Journal: Cell Genomics

Article Title: Single-cell profiling of bone metastasis ecosystems from multiple cancer types reveals convergent and divergent mechanisms of bone colonization

doi: 10.1016/j.xgen.2025.100888

Figure Lengend Snippet: Bone stromal drives divergent bone colonization and immune evasion mechanisms (A) Analysis of cell-cell communication signal flow. Outgoing signal strength is shown on the x axis and incoming signal strength on the y axis, comparing the Mφ-OC and Treg-Tex archetypes with healthy samples serving as references. (B) Identification of key ligand-receptor pairs that differentially regulate the OC populations. This analysis compares the relative signaling strengths between the Mφ-OC and Treg-Tex archetypes, focusing on osteoclasts as the signal receivers (from A). (C) Schematic illustration of in vitro experimental validation for estimated signaling molecules. CD14 + monocytes isolated from human peripheral blood were enriched for osteoclastogenesis induction, with selected factors added to the culture medium to test their predicted roles in regulating differential osteoclastogenesis. Osteoclastogenesis was then evaluated by both qPCR and TRAP staining. (D) qPCR analysis of osteoclast signature genes to validate differential osteoclastogenesis regulation by estimated signaling molecules. Each signaling factor was tested using graded concentrations: TWEAK (TNFSF12; 0.1, 1, 10 ng/μL), COMP (5, 50, 500 ng/μL), and NRG1 (10, 100, 1000 ng/μL), TNFSF10 (1, 10, 100 ng/μL), SEMA4A (1, 10, 100 ng/μL), EFNA5 (1, 10, 100 ng/μL), BMP8A (1, 10, 100 ng/μL). Each condition has five replicates. Statistical significance was assessed using one-way ANOVA, with significance levels: ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001.

Article Snippet: recombinant human EFNA5 , Sino Biological , Cat#10192-H08H-100.

Techniques: In Vitro, Biomarker Discovery, Isolation, Staining

Journal: bioRxiv

Article Title: DCHS1 Modulates Forebrain Proportions in Modern Humans via a Glycosylation Change

doi: 10.1101/2025.05.14.654031

Figure Lengend Snippet: (a) Schematic representation of the selection process for ephrin signaling interactions. Co-immunoprecipitation mass spectrometry identified 5157 proteins, of which 1327 were differentially bound (DB; p < 0.05, FC > 1 vs. GFP). In parallel, CellChat analysis of scRNA-seq data tested 229 ligand–receptor networks, identifying 16 differentially regulated (DR; p < 0.05) interactions based on signaling strength. Ephrin signaling was selected as a key candidate pathway by intersecting both datasets, guiding further analysis of its role in aDCHS1 and hDCHS1 organoids. (b) Significant signaling pathways ranked based on differences in overall information flow within the inferred networks between aDCHS1 and hDCHS1. Pathways enriched in aDCHS1 are shown in teal, equally enriched pathways in black, and pathways enriched in hDCHS1 in yellow. (c) Fold-change differences in protein abundance from immunoprecipitation (IP) analysis between aDCHS1 and hDCHS1. (d) Representative fluorescence images of DAPI (blue), DCHS1 (green), and EPHA4 (magenta) in control 60-day-old neural organoids. V = ventricle; scale bars: 25 µm (individual channels) and 10 µm (merged image). (e) Representative fluorescence images of 60-day-old hDCHS1 and aDCHS1 neural organoids subjected to proximity ligation assay (PLA) to detect DCHS1-EPHA4 interactions. Nuclei were stained with DAPI. Images were acquired at 63× magnification. V = ventricle; scale bar: 10 µm. (f) Differential expression analysis of cell-cell communication events potentially deregulated between aDCHS1 and hDCHS1 related to the EPHA4 receptor. Dot color indicates enrichment in hDCHS1 (yellow) or aDCHS1 (teal). (g) Representative immunohistochemistry (IHC) images and quantification of PAX6+ and MEIS2+ cells in 30-day-old neural organoids derived from human iPSCs, treated with EFNA5, EFNB2, or left untreated. Statistical significance was assessed using a binomial test by comparing each treated condition to the untreated condition individually. For PAX6 (Batch=1), n = 4 organoids per condition; total number of ventricles: Untreated = 23, EFNA5 = 62, EFNB2 = 45. For MEIS2 (Batch=1), n = 4 organoids per condition; total number of ventricles: Untreated = 30, EFNA5 = 35, EFNB2 = 49. (h) Dot plot showing the expression of EPHA4, EFNA5, EFNB2, EFNB3 and EFNB1 genes in the Excitatory, Inhibitory and Striatal lineage. Dot color represents the average expression level, and dot size indicates the proportion of cells expressing each gene.

Article Snippet: Human brain organoids were treated with either recombinant EFNA5 (MCE, Cat. No.: HY-P70379) or EFNB2 (MCE, Cat. No.: HY-P77645) protein to study their effects on organoid development.

Techniques: Selection, Immunoprecipitation, Mass Spectrometry, Protein-Protein interactions, Quantitative Proteomics, Fluorescence, Control, Proximity Ligation Assay, Staining, Immunohistochemistry, Derivative Assay, Expressing

Journal: Discover Oncology

Article Title: EFNA5 suppresses cell proliferation and tumor metastasis in hepatoma via epithelial-to-mesenchymal transition

doi: 10.1007/s12672-024-01454-7

Figure Lengend Snippet: EFNA5 expression is associated with good prognosis in hepatoma. A TCGA analysis of EFNA5 expression difference between liver tumor tissue and normal liver tissue. ** P < 0.01. B KM-plotter analysis of connection between EFNA5 expression and prognosis in hepatoma. C STRING online analysis of EFNA5 and related genes. D GO enrichment analysis of differential genes in hepatoma. E KEGG enrichment analysis of differential genes in hepatoma. F , G Representative IHC images and average density scores of EFNA5 expression in hepatoma and adjacent tissues

Article Snippet: In this experiment, the used antibodies are as follows: EFNA5 (Cat. No. ABP50058, Abbkine), GAPDH (Cat. No. AP0063, Bioworld Technology), B-actin (Cat. No. 8480, CST), EGFR (Cat. No. 51067-2-AP, PTG), E-cadherin (Cat. No. 20874-1-AP, PTG), N-cadherin (Cat. No. 13769-1-AP, PTG), c-Jun (Cat. No. 9165, CST), c-Myc (Cat. No. ab32072, Abcam), and vimentin (VIM) (Cat. No. 60330-1-Ig, PTG); HRP labeled anti-rabbit/mouse secondary antibody were purchased from Epitomics Biotechnology company.

Techniques: Expressing

Journal: Discover Oncology

Article Title: EFNA5 suppresses cell proliferation and tumor metastasis in hepatoma via epithelial-to-mesenchymal transition

doi: 10.1007/s12672-024-01454-7

Figure Lengend Snippet: EFNA5 inhibits the proliferation of hepatoma cells. A EFNA5 expression in hepatoma cell lines and normal hepatic epithelial cell line at the RNA levels by quantitative real-time PCR. *** P < 0.001. B Expression of EFNA5 in EFNA5-overexpressing HepG2 and LM3 cells, as detected by quantitative real-time PCR assays. C , D The proliferation ability of EFNA5 overexpressed hepatoma cells in LM3 and HepG2 cells was measured by CCK-8 method compared with the control group

Article Snippet: In this experiment, the used antibodies are as follows: EFNA5 (Cat. No. ABP50058, Abbkine), GAPDH (Cat. No. AP0063, Bioworld Technology), B-actin (Cat. No. 8480, CST), EGFR (Cat. No. 51067-2-AP, PTG), E-cadherin (Cat. No. 20874-1-AP, PTG), N-cadherin (Cat. No. 13769-1-AP, PTG), c-Jun (Cat. No. 9165, CST), c-Myc (Cat. No. ab32072, Abcam), and vimentin (VIM) (Cat. No. 60330-1-Ig, PTG); HRP labeled anti-rabbit/mouse secondary antibody were purchased from Epitomics Biotechnology company.

Techniques: Expressing, Real-time Polymerase Chain Reaction, CCK-8 Assay, Control

Journal: Discover Oncology

Article Title: EFNA5 suppresses cell proliferation and tumor metastasis in hepatoma via epithelial-to-mesenchymal transition

doi: 10.1007/s12672-024-01454-7

Figure Lengend Snippet: EFNA5 can inhibit the migration and invasion of hepatoma cells. A , B Representative images and quantitative analysis of cell migration based on Transwell assays. C , D The representative images and quantitative dat of the EdU assay in HepG2 and LM3

Article Snippet: In this experiment, the used antibodies are as follows: EFNA5 (Cat. No. ABP50058, Abbkine), GAPDH (Cat. No. AP0063, Bioworld Technology), B-actin (Cat. No. 8480, CST), EGFR (Cat. No. 51067-2-AP, PTG), E-cadherin (Cat. No. 20874-1-AP, PTG), N-cadherin (Cat. No. 13769-1-AP, PTG), c-Jun (Cat. No. 9165, CST), c-Myc (Cat. No. ab32072, Abcam), and vimentin (VIM) (Cat. No. 60330-1-Ig, PTG); HRP labeled anti-rabbit/mouse secondary antibody were purchased from Epitomics Biotechnology company.

Techniques: Migration, EdU Assay

Journal: Discover Oncology

Article Title: EFNA5 suppresses cell proliferation and tumor metastasis in hepatoma via epithelial-to-mesenchymal transition

doi: 10.1007/s12672-024-01454-7

Figure Lengend Snippet: EFNA5 inhibits EMT in hepatoma cells. A – C Analysis of epithelial–mesenchymal transition markers by western blotting and quantitative analysis in EFNA5 overexpression cell lysates. Overexpression of EFNA5 suppressed the protein levels of GAPDH, c-Myc, c-Jun, E-cadherin, N-cadherin, VIM, EGFR, and EFNA5 in HepG2 and LM3 cells

Article Snippet: In this experiment, the used antibodies are as follows: EFNA5 (Cat. No. ABP50058, Abbkine), GAPDH (Cat. No. AP0063, Bioworld Technology), B-actin (Cat. No. 8480, CST), EGFR (Cat. No. 51067-2-AP, PTG), E-cadherin (Cat. No. 20874-1-AP, PTG), N-cadherin (Cat. No. 13769-1-AP, PTG), c-Jun (Cat. No. 9165, CST), c-Myc (Cat. No. ab32072, Abcam), and vimentin (VIM) (Cat. No. 60330-1-Ig, PTG); HRP labeled anti-rabbit/mouse secondary antibody were purchased from Epitomics Biotechnology company.

Techniques: Western Blot, Over Expression