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p53 plasmid  (Addgene inc)
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Addgene inc p53 plasmid
Fig. 4 <t>p53</t> upregulation determines the action of the combination through UMPS inhibition-mediated apoptosis in only NSCLC with wild type p53. A The tendency for co-occurrence of mutant TP53 and UMPS tested in NSCLC patients in seven datasets. B The basal expression levels of UMPS and p53 in NSCLC. C The correlation between p53 and UMPS expression in NSCLC. D NSCLC was treated with the combination of SH003 and DTX for 24 h and the expression of p53 was determined by western blotting. E The correlation of <t>p53</t> <t>protein</t> levels and cell viability was changed by the combination in NSCLC. F, G H460 and A549 cells were treated with SH003 and/ or DTX for 24 h following p53 knockdown. H, I H1703 and H358 cells were treated with SH003 and/or DTX for 24 h following p53 overexpression. The cell viability and protein expression levels were measured. Statistical significance was determined by one-way ANOVA with Tukey’s test. *p < 0.05; **p < 0.01
P53 Plasmid, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Fig. 4 p53 upregulation determines the action of the combination through UMPS inhibition-mediated apoptosis in only NSCLC with wild type p53. A The tendency for co-occurrence of mutant TP53 and UMPS tested in NSCLC patients in seven datasets. B The basal expression levels of UMPS and p53 in NSCLC. C The correlation between p53 and UMPS expression in NSCLC. D NSCLC was treated with the combination of SH003 and DTX for 24 h and the expression of p53 was determined by western blotting. E The correlation of p53 protein levels and cell viability was changed by the combination in NSCLC. F, G H460 and A549 cells were treated with SH003 and/ or DTX for 24 h following p53 knockdown. H, I H1703 and H358 cells were treated with SH003 and/or DTX for 24 h following p53 overexpression. The cell viability and protein expression levels were measured. Statistical significance was determined by one-way ANOVA with Tukey’s test. *p < 0.05; **p < 0.01

Journal: Cancer cell international

Article Title: p53 activation enhances the sensitivity of non-small cell lung cancer to the combination of SH003 and docetaxel by inhibiting de novo pyrimidine synthesis.

doi: 10.1186/s12935-024-03337-x

Figure Lengend Snippet: Fig. 4 p53 upregulation determines the action of the combination through UMPS inhibition-mediated apoptosis in only NSCLC with wild type p53. A The tendency for co-occurrence of mutant TP53 and UMPS tested in NSCLC patients in seven datasets. B The basal expression levels of UMPS and p53 in NSCLC. C The correlation between p53 and UMPS expression in NSCLC. D NSCLC was treated with the combination of SH003 and DTX for 24 h and the expression of p53 was determined by western blotting. E The correlation of p53 protein levels and cell viability was changed by the combination in NSCLC. F, G H460 and A549 cells were treated with SH003 and/ or DTX for 24 h following p53 knockdown. H, I H1703 and H358 cells were treated with SH003 and/or DTX for 24 h following p53 overexpression. The cell viability and protein expression levels were measured. Statistical significance was determined by one-way ANOVA with Tukey’s test. *p < 0.05; **p < 0.01

Article Snippet: Cells were transfected using Lipofectamine RNAiMAX reagent or Lipofectamine 3000 (Thermo Scientific, USA). p53 siRNA was obtained from Santa Cruz (sc-29435, USA) and p53 plasmid was purchased from Addgene (#69003).

Techniques: Inhibition, Mutagenesis, Expressing, Western Blot, Knockdown, Over Expression

Fig. 5 Combination treatment-mediated p53 activation induces replication stress and DNA damage through reduction of the UMP pool in only H460 cells. A H460 cells were treated with the combination for 6 h and stained with anti-BrdU. BrdU-negative cells in S phase were analyzed by flow cytometry. The flow cytometry image shows one representative result. B Bar graph indicates the proportion of cells in S-phase arrest. C H460 cells were treated with SH003 and/or DTX for 24 h, and the cell cycle was analyzed by staining with PI. Histogram represents sub-G1-phase cells. D Western blot analysis of a DNA damage marker, γ-H2AX, and p-p53. E Immunofluorescence analysis of γ-H2AX in the cell nuclei after exposure to SH003 and/or DTX for 24 h in H460 cells. F Cells were treated with the combination followed by uridine for 24 h. The expression of γ-H2AX protein was analyzed by western blotting. G H460 cells were treated with SH003 and DTX for 24 h following p53 knockdown, fixed, and incubated with anti-γ-H2AX. The intensity of γ-H2AX foci was calculated using Image J. H Confocal image indicated the formation of γ-H2AX foci in p53-overexpressing H358 cells. Bar graph showed the relative intensity of γ-H2AX foci. I Upon the transfection of H460 and A549 cells with sip53, the protein levels of p21 and γ-H2AX were detected by western blotting. J Upon the overexpression of p53 vector in H358 and H1703 cells, the protein levels of p21 and γ-H2AX were determined by western blotting. Statistical significance was determined by one-way ANOVA with Tukey’s test. *p < 0.05; **p < 0.01

Journal: Cancer cell international

Article Title: p53 activation enhances the sensitivity of non-small cell lung cancer to the combination of SH003 and docetaxel by inhibiting de novo pyrimidine synthesis.

doi: 10.1186/s12935-024-03337-x

Figure Lengend Snippet: Fig. 5 Combination treatment-mediated p53 activation induces replication stress and DNA damage through reduction of the UMP pool in only H460 cells. A H460 cells were treated with the combination for 6 h and stained with anti-BrdU. BrdU-negative cells in S phase were analyzed by flow cytometry. The flow cytometry image shows one representative result. B Bar graph indicates the proportion of cells in S-phase arrest. C H460 cells were treated with SH003 and/or DTX for 24 h, and the cell cycle was analyzed by staining with PI. Histogram represents sub-G1-phase cells. D Western blot analysis of a DNA damage marker, γ-H2AX, and p-p53. E Immunofluorescence analysis of γ-H2AX in the cell nuclei after exposure to SH003 and/or DTX for 24 h in H460 cells. F Cells were treated with the combination followed by uridine for 24 h. The expression of γ-H2AX protein was analyzed by western blotting. G H460 cells were treated with SH003 and DTX for 24 h following p53 knockdown, fixed, and incubated with anti-γ-H2AX. The intensity of γ-H2AX foci was calculated using Image J. H Confocal image indicated the formation of γ-H2AX foci in p53-overexpressing H358 cells. Bar graph showed the relative intensity of γ-H2AX foci. I Upon the transfection of H460 and A549 cells with sip53, the protein levels of p21 and γ-H2AX were detected by western blotting. J Upon the overexpression of p53 vector in H358 and H1703 cells, the protein levels of p21 and γ-H2AX were determined by western blotting. Statistical significance was determined by one-way ANOVA with Tukey’s test. *p < 0.05; **p < 0.01

Article Snippet: Cells were transfected using Lipofectamine RNAiMAX reagent or Lipofectamine 3000 (Thermo Scientific, USA). p53 siRNA was obtained from Santa Cruz (sc-29435, USA) and p53 plasmid was purchased from Addgene (#69003).

Techniques: Activation Assay, Staining, Flow Cytometry, Western Blot, Marker, Immunofluorescence, Expressing, Knockdown, Incubation, Transfection, Over Expression, Plasmid Preparation

Fig. 6 A schematic of the mechanism by which the combination of SH003 and DTX induces NSCLC cell death. Treatment with SH003 and DTX inhibited the de novo pyrimidine synthesis pathway by activating p53 in p53 wild type NSCLC cells. The reduction of pyrimidine synthesis-related UMPS enzyme levels in turn caused replication stress, DNA damage, and apoptosis. In NSCLC cells harboring p53 mutation or null type, combination treatment induced apoptosis independent of p53-mediated metabolic perturbations

Journal: Cancer cell international

Article Title: p53 activation enhances the sensitivity of non-small cell lung cancer to the combination of SH003 and docetaxel by inhibiting de novo pyrimidine synthesis.

doi: 10.1186/s12935-024-03337-x

Figure Lengend Snippet: Fig. 6 A schematic of the mechanism by which the combination of SH003 and DTX induces NSCLC cell death. Treatment with SH003 and DTX inhibited the de novo pyrimidine synthesis pathway by activating p53 in p53 wild type NSCLC cells. The reduction of pyrimidine synthesis-related UMPS enzyme levels in turn caused replication stress, DNA damage, and apoptosis. In NSCLC cells harboring p53 mutation or null type, combination treatment induced apoptosis independent of p53-mediated metabolic perturbations

Article Snippet: Cells were transfected using Lipofectamine RNAiMAX reagent or Lipofectamine 3000 (Thermo Scientific, USA). p53 siRNA was obtained from Santa Cruz (sc-29435, USA) and p53 plasmid was purchased from Addgene (#69003).

Techniques: Mutagenesis