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CD133 and CXCR4 are overexpressed in PDAC. ( A ) Box plots represent relative mRNA expression for the gene signatures PROM1, CXCR4 or PROM1 and CXCR4 in normal tissue compared to PDAC tumor tissue (TCGA and GTEx database, GEPIA). ( B ) Protein–protein interactions of PROM1 (CD133) and CXCR4 with relevant factors involved in metastasis (green) and CSCs (red) (STRING). ( C ) Screening for percent CD133 + cells and ( D ) CD133 + CXCR4 + found in adherent cell culture of indicated cell lines. ( E ) Experimental scheme to evaluate CD133 and CXCR4 surface expression to identify patient derived xenografts (PDX) or patient derived organoids (PDO) crosstalk with pancreatic stellate cells (PSCs) at the protein level. ( F ) FACS analysis performed on Panc354 and MetPO1 when exposed to no conditioned media (grey), conditioned media from non—primed PSCs (blue) or conditioned media from primed PSCs (pink) for CD133 + cells, CXCR4 + cells <t>and</t> <t>CD133</t> + CXCR4 + cells represented as fold change against no conditioned media. ( G ) Representative cytometry blots. Error bars represent the standard deviation. n = 3 for all experiments unless otherwise depicted in the datasets. * p < 0.05, ns = not significant.
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COP1 knockdown reduces motility, and stemness in HCC cells. (a‐b) Migration (a) or invasion (b) assay showing reduced motility in Huh7 and HepG2 cells treated with COP1‐siRNA, as quantified by the relative migration or invaded area. Statistical significance: *, p < 0.05; ** p < 0.01; *** p < 0.001 vs. control. (c) Sphere formation assay images and quantitative data from Huh7 and HepG2 cells, demonstrating a decrease in both the number and size of spheres in COP1‐siRNA‐treated cells. (d) Sphere formation assay images and quantitative data from PLC/PRF/5 <t>CD133+</t> cells. Compared to the control grpup, both the sphere number and size decreased upon COP1‐siRNA treatment. Scale bar, 100 μm Statistical significance: *, p < 0.05; *** p < 0.001 vs. control.
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Image Search Results


CD133 and CXCR4 are overexpressed in PDAC. ( A ) Box plots represent relative mRNA expression for the gene signatures PROM1, CXCR4 or PROM1 and CXCR4 in normal tissue compared to PDAC tumor tissue (TCGA and GTEx database, GEPIA). ( B ) Protein–protein interactions of PROM1 (CD133) and CXCR4 with relevant factors involved in metastasis (green) and CSCs (red) (STRING). ( C ) Screening for percent CD133 + cells and ( D ) CD133 + CXCR4 + found in adherent cell culture of indicated cell lines. ( E ) Experimental scheme to evaluate CD133 and CXCR4 surface expression to identify patient derived xenografts (PDX) or patient derived organoids (PDO) crosstalk with pancreatic stellate cells (PSCs) at the protein level. ( F ) FACS analysis performed on Panc354 and MetPO1 when exposed to no conditioned media (grey), conditioned media from non—primed PSCs (blue) or conditioned media from primed PSCs (pink) for CD133 + cells, CXCR4 + cells and CD133 + CXCR4 + cells represented as fold change against no conditioned media. ( G ) Representative cytometry blots. Error bars represent the standard deviation. n = 3 for all experiments unless otherwise depicted in the datasets. * p < 0.05, ns = not significant.

Journal: Scientific Reports

Article Title: A CXCR4 targeting peptide delivered by silica nanoparticles eliminates migrating cancer stem cells in pancreatic ductal adenocarcinoma

doi: 10.1038/s41598-026-48584-2

Figure Lengend Snippet: CD133 and CXCR4 are overexpressed in PDAC. ( A ) Box plots represent relative mRNA expression for the gene signatures PROM1, CXCR4 or PROM1 and CXCR4 in normal tissue compared to PDAC tumor tissue (TCGA and GTEx database, GEPIA). ( B ) Protein–protein interactions of PROM1 (CD133) and CXCR4 with relevant factors involved in metastasis (green) and CSCs (red) (STRING). ( C ) Screening for percent CD133 + cells and ( D ) CD133 + CXCR4 + found in adherent cell culture of indicated cell lines. ( E ) Experimental scheme to evaluate CD133 and CXCR4 surface expression to identify patient derived xenografts (PDX) or patient derived organoids (PDO) crosstalk with pancreatic stellate cells (PSCs) at the protein level. ( F ) FACS analysis performed on Panc354 and MetPO1 when exposed to no conditioned media (grey), conditioned media from non—primed PSCs (blue) or conditioned media from primed PSCs (pink) for CD133 + cells, CXCR4 + cells and CD133 + CXCR4 + cells represented as fold change against no conditioned media. ( G ) Representative cytometry blots. Error bars represent the standard deviation. n = 3 for all experiments unless otherwise depicted in the datasets. * p < 0.05, ns = not significant.

Article Snippet: Mouse CD133/1 IgG1κ (AC133) , PE , Miltenyi Biotec , 130-113-108.

Techniques: Expressing, Protein-Protein interactions, Cell Culture, Derivative Assay, Cytometry, Standard Deviation

BMI1 downstream CXCL12–CXCR4 regulates EMT and stemness. ( A ) Protein–protein interactions of CXCL12 and CXCR4 with relevant factors involved in metastasis (red), stemness (purple), sonic hedgehog signaling (blue), AKT signaling (grey) and NFκB pathway (yellow) (STRING). ( B ) BMI1 gene expression analysis and western blot analysis. GAPDH was used as a loading control. Intensity ratios (IR) calculated against control lane using ImageJ. Cropped blot for clarity. ( C ) Gene expression analysis with genes involved in EMT using qRT-PCR. ( D ) Immunofluorescence quantifications and representative micrographs for indicated cell lines with white arrowheads marking mesenchymal structures of actin filaments stained with Phalloidin (pink) and nucleus stained with DAPI (blue). ( E ) Migration assays towards serum containing media. ( F ) Experimental scheme to evaluate CD133 and CXCR4 surface expression using flow cytometry for Panc354 and MetPO1 (sh_ SCR , sh1_ BMI1 and sh2_ BMI1 ) with (or without) CXCL12. ( G ) Flow cytometry analysis of CD133 + cells and CD133 + CXCR4 + cells in MetPO1 (sh_ SCR , sh1_ BMI1 and sh2_ BMI1 ) treated with (or without) CXCL12. ( H ) Representative cytometry plots for MetPO1 cell line. Error bars represent the standard deviation. n = 3 for all experiments unless otherwise depicted in the datasets. * p < 0.05, ns = not significant.

Journal: Scientific Reports

Article Title: A CXCR4 targeting peptide delivered by silica nanoparticles eliminates migrating cancer stem cells in pancreatic ductal adenocarcinoma

doi: 10.1038/s41598-026-48584-2

Figure Lengend Snippet: BMI1 downstream CXCL12–CXCR4 regulates EMT and stemness. ( A ) Protein–protein interactions of CXCL12 and CXCR4 with relevant factors involved in metastasis (red), stemness (purple), sonic hedgehog signaling (blue), AKT signaling (grey) and NFκB pathway (yellow) (STRING). ( B ) BMI1 gene expression analysis and western blot analysis. GAPDH was used as a loading control. Intensity ratios (IR) calculated against control lane using ImageJ. Cropped blot for clarity. ( C ) Gene expression analysis with genes involved in EMT using qRT-PCR. ( D ) Immunofluorescence quantifications and representative micrographs for indicated cell lines with white arrowheads marking mesenchymal structures of actin filaments stained with Phalloidin (pink) and nucleus stained with DAPI (blue). ( E ) Migration assays towards serum containing media. ( F ) Experimental scheme to evaluate CD133 and CXCR4 surface expression using flow cytometry for Panc354 and MetPO1 (sh_ SCR , sh1_ BMI1 and sh2_ BMI1 ) with (or without) CXCL12. ( G ) Flow cytometry analysis of CD133 + cells and CD133 + CXCR4 + cells in MetPO1 (sh_ SCR , sh1_ BMI1 and sh2_ BMI1 ) treated with (or without) CXCL12. ( H ) Representative cytometry plots for MetPO1 cell line. Error bars represent the standard deviation. n = 3 for all experiments unless otherwise depicted in the datasets. * p < 0.05, ns = not significant.

Article Snippet: Mouse CD133/1 IgG1κ (AC133) , PE , Miltenyi Biotec , 130-113-108.

Techniques: Protein-Protein interactions, Gene Expression, Western Blot, Control, Quantitative RT-PCR, Immunofluorescence, Staining, Migration, Expressing, Flow Cytometry, Cytometry, Standard Deviation

COP1 knockdown reduces motility, and stemness in HCC cells. (a‐b) Migration (a) or invasion (b) assay showing reduced motility in Huh7 and HepG2 cells treated with COP1‐siRNA, as quantified by the relative migration or invaded area. Statistical significance: *, p < 0.05; ** p < 0.01; *** p < 0.001 vs. control. (c) Sphere formation assay images and quantitative data from Huh7 and HepG2 cells, demonstrating a decrease in both the number and size of spheres in COP1‐siRNA‐treated cells. (d) Sphere formation assay images and quantitative data from PLC/PRF/5 CD133+ cells. Compared to the control grpup, both the sphere number and size decreased upon COP1‐siRNA treatment. Scale bar, 100 μm Statistical significance: *, p < 0.05; *** p < 0.001 vs. control.

Journal: Genes to Cells

Article Title: Functional Role of COP1 Gene in Hepatocellular Carcinoma Lipid Metabolism and Stemness

doi: 10.1111/gtc.70108

Figure Lengend Snippet: COP1 knockdown reduces motility, and stemness in HCC cells. (a‐b) Migration (a) or invasion (b) assay showing reduced motility in Huh7 and HepG2 cells treated with COP1‐siRNA, as quantified by the relative migration or invaded area. Statistical significance: *, p < 0.05; ** p < 0.01; *** p < 0.001 vs. control. (c) Sphere formation assay images and quantitative data from Huh7 and HepG2 cells, demonstrating a decrease in both the number and size of spheres in COP1‐siRNA‐treated cells. (d) Sphere formation assay images and quantitative data from PLC/PRF/5 CD133+ cells. Compared to the control grpup, both the sphere number and size decreased upon COP1‐siRNA treatment. Scale bar, 100 μm Statistical significance: *, p < 0.05; *** p < 0.001 vs. control.

Article Snippet: The cells were treated with FcR Blocking Reagent and CD133 MicroBeads (130‐100‐857, Miltenyi Biotec, Bergisch Gladbach, Germany) according to the manufacturer's instructions and incubated for 15 min at 4°C in the dark.

Techniques: Knockdown, Migration, Control, Tube Formation Assay