu by inducing pro-death autophagy. (A) HCT116p53 +/+ and HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the protein expression of LC3B, Beclin-1, and Active caspase-3 were examined by Western blot; (B) HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the autophagy flow was observed by immunofluorescence, red arrow indicates autolysosomes; (C) HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the occurrence of autophagy was observed by transmission electron microscope; (D) HCT116p53 –/– cells were treated with 5-Fu + β-elemene, 5-Fu + β-elemene + Bafilomycin A1, the cell viability was examined by CCK8. (*** p
Figure Legend Snippet: β-elemene reverse the resistance of HCT116p53 –/– cells to 5-Fu by inducing pro-death autophagy. (A) HCT116p53 +/+ and HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the protein expression of LC3B, Beclin-1, and Active caspase-3 were examined by Western blot; (B) HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the autophagy flow was observed by immunofluorescence, red arrow indicates autolysosomes; (C) HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the occurrence of autophagy was observed by transmission electron microscope; (D) HCT116p53 –/– cells were treated with 5-Fu + β-elemene, 5-Fu + β-elemene + Bafilomycin A1, the cell viability was examined by CCK8. (*** p

Techniques Used: Expressing, Western Blot, Immunofluorescence, Transmission Assay, Microscopy

5-Fu and β-elemene inhibits proliferation of colorectal cancer cells. (A) HCT116p53 +/+ and HCT116p53 –/– cells were treated with different concentrations of 5-Fu for 24 h, or treated with β-elemene for 24, 48, and 72 h, the cell viability was examined by CCK8; (B) the cell proliferation was detected by a clone formation assays; (C) the apoptosis rate of cells was examined by flow cytometry. ( ∗ p
Figure Legend Snippet: 5-Fu and β-elemene inhibits proliferation of colorectal cancer cells. (A) HCT116p53 +/+ and HCT116p53 –/– cells were treated with different concentrations of 5-Fu for 24 h, or treated with β-elemene for 24, 48, and 72 h, the cell viability was examined by CCK8; (B) the cell proliferation was detected by a clone formation assays; (C) the apoptosis rate of cells was examined by flow cytometry. ( ∗ p

Techniques Used: Flow Cytometry

β-elemene reverse the resistance of HCT116p53 –/– cells to 5-Fu by inducing Cyclin D3- dependent cycle arrest. (A) HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the expression of cell cycle-related proteins were examined by Western blot; (B) HCT116p53 –/– cells were treated with 5-Fu + β-elemene, Cyclin-D3, 5-Fu + β-elemene + Cyclin D3, the protein expression of Cyclin D3 and CDK6 were examined by Western blot; (C) Overexpression Cyclin D3 of HCT116p53 –/– cells and treated with 5-Fu, β-elemene, 5-Fu + β-elemene, the cell viability was examined by CCK8. (** p
Figure Legend Snippet: β-elemene reverse the resistance of HCT116p53 –/– cells to 5-Fu by inducing Cyclin D3- dependent cycle arrest. (A) HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the expression of cell cycle-related proteins were examined by Western blot; (B) HCT116p53 –/– cells were treated with 5-Fu + β-elemene, Cyclin-D3, 5-Fu + β-elemene + Cyclin D3, the protein expression of Cyclin D3 and CDK6 were examined by Western blot; (C) Overexpression Cyclin D3 of HCT116p53 –/– cells and treated with 5-Fu, β-elemene, 5-Fu + β-elemene, the cell viability was examined by CCK8. (** p

Techniques Used: Expressing, Western Blot, Over Expression

Effect of β-elemene combined with 5-Fu on tumorigenicity of HCT116p53 –/– cells in vivo. (A) The tumor tissue; (B) Tumor volume curve. (* p
Figure Legend Snippet: Effect of β-elemene combined with 5-Fu on tumorigenicity of HCT116p53 –/– cells in vivo. (A) The tumor tissue; (B) Tumor volume curve. (* p

Techniques Used: In Vivo

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    Supelco β elemene
    <t>β-elemene</t> reverse the resistance of HCT116p53 –/– cells to 5-Fu by inducing pro-death autophagy. (A) HCT116p53 +/+ and HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the protein expression of LC3B, Beclin-1, and Active caspase-3 were examined by Western blot; (B) HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the autophagy flow was observed by immunofluorescence, red arrow indicates autolysosomes; (C) HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the occurrence of autophagy was observed by transmission electron microscope; (D) HCT116p53 –/– cells were treated with 5-Fu + β-elemene, 5-Fu + β-elemene + Bafilomycin A1, the cell viability was examined by CCK8. (*** p
    β Elemene, supplied by Supelco, used in various techniques. Bioz Stars score: 89/100, based on 0 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/β elemene/product/Supelco
    Average 89 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    β elemene - by Bioz Stars, 2020-09
    89/100 stars
      Buy from Supplier

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    β-elemene reverse the resistance of HCT116p53 –/– cells to 5-Fu by inducing pro-death autophagy. (A) HCT116p53 +/+ and HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the protein expression of LC3B, Beclin-1, and Active caspase-3 were examined by Western blot; (B) HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the autophagy flow was observed by immunofluorescence, red arrow indicates autolysosomes; (C) HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the occurrence of autophagy was observed by transmission electron microscope; (D) HCT116p53 –/– cells were treated with 5-Fu + β-elemene, 5-Fu + β-elemene + Bafilomycin A1, the cell viability was examined by CCK8. (*** p

    Journal: Frontiers in Bioengineering and Biotechnology

    Article Title: β-Elemene Reverses the Resistance of p53-Deficient Colorectal Cancer Cells to 5-Fluorouracil by Inducing Pro-death Autophagy and Cyclin D3-Dependent Cycle Arrest

    doi: 10.3389/fbioe.2020.00378

    Figure Lengend Snippet: β-elemene reverse the resistance of HCT116p53 –/– cells to 5-Fu by inducing pro-death autophagy. (A) HCT116p53 +/+ and HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the protein expression of LC3B, Beclin-1, and Active caspase-3 were examined by Western blot; (B) HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the autophagy flow was observed by immunofluorescence, red arrow indicates autolysosomes; (C) HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the occurrence of autophagy was observed by transmission electron microscope; (D) HCT116p53 –/– cells were treated with 5-Fu + β-elemene, 5-Fu + β-elemene + Bafilomycin A1, the cell viability was examined by CCK8. (*** p

    Article Snippet: Anti-rabbit IgG, HRP-linked Antibody (#7074) and Anti-mouse IgG, HRP-linked Antibody (#7076) were also obtained from CST. β-elemene was obtained from LKT lab (E4418, purity ≥98%), β-elemene was dissolved in ethanol (02483, Supelco).

    Techniques: Expressing, Western Blot, Immunofluorescence, Transmission Assay, Microscopy

    5-Fu and β-elemene inhibits proliferation of colorectal cancer cells. (A) HCT116p53 +/+ and HCT116p53 –/– cells were treated with different concentrations of 5-Fu for 24 h, or treated with β-elemene for 24, 48, and 72 h, the cell viability was examined by CCK8; (B) the cell proliferation was detected by a clone formation assays; (C) the apoptosis rate of cells was examined by flow cytometry. ( ∗ p

    Journal: Frontiers in Bioengineering and Biotechnology

    Article Title: β-Elemene Reverses the Resistance of p53-Deficient Colorectal Cancer Cells to 5-Fluorouracil by Inducing Pro-death Autophagy and Cyclin D3-Dependent Cycle Arrest

    doi: 10.3389/fbioe.2020.00378

    Figure Lengend Snippet: 5-Fu and β-elemene inhibits proliferation of colorectal cancer cells. (A) HCT116p53 +/+ and HCT116p53 –/– cells were treated with different concentrations of 5-Fu for 24 h, or treated with β-elemene for 24, 48, and 72 h, the cell viability was examined by CCK8; (B) the cell proliferation was detected by a clone formation assays; (C) the apoptosis rate of cells was examined by flow cytometry. ( ∗ p

    Article Snippet: Anti-rabbit IgG, HRP-linked Antibody (#7074) and Anti-mouse IgG, HRP-linked Antibody (#7076) were also obtained from CST. β-elemene was obtained from LKT lab (E4418, purity ≥98%), β-elemene was dissolved in ethanol (02483, Supelco).

    Techniques: Flow Cytometry

    β-elemene reverse the resistance of HCT116p53 –/– cells to 5-Fu by inducing Cyclin D3- dependent cycle arrest. (A) HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the expression of cell cycle-related proteins were examined by Western blot; (B) HCT116p53 –/– cells were treated with 5-Fu + β-elemene, Cyclin-D3, 5-Fu + β-elemene + Cyclin D3, the protein expression of Cyclin D3 and CDK6 were examined by Western blot; (C) Overexpression Cyclin D3 of HCT116p53 –/– cells and treated with 5-Fu, β-elemene, 5-Fu + β-elemene, the cell viability was examined by CCK8. (** p

    Journal: Frontiers in Bioengineering and Biotechnology

    Article Title: β-Elemene Reverses the Resistance of p53-Deficient Colorectal Cancer Cells to 5-Fluorouracil by Inducing Pro-death Autophagy and Cyclin D3-Dependent Cycle Arrest

    doi: 10.3389/fbioe.2020.00378

    Figure Lengend Snippet: β-elemene reverse the resistance of HCT116p53 –/– cells to 5-Fu by inducing Cyclin D3- dependent cycle arrest. (A) HCT116p53 –/– cells were treated with control, 5-Fu, β-elemene, 5-Fu + β-elemene, the expression of cell cycle-related proteins were examined by Western blot; (B) HCT116p53 –/– cells were treated with 5-Fu + β-elemene, Cyclin-D3, 5-Fu + β-elemene + Cyclin D3, the protein expression of Cyclin D3 and CDK6 were examined by Western blot; (C) Overexpression Cyclin D3 of HCT116p53 –/– cells and treated with 5-Fu, β-elemene, 5-Fu + β-elemene, the cell viability was examined by CCK8. (** p

    Article Snippet: Anti-rabbit IgG, HRP-linked Antibody (#7074) and Anti-mouse IgG, HRP-linked Antibody (#7076) were also obtained from CST. β-elemene was obtained from LKT lab (E4418, purity ≥98%), β-elemene was dissolved in ethanol (02483, Supelco).

    Techniques: Expressing, Western Blot, Over Expression

    Effect of β-elemene combined with 5-Fu on tumorigenicity of HCT116p53 –/– cells in vivo. (A) The tumor tissue; (B) Tumor volume curve. (* p

    Journal: Frontiers in Bioengineering and Biotechnology

    Article Title: β-Elemene Reverses the Resistance of p53-Deficient Colorectal Cancer Cells to 5-Fluorouracil by Inducing Pro-death Autophagy and Cyclin D3-Dependent Cycle Arrest

    doi: 10.3389/fbioe.2020.00378

    Figure Lengend Snippet: Effect of β-elemene combined with 5-Fu on tumorigenicity of HCT116p53 –/– cells in vivo. (A) The tumor tissue; (B) Tumor volume curve. (* p

    Article Snippet: Anti-rabbit IgG, HRP-linked Antibody (#7074) and Anti-mouse IgG, HRP-linked Antibody (#7076) were also obtained from CST. β-elemene was obtained from LKT lab (E4418, purity ≥98%), β-elemene was dissolved in ethanol (02483, Supelco).

    Techniques: In Vivo