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Human Protein Atlas representative immunohistochemistry ihc images illustrating tfr1 protein expression
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Human Protein Atlas plk1 protein expression
Molecular dynamics results of NC and <t>PLK1.</t> (A) Three-dimensional representation of the protein–ligand complex. The overall protein structure is shown in cartoon format (left), with the ligand depicted as sticks within the binding pocket. The right panel shows an enlarged view of the binding site, highlighting the spatial arrangement of the ligand and surrounding amino acid residues (e.g., LEU-59, LEU-132, LYS-82, PHE-183, and ASP-194), along with the distances of their interactions. (B) Summary of protein–ligand interaction analysis. The table presents hydrophobic interactions, hydrogen bonds, and π-stacking interactions, including details such as interacting residues, atom indices, interaction distances, angles, and related geometric parameters.
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Image Search Results


Integrated in silico and experimental analysis of transferrin receptor 1 (TfR1 / TFRC) expression in gliomas and representative cell lines. Box-plot summary of TFRC mRNA expression obtained from GEPIA (Gene Expression Profiling Interactive Analysis) based on tumor and normal samples from the TCGA and the GTEx databases (accessed March 2025). ( A ) Comparison of TFRC expression in high-grade gliomas (GBM) vs. low-grade glioma (LGG) (n indicated on each plot). ( B ) TFRC expression stratified by canonical GBM molecular subtype (classical, mesenchymal, neural, proneural). Boxes represent the interquartile range, horizontal lines the median, whiskers extend to 1.5×IQR, and individual data points are overlaid. Brackets with asterisks denote statistically significant pairwise differences (see Methods for statistical test). ( C ) TfR1 expression levels in GBM cell lines and HEK293 (non-tumor control). Data taken and adapted from the Human Protein Atlas. ( D ) Representative flow-cytometry histograms of surface TfR1 staining in U87MG, T98G, MO59K and HEK293 cells. Traces correspond to unstained control (red), secondary-only control (anti-mouse IgG–AF647; Orange) and specific anti-CD71 primary staining followed by anti-mouse-AF647 secondary (blue). The horizontal bracket on each histogram indicates the gate used to define TfR1-positive events. ( E ) gMFI of the CD71 signal (mean ± SD; n = biological replicates indicated in Methods), and ( F ) percentage of TfR1-positive cells. Data were normalized to appropriate controls. Statistical comparisons were performed as described in Methods (* p < 0.05 ).

Journal: International Journal of Nanomedicine

Article Title: Transferrin-Functionalized Conjugated Polymer Nanoparticles for Enhanced Photodynamic Therapy of Glioblastoma

doi: 10.2147/IJN.S592688

Figure Lengend Snippet: Integrated in silico and experimental analysis of transferrin receptor 1 (TfR1 / TFRC) expression in gliomas and representative cell lines. Box-plot summary of TFRC mRNA expression obtained from GEPIA (Gene Expression Profiling Interactive Analysis) based on tumor and normal samples from the TCGA and the GTEx databases (accessed March 2025). ( A ) Comparison of TFRC expression in high-grade gliomas (GBM) vs. low-grade glioma (LGG) (n indicated on each plot). ( B ) TFRC expression stratified by canonical GBM molecular subtype (classical, mesenchymal, neural, proneural). Boxes represent the interquartile range, horizontal lines the median, whiskers extend to 1.5×IQR, and individual data points are overlaid. Brackets with asterisks denote statistically significant pairwise differences (see Methods for statistical test). ( C ) TfR1 expression levels in GBM cell lines and HEK293 (non-tumor control). Data taken and adapted from the Human Protein Atlas. ( D ) Representative flow-cytometry histograms of surface TfR1 staining in U87MG, T98G, MO59K and HEK293 cells. Traces correspond to unstained control (red), secondary-only control (anti-mouse IgG–AF647; Orange) and specific anti-CD71 primary staining followed by anti-mouse-AF647 secondary (blue). The horizontal bracket on each histogram indicates the gate used to define TfR1-positive events. ( E ) gMFI of the CD71 signal (mean ± SD; n = biological replicates indicated in Methods), and ( F ) percentage of TfR1-positive cells. Data were normalized to appropriate controls. Statistical comparisons were performed as described in Methods (* p < 0.05 ).

Article Snippet: In addition, representative immunohistochemistry (IHC) images illustrating TfR1 protein expression in human brain tissues were retrieved from the Human Protein Atlas (HPA) database ( https://www.proteinatlas.org ), an open-access resource providing antibody-based protein expression profiles across normal and cancer tissues.

Techniques: In Silico, Expressing, Gene Expression, Comparison, Control, Flow Cytometry, Staining

Journal: Cell Genomics

Article Title: MultiSP deciphers tissue structure and multicellular communication from spatial multi-omics data

doi: 10.1016/j.xgen.2026.101141

Figure Lengend Snippet:

Article Snippet: 10× Visium human tonsil gene and protein expression data , 10× Genomics , https://www.10xgenomics.com/resources/datasets/gene-protein-expression-library-of-human-tonsil-cytassist-ffpe-2-standard.

Techniques: Expressing, Software

Molecular dynamics results of NC and PLK1. (A) Three-dimensional representation of the protein–ligand complex. The overall protein structure is shown in cartoon format (left), with the ligand depicted as sticks within the binding pocket. The right panel shows an enlarged view of the binding site, highlighting the spatial arrangement of the ligand and surrounding amino acid residues (e.g., LEU-59, LEU-132, LYS-82, PHE-183, and ASP-194), along with the distances of their interactions. (B) Summary of protein–ligand interaction analysis. The table presents hydrophobic interactions, hydrogen bonds, and π-stacking interactions, including details such as interacting residues, atom indices, interaction distances, angles, and related geometric parameters.

Journal: Frontiers in Oncology

Article Title: Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study

doi: 10.3389/fonc.2026.1824796

Figure Lengend Snippet: Molecular dynamics results of NC and PLK1. (A) Three-dimensional representation of the protein–ligand complex. The overall protein structure is shown in cartoon format (left), with the ligand depicted as sticks within the binding pocket. The right panel shows an enlarged view of the binding site, highlighting the spatial arrangement of the ligand and surrounding amino acid residues (e.g., LEU-59, LEU-132, LYS-82, PHE-183, and ASP-194), along with the distances of their interactions. (B) Summary of protein–ligand interaction analysis. The table presents hydrophobic interactions, hydrogen bonds, and π-stacking interactions, including details such as interacting residues, atom indices, interaction distances, angles, and related geometric parameters.

Article Snippet: PLK1 protein expression in CRC was validated by immunohistochemistry (IHC) using data from the Human Protein Atlas (HPA, antibody HPA053229).

Techniques: Binding Assay

Molecular dynamics results of NC and PLK1. (A) Root mean square deviation (RMSD) of the complex, protein, and ligand as a function of simulation time. (B) Root mean square fluctuation (RMSF) of protein residues. (C) Solvent-accessible surface area (SASA) of the complex over time. (D) Radius of gyration (Rg) of the complex during the simulation. (E) Number of hydrogen bonds formed between the protein and ligand over time. (F) Gibbs free energy landscape as a function of RMSD and Rg, presented in both 2D contour and 3D surface plots. (G) Binding free energy components, including van der Waals, electrostatic, polar solvation, nonpolar solvation, and total energy contributions. (H) Per-residue binding energy contribution of amino acids to the ligand. (I) Representative structures of the protein–ligand complex at 0 ns, 50 ns, and 100 ns during the simulation. NC, Nitidine Chloride; PLK1, polo-like kinase 1; PCA, principal component analysis; RMSD, root mean square deviation; Rg, radius of gyration; RMSF, root mean square fluctuation.

Journal: Frontiers in Oncology

Article Title: Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study

doi: 10.3389/fonc.2026.1824796

Figure Lengend Snippet: Molecular dynamics results of NC and PLK1. (A) Root mean square deviation (RMSD) of the complex, protein, and ligand as a function of simulation time. (B) Root mean square fluctuation (RMSF) of protein residues. (C) Solvent-accessible surface area (SASA) of the complex over time. (D) Radius of gyration (Rg) of the complex during the simulation. (E) Number of hydrogen bonds formed between the protein and ligand over time. (F) Gibbs free energy landscape as a function of RMSD and Rg, presented in both 2D contour and 3D surface plots. (G) Binding free energy components, including van der Waals, electrostatic, polar solvation, nonpolar solvation, and total energy contributions. (H) Per-residue binding energy contribution of amino acids to the ligand. (I) Representative structures of the protein–ligand complex at 0 ns, 50 ns, and 100 ns during the simulation. NC, Nitidine Chloride; PLK1, polo-like kinase 1; PCA, principal component analysis; RMSD, root mean square deviation; Rg, radius of gyration; RMSF, root mean square fluctuation.

Article Snippet: PLK1 protein expression in CRC was validated by immunohistochemistry (IHC) using data from the Human Protein Atlas (HPA, antibody HPA053229).

Techniques: Solvent, Binding Assay, Residue

Single-cell identification of malignant cell populations and proliferation-associated gene expression in colorectal cancer (CRC). (A) UMAP visualization showing the major cell populations in CRC samples, including B cells, cancer-associated fibroblasts (CAFs), endothelial cells, macrophages, malignant epithelial cells, and T/NK cells. (B) Identification of malignant cells based on inferred copy number variation (CNV). The left panel shows the distribution of high-CNV (malignant) and low-CNV (normal-like) cells in UMAP space, while the right panel presents total CNV scores across different cell types or malignant epithelial subpopulations. (C) UMAP feature plots showing the expression patterns of the proliferation-related genes MKI67 and PLK1 at the single-cell level in CRC samples.

Journal: Frontiers in Oncology

Article Title: Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study

doi: 10.3389/fonc.2026.1824796

Figure Lengend Snippet: Single-cell identification of malignant cell populations and proliferation-associated gene expression in colorectal cancer (CRC). (A) UMAP visualization showing the major cell populations in CRC samples, including B cells, cancer-associated fibroblasts (CAFs), endothelial cells, macrophages, malignant epithelial cells, and T/NK cells. (B) Identification of malignant cells based on inferred copy number variation (CNV). The left panel shows the distribution of high-CNV (malignant) and low-CNV (normal-like) cells in UMAP space, while the right panel presents total CNV scores across different cell types or malignant epithelial subpopulations. (C) UMAP feature plots showing the expression patterns of the proliferation-related genes MKI67 and PLK1 at the single-cell level in CRC samples.

Article Snippet: PLK1 protein expression in CRC was validated by immunohistochemistry (IHC) using data from the Human Protein Atlas (HPA, antibody HPA053229).

Techniques: Single Cell, Gene Expression, Expressing

Batch effect assessment and correction in the integrated multi-platform colon cancer gene expression dataset for PLK1 biomarker analysis.

Journal: Frontiers in Oncology

Article Title: Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study

doi: 10.3389/fonc.2026.1824796

Figure Lengend Snippet: Batch effect assessment and correction in the integrated multi-platform colon cancer gene expression dataset for PLK1 biomarker analysis.

Article Snippet: PLK1 protein expression in CRC was validated by immunohistochemistry (IHC) using data from the Human Protein Atlas (HPA, antibody HPA053229).

Techniques: Gene Expression, Biomarker Discovery

PLK1 is highly expressed at the mRNA level in CRC (non-CRC: 1260 samples; CRC: 2259 samples). (A) Inclusion flowchart of mRNA datasets. (B) SMD diagram, funnel plot, and SROC diagram. PLK1: polo-like kinase 1; CRC, colorectal cancer; SMD, standardized mean difference; SROC, summary receiver operating characteristic.

Journal: Frontiers in Oncology

Article Title: Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study

doi: 10.3389/fonc.2026.1824796

Figure Lengend Snippet: PLK1 is highly expressed at the mRNA level in CRC (non-CRC: 1260 samples; CRC: 2259 samples). (A) Inclusion flowchart of mRNA datasets. (B) SMD diagram, funnel plot, and SROC diagram. PLK1: polo-like kinase 1; CRC, colorectal cancer; SMD, standardized mean difference; SROC, summary receiver operating characteristic.

Article Snippet: PLK1 protein expression in CRC was validated by immunohistochemistry (IHC) using data from the Human Protein Atlas (HPA, antibody HPA053229).

Techniques:

GSEA analysis of PLK1-coexpressed genes in CRC (R>0.5, P<0.05). (A) Pathway enrichment results. (B) Enrichment pathway network diagram. It shows the relationship between various pathways; the node size represents the number of gene sets, and the color represents the enrichment intensity, revealing that PLK1 is mainly involved in the cell cycle regulatory network. PLK1: polo-like kinase 1; CRC, colorectal cancer; GSEA, Gene Set Enrichment Analysis.

Journal: Frontiers in Oncology

Article Title: Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study

doi: 10.3389/fonc.2026.1824796

Figure Lengend Snippet: GSEA analysis of PLK1-coexpressed genes in CRC (R>0.5, P<0.05). (A) Pathway enrichment results. (B) Enrichment pathway network diagram. It shows the relationship between various pathways; the node size represents the number of gene sets, and the color represents the enrichment intensity, revealing that PLK1 is mainly involved in the cell cycle regulatory network. PLK1: polo-like kinase 1; CRC, colorectal cancer; GSEA, Gene Set Enrichment Analysis.

Article Snippet: PLK1 protein expression in CRC was validated by immunohistochemistry (IHC) using data from the Human Protein Atlas (HPA, antibody HPA053229).

Techniques:

PLK1 is highly expressed at the protein level in CRC. (A) Immunohistochemical staining. (B) Expression density distribution diagram. (C) Comparison of expression levels. (D) ROC curve analysis. Data in B-D are from Proteomic Data Commons (30 normal cases vs 42 CRC cases). PLK1, polo-like kinase 1; CRC, colorectal cancer; ROC, receiver operating characteristic.

Journal: Frontiers in Oncology

Article Title: Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study

doi: 10.3389/fonc.2026.1824796

Figure Lengend Snippet: PLK1 is highly expressed at the protein level in CRC. (A) Immunohistochemical staining. (B) Expression density distribution diagram. (C) Comparison of expression levels. (D) ROC curve analysis. Data in B-D are from Proteomic Data Commons (30 normal cases vs 42 CRC cases). PLK1, polo-like kinase 1; CRC, colorectal cancer; ROC, receiver operating characteristic.

Article Snippet: PLK1 protein expression in CRC was validated by immunohistochemistry (IHC) using data from the Human Protein Atlas (HPA, antibody HPA053229).

Techniques: Immunohistochemical staining, Staining, Expressing, Comparison

Spatial transcriptomics reveals PLK1-related spatial distribution patterns and microenvironmental features in tumor tissue. (A) Spatial maps showing LogTPM expression of proliferation markers PLK1 and MKI67, neutrophil fraction, and inferred cell-type fractions (malignant, macrophage, endothelial, CAF, plasma, B cell, CD4 + T cell, CD8 + T cell, NK cell, cDC, pDC, and mast cell). (B) Correlation heatmap of cell-type abundances estimated by multiple deconvolution algorithms (CIBERSORT, CIBERSORT_ABS, EPIC, ESTIMATE, MCPcounter, Quantiseq, TIMER, xCell) across GEO datasets. (C) Histogram of permuted Lee’s L spatial statistic (observed L = −0.156).

Journal: Frontiers in Oncology

Article Title: Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study

doi: 10.3389/fonc.2026.1824796

Figure Lengend Snippet: Spatial transcriptomics reveals PLK1-related spatial distribution patterns and microenvironmental features in tumor tissue. (A) Spatial maps showing LogTPM expression of proliferation markers PLK1 and MKI67, neutrophil fraction, and inferred cell-type fractions (malignant, macrophage, endothelial, CAF, plasma, B cell, CD4 + T cell, CD8 + T cell, NK cell, cDC, pDC, and mast cell). (B) Correlation heatmap of cell-type abundances estimated by multiple deconvolution algorithms (CIBERSORT, CIBERSORT_ABS, EPIC, ESTIMATE, MCPcounter, Quantiseq, TIMER, xCell) across GEO datasets. (C) Histogram of permuted Lee’s L spatial statistic (observed L = −0.156).

Article Snippet: PLK1 protein expression in CRC was validated by immunohistochemistry (IHC) using data from the Human Protein Atlas (HPA, antibody HPA053229).

Techniques: Spatial Transcriptomics, Expressing, Clinical Proteomics

Knockdown of PLK1 inhibits CRC-related cells. A negative CRISPR score indicates that the gene is essential for cell survival, and a more negative score indicates a more significant inhibition of cell growth after knockdown. PLK1, polo-like kinase 1; CRC, colorectal cancer; CRISPR, clustered regularly interspaced short palindromic repeats.

Journal: Frontiers in Oncology

Article Title: Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study

doi: 10.3389/fonc.2026.1824796

Figure Lengend Snippet: Knockdown of PLK1 inhibits CRC-related cells. A negative CRISPR score indicates that the gene is essential for cell survival, and a more negative score indicates a more significant inhibition of cell growth after knockdown. PLK1, polo-like kinase 1; CRC, colorectal cancer; CRISPR, clustered regularly interspaced short palindromic repeats.

Article Snippet: PLK1 protein expression in CRC was validated by immunohistochemistry (IHC) using data from the Human Protein Atlas (HPA, antibody HPA053229).

Techniques: Knockdown, CRISPR, Inhibition

PLK1 is downregulated at the mRNA and protein levels after NC treatment. (A) Transcriptome sequencing verification. The mRNA expression of PLK1 in HCT116 cells was significantly downregulated after NC treatment. P < 0.01 vs control group. (B) RT-qPCR verification. The mRNA expression level of PLK1 was significantly reduced after treatment with NC (6 μmol/L) for 48h. Data are expressed as mean ± standard deviation. ***P < 0.001 vs control group. (C) In vivo immunohistochemical verification. Detection of PLK1 protein expression in ectopic xenograft tissues of mice. NC downregulated PLK1 protein expression in a dose-dependent manner, and the bar chart in the lower right corner shows the quantitative analysis of the average optical density value of each group. ***P < 0.001 vs control group. NC, Nitidine Chloride; PLK1, polo-like kinase 1.

Journal: Frontiers in Oncology

Article Title: Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study

doi: 10.3389/fonc.2026.1824796

Figure Lengend Snippet: PLK1 is downregulated at the mRNA and protein levels after NC treatment. (A) Transcriptome sequencing verification. The mRNA expression of PLK1 in HCT116 cells was significantly downregulated after NC treatment. P < 0.01 vs control group. (B) RT-qPCR verification. The mRNA expression level of PLK1 was significantly reduced after treatment with NC (6 μmol/L) for 48h. Data are expressed as mean ± standard deviation. ***P < 0.001 vs control group. (C) In vivo immunohistochemical verification. Detection of PLK1 protein expression in ectopic xenograft tissues of mice. NC downregulated PLK1 protein expression in a dose-dependent manner, and the bar chart in the lower right corner shows the quantitative analysis of the average optical density value of each group. ***P < 0.001 vs control group. NC, Nitidine Chloride; PLK1, polo-like kinase 1.

Article Snippet: PLK1 protein expression in CRC was validated by immunohistochemistry (IHC) using data from the Human Protein Atlas (HPA, antibody HPA053229).

Techniques: Sequencing, Expressing, Control, Quantitative RT-PCR, Standard Deviation, In Vivo, Immunohistochemical staining

MYCN directly binds to the PLK1 promoter and both genes are downregulated by Nitidine Chloride. (A) Genome browser tracks showing MYCN ChIP-seq signal and H3K27ac enrichment across the PLK1 genomic locus. The genomic coordinates and gene annotation are shown below. (B) Sequence logo representing the predicted MYCN–MAX binding motif (E-box) identified within the PLK1 promoter region. (C) Structural model of the MYCN–MAX complex in association with the PLK1 promoter DNA sequence generated by AlphaFold-Multimer and protein–DNA docking. The structure is colored according to pLDDT confidence scores. (D) Predicted aligned error (PAE) plot of the MYCN–MAX complex, indicating the confidence of relative positioning between residues.

Journal: Frontiers in Oncology

Article Title: Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study

doi: 10.3389/fonc.2026.1824796

Figure Lengend Snippet: MYCN directly binds to the PLK1 promoter and both genes are downregulated by Nitidine Chloride. (A) Genome browser tracks showing MYCN ChIP-seq signal and H3K27ac enrichment across the PLK1 genomic locus. The genomic coordinates and gene annotation are shown below. (B) Sequence logo representing the predicted MYCN–MAX binding motif (E-box) identified within the PLK1 promoter region. (C) Structural model of the MYCN–MAX complex in association with the PLK1 promoter DNA sequence generated by AlphaFold-Multimer and protein–DNA docking. The structure is colored according to pLDDT confidence scores. (D) Predicted aligned error (PAE) plot of the MYCN–MAX complex, indicating the confidence of relative positioning between residues.

Article Snippet: PLK1 protein expression in CRC was validated by immunohistochemistry (IHC) using data from the Human Protein Atlas (HPA, antibody HPA053229).

Techniques: ChIP-sequencing, Sequencing, Binding Assay, Generated

High MYCN mRNA expression in CRC. (A) Forest plot showing the standardized mean difference (SMD) in MYCN mRNA expression levels between CRC (experimental) and normal control groups across multiple studies/datasets, with pooled estimates for common-effect and random-effects models, heterogeneity statistics, summary receiver operating characteristic (SROC) curve, and publication bias tests (Egger’s and Begg’s). (B) Heatmap of Pearson correlation coefficients (R) between PLK1 and MYCN mRNA expression across the listed studies (significant correlations marked with asterisks).

Journal: Frontiers in Oncology

Article Title: Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study

doi: 10.3389/fonc.2026.1824796

Figure Lengend Snippet: High MYCN mRNA expression in CRC. (A) Forest plot showing the standardized mean difference (SMD) in MYCN mRNA expression levels between CRC (experimental) and normal control groups across multiple studies/datasets, with pooled estimates for common-effect and random-effects models, heterogeneity statistics, summary receiver operating characteristic (SROC) curve, and publication bias tests (Egger’s and Begg’s). (B) Heatmap of Pearson correlation coefficients (R) between PLK1 and MYCN mRNA expression across the listed studies (significant correlations marked with asterisks).

Article Snippet: PLK1 protein expression in CRC was validated by immunohistochemistry (IHC) using data from the Human Protein Atlas (HPA, antibody HPA053229).

Techniques: Expressing, Control