Journal: The Journal of thoracic and cardiovascular surgery

Article Title: Loss of p53, rather than beta-catenin overexpression, induces survivin-mediated resistance to apoptosis in an esophageal cancer cell line.

doi: 10.1016/j.jtcvs.2009.11.038

Figure Lengend Snippet: FIGURE 4. TE7 cells exhibit a loss of p53 with resulting increased survi- vin transcription. A, Representative immunoblots of p53 protein expression in nhEso and TE7 cells. B, Schematic representation of the survivin pro- moter-luciferase reporter construct that included 2 TCF-b-catenin binding

Article Snippet: Co-transfection assays were carried out in nhEso and TE7 cells using 0.3 mg of survivin luciferase reporter gene plasmid, 0.3 mg of either an empty expression vector or an overexpression vector encoding the tumor protein p53 (OriGene Technologies Inc, Rockville, Md), in 0.7 mL Lipofectamine reagent.

Techniques: Western Blot, Expressing, Luciferase, Construct, Binding Assay

Journal: The Journal of thoracic and cardiovascular surgery

Article Title: Loss of p53, rather than beta-catenin overexpression, induces survivin-mediated resistance to apoptosis in an esophageal cancer cell line.

doi: 10.1016/j.jtcvs.2009.11.038

Figure Lengend Snippet: FIGURE 5. Effect of p53 overexpression on survivin promoter activity and survivin mRNA transcription in nhEso and TE7 cells. A, Reporter gene activity in nhEso and TE7 cells after overexpression of p53. Cells were co-transfected with the survivin reporter construct and the expression vector containing human p53 cDNA (p53) or control vector lacking p53 (control) using Lipofectamine (Invitrogen, Carlsbad, Calif). Twenty-four

Article Snippet: Co-transfection assays were carried out in nhEso and TE7 cells using 0.3 mg of survivin luciferase reporter gene plasmid, 0.3 mg of either an empty expression vector or an overexpression vector encoding the tumor protein p53 (OriGene Technologies Inc, Rockville, Md), in 0.7 mL Lipofectamine reagent.

Techniques: Over Expression, Activity Assay, Transfection, Construct, Expressing, Plasmid Preparation, Control

Journal: Journal of Cancer

Article Title: Upregulation of nucleoprotein AHNAK is associated with poor outcome of pancreatic ductal adenocarcinoma prognosis via mediating epithelial-mesenchymal transition

doi: 10.7150/jca.31291

Figure Lengend Snippet: AHNAK mediates the EMT to promote PDAC cell proliferation and migration via TP53 signaling pathway. A: GSEA was carried out in the paired PDAC samples in GEO database. It showed that most biomarkers were involved in the EMT phenotype. B: Western blotting analysis showed that AHNAK suppression caused an increase in E-cadherin but a decrease in N-cadherin. C and D: The qPCR results showed the alteration of gene expression in EMT phenotype after knockdown of AHNAK.

Article Snippet: Recombinant p53 protein was purchased from Origene (Catalog: TP710022) and Cell culture experiments were used to verify the predictions.

Techniques: Migration, Western Blot, Gene Expression, Knockdown

Journal: Journal of Cancer

Article Title: Upregulation of nucleoprotein AHNAK is associated with poor outcome of pancreatic ductal adenocarcinoma prognosis via mediating epithelial-mesenchymal transition

doi: 10.7150/jca.31291

Figure Lengend Snippet: AHNAK mediates the EMT via TP53 signaling pathway. A: Western blot analysis showed that after knockdown of AHNAK, only expression of TP53 was altered, while other markers, including AKT and ERK. The phosphorylated level of TP53, AKT and ERK also showed no alterations. B: qRT-PCR showed the alteration of markers in TP53 signaling pathway. C: GSEA suggested an enrichment of TP53 signaling pathway in PDAC by analyzing the GEO database. D: Western blot showed after the recombinant TP53 protein was added into the AHNAK deficiency cell lines, E-cad, the epithelial markers of EMT phenotype was restored. E and F: CCK-8 and Transwell assays showed that recombinant TP53 could restore cellular proliferation and migration.

Article Snippet: Recombinant p53 protein was purchased from Origene (Catalog: TP710022) and Cell culture experiments were used to verify the predictions.

Techniques: Western Blot, Knockdown, Expressing, Quantitative RT-PCR, Recombinant, CCK-8 Assay, Migration

Journal: PLoS ONE

Article Title: Expression of Galectin-7 Is Induced in Breast Cancer Cells by Mutant p53

doi: 10.1371/journal.pone.0072468

Figure Lengend Snippet: mutant is inhibited by CAPE . ( A ) Inhibition of galectin-7 mRNA levels by CAPE in MDA-MB-453 cells transfected with the expression vector encoding p53 R175H or with the (empty) pCDNA3.1 control vector (CTRL). GAPDH was used as loading control. ( B ) Effect of CAPE on NF-κB reporter activity in MDA-MB-453 cells transfected with the expression vector encoding p53 R175H or with the (empty) pCDNA3.1 control vector (CTRL). Transfection efficiency was normalized by co-transfection with a β-galactosidase reporter vector.

Article Snippet: The vector encoding the wild-type human p53 gene was purchased from Origene (Burlington, MA).

Techniques: Mutagenesis, Inhibition, Transfection, Expressing, Plasmid Preparation, Control, Activity Assay, Cotransfection

Journal: Science Advances

Article Title: Identifying the substrate proteins of U-box E3s E4B and CHIP by orthogonal ubiquitin transfer

doi: 10.1126/sciadv.1701393

Figure Lengend Snippet: ( A ) fE4B-KB2 and fE4B-KB12 could assemble an OUT cascade with xUba1 and xUbcH5b to mediate xUB transfer to p53. The efficiency of p53 ubiquitination by xUB and the OUT cascade was similar to p53 ubiquitination with wt UB and the wt Uba1-UbcH5b-fE4B cascade. In contrast, wt E4B could not pair with xUba1-xUbcH5b to transfer xUB to p53, suggesting the orthogonality between the OUT cascade and native E3s. Mutant fE4B KB2 or KB12 could not pair with wt Uba1–wt UbcH5b to transfer wt UB to p53. ( B ) Similar to E4B OUT cascade, CHIP-KB2 and CHIP-KB12 could relay with xUba1-xUbcH5b to transfer xUB to p53. The efficiency of xUB modification of p53 by the CHIP OUT cascades was similar to that of p53 modification by wt UB going through the wt Uba1-UbcH5b-CHIP cascade. xUB could not be transferred to p53 with the crossover cascade of xUba1-xUbcH5b–wt CHIP. wt UB could not be transferred to p53 with the crossover cascade of wt Uba1–wt UbcH5b–mutant CHIP (KB2 or KB12).

Article Snippet: Anti-flag (M2) antibody (F3165) was from Sigma-Aldrich. p53 protein (SP-452-020) was from R&D Systems.

Techniques: Ubiquitin Proteomics, Mutagenesis, Modification

Journal: Cancer Research Communications

Article Title: Cancer Relevance of Circulating Antibodies Against LINE-1 Antigens in Humans

doi: 10.1158/2767-9764.CRC-23-0289

Figure Lengend Snippet: Approach and proof of concept. A, Hypotheses: proteins encoded by L1 are expected to be recognized as tumor-associated antigens and become targets for antibody response. This response is stimulated by the cGAS-STING-mediated induction of inflammation. Circulating Abs to L1 antigens can be used as cancer biomarkers if detected by anti-ORF1p and anti-ORF2p immunoassays. Comparison of antibody levels in healthy individuals ( N = 137) and patients with cancer ( N = 331) in the assays for anti-ORF1p ( B ), anti-ORF2p ( C ), and p53 ( D ). The significance of differences is assessed by Mann–Whitney U test. E, Spearman correlation between anti-ORF1p IgG titers and anti-p53 IgG signals in serum samples of patients with cancer ( N = 331). All P value less than 0.05 is considered significant.

Article Snippet: Recombinant Human Tumor Protein p53 (RayBiotech, Code 230-00639-10) was diluted to 1 μg/mL in a 2 mol/L urea/PBS coating buffer; or each of 17 ORF1p 25-mer peptides conjugated with BSA were diluted to 2 μg/mL in PBS coating buffer and added to Black MaxiSorp 96-well assay plates (50 μL/well).

Techniques: Comparison, MANN-WHITNEY

Journal: Journal of Clinical Medicine

Article Title: The Impact of Osteopontin and Galectin-7 on the Preoperative Diagnosis of Ovarian Tumors: A Case–Control Study

doi: 10.3390/jcm15062178

Figure Lengend Snippet: Distributions of osteopontin and galectin-7 in controls (normal) vs. cases (benign and malignant). No statistically significant differences were observed between groups for osteopontin ( p = 0.562) or galectin-7 ( p = 0.138).

Article Snippet: Osteopontin and galectin-7 concentrations were quantified from serum using commercially available ELISA kits by Boster Biological Technology (Pleasanton, CA, USA).

Techniques:

Journal: Journal of Clinical Medicine

Article Title: The Impact of Osteopontin and Galectin-7 on the Preoperative Diagnosis of Ovarian Tumors: A Case–Control Study

doi: 10.3390/jcm15062178

Figure Lengend Snippet: Receiver operating characteristic (ROC) curves for osteopontin and galectin-7.

Article Snippet: Osteopontin and galectin-7 concentrations were quantified from serum using commercially available ELISA kits by Boster Biological Technology (Pleasanton, CA, USA).

Techniques:

Journal: Journal of Clinical Medicine

Article Title: The Impact of Osteopontin and Galectin-7 on the Preoperative Diagnosis of Ovarian Tumors: A Case–Control Study

doi: 10.3390/jcm15062178

Figure Lengend Snippet: Receiver operating characteristic (ROC) curves for osteopontin (blue), galectin-7 (red), and the combined logistic regression model (green) in discriminating malignant from benign ovarian tumors.

Article Snippet: Osteopontin and galectin-7 concentrations were quantified from serum using commercially available ELISA kits by Boster Biological Technology (Pleasanton, CA, USA).

Techniques: