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Human Protein Atlas vcam1 protein expression
<t>VCAM1</t> is expressed in glioma stem cells of eGFP+ 73C and eGFP+ GL261-luc tumor models in vivo. (A) Schematic timeline illustrating glioma cell implantation and acute cell staining. Gliomas were induced by intracranial implantation of 5,000–6,000 eGFP + 73C or eGFP + GL261-luc tumor cells in C57BL/6J mice. Acute cell staining was performed on day 12 post-implantation for eGFP + 73C and on day 20 for eGFP + GL261-luc. (B) Co-staining of VCAM1 with other glioma stem cell markers (SOX2, CD133, Nestin) and Ki-67 in acutely isolated eGFP + 73C glioma at 12 days post-implantation. Scale bar, 10 μm. (C) Co-staining of VCAM1 with other glioma stem cell markers (SOX2, CD133, Nestin) and Ki-67 in acutely isolated eGFP + GL261-luc glioma at 20 days post-implantation. Scale bar, 10 μm. (D) Quantitative analysis of the percentage of VCAM1-expressing cells in different glioma stem cell type populations in eGFP + 73C glioma. Data represent mean ± SEM (n = 6 biological replicates). Six randomly selected 500 × 500 μm regions were analyzed per sample. (E) Quantitative analysis of the percentage of VCAM1-expressing cells in different glioma stem cell type populations in eGFP + GL261-luc glioma. Data represent mean ± SEM, n = 6 repeats. Six 500 μm×500 μm regions were randomly selected.
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1) Product Images from "Glia-derived VCAM1 promotes glioma progression"

Article Title: Glia-derived VCAM1 promotes glioma progression

Journal: Frontiers in Oncology

doi: 10.3389/fonc.2026.1802953

VCAM1 is expressed in glioma stem cells of eGFP+ 73C and eGFP+ GL261-luc tumor models in vivo. (A) Schematic timeline illustrating glioma cell implantation and acute cell staining. Gliomas were induced by intracranial implantation of 5,000–6,000 eGFP + 73C or eGFP + GL261-luc tumor cells in C57BL/6J mice. Acute cell staining was performed on day 12 post-implantation for eGFP + 73C and on day 20 for eGFP + GL261-luc. (B) Co-staining of VCAM1 with other glioma stem cell markers (SOX2, CD133, Nestin) and Ki-67 in acutely isolated eGFP + 73C glioma at 12 days post-implantation. Scale bar, 10 μm. (C) Co-staining of VCAM1 with other glioma stem cell markers (SOX2, CD133, Nestin) and Ki-67 in acutely isolated eGFP + GL261-luc glioma at 20 days post-implantation. Scale bar, 10 μm. (D) Quantitative analysis of the percentage of VCAM1-expressing cells in different glioma stem cell type populations in eGFP + 73C glioma. Data represent mean ± SEM (n = 6 biological replicates). Six randomly selected 500 × 500 μm regions were analyzed per sample. (E) Quantitative analysis of the percentage of VCAM1-expressing cells in different glioma stem cell type populations in eGFP + GL261-luc glioma. Data represent mean ± SEM, n = 6 repeats. Six 500 μm×500 μm regions were randomly selected.
Figure Legend Snippet: VCAM1 is expressed in glioma stem cells of eGFP+ 73C and eGFP+ GL261-luc tumor models in vivo. (A) Schematic timeline illustrating glioma cell implantation and acute cell staining. Gliomas were induced by intracranial implantation of 5,000–6,000 eGFP + 73C or eGFP + GL261-luc tumor cells in C57BL/6J mice. Acute cell staining was performed on day 12 post-implantation for eGFP + 73C and on day 20 for eGFP + GL261-luc. (B) Co-staining of VCAM1 with other glioma stem cell markers (SOX2, CD133, Nestin) and Ki-67 in acutely isolated eGFP + 73C glioma at 12 days post-implantation. Scale bar, 10 μm. (C) Co-staining of VCAM1 with other glioma stem cell markers (SOX2, CD133, Nestin) and Ki-67 in acutely isolated eGFP + GL261-luc glioma at 20 days post-implantation. Scale bar, 10 μm. (D) Quantitative analysis of the percentage of VCAM1-expressing cells in different glioma stem cell type populations in eGFP + 73C glioma. Data represent mean ± SEM (n = 6 biological replicates). Six randomly selected 500 × 500 μm regions were analyzed per sample. (E) Quantitative analysis of the percentage of VCAM1-expressing cells in different glioma stem cell type populations in eGFP + GL261-luc glioma. Data represent mean ± SEM, n = 6 repeats. Six 500 μm×500 μm regions were randomly selected.

Techniques Used: In Vivo, Staining, Isolation, Expressing

VCAM1 is expressed in glioma stem cell-like cells of gDAM-induced primary glioma in vivo . (A) Schematic timeline for the application of the gDAM method in C57BL/6J mice, involving the injection of a plasmid combination and proline mixture for gliomagenesis. (B) Labeling of tdTomato-expressing astrocytes in the brain of Ai14 mice using a Cre-expressing plasmid delivered via the gDAM method. Scale bar, 100 μm. (C) An astrocyte expressing tdTomato with characteristic endfoot structures. Scale bar, 20 μm. (D) gDAM-induced primary glioma observed at five months, showing immunostaining for Ki67 (green), VCAM1 (purple), and mCherry + tumor cells (red). Scale bar, 2 mm. (E) SOX2-expressing mCherry + tumor cells in a five-month-old primary glioma, indicated by yellow arrows. Scale bar, 20 μm. (F) Expression patterns of VCAM1, SOX2 and tumor cells in GC and TSM. GC, glioma core; TSM, tumor substantial margins. Scale bar, 20 μm. (G) The proportion of SOX2 + mCherry + cells relative to the total mCherry + cells in the GC and the TSM. * p = 0.0313. Data are presented as mean ± SEM (n = 6 randomly selected fields derived from 3 mice per group). Statistical significance was determined by unpaired two-tailed Student’s t-test. (H) Relative fluorescence intensity of VCAM1 in the GC and TSM, based on randomly selected 200 μm × 200 μm regions. n.s. p = 0.1563. Data are presented as mean ± SEM (n = 6 randomly selected fields derived from 3 mice per group). Statistical significance was determined by unpaired two-tailed Student’s t-test.
Figure Legend Snippet: VCAM1 is expressed in glioma stem cell-like cells of gDAM-induced primary glioma in vivo . (A) Schematic timeline for the application of the gDAM method in C57BL/6J mice, involving the injection of a plasmid combination and proline mixture for gliomagenesis. (B) Labeling of tdTomato-expressing astrocytes in the brain of Ai14 mice using a Cre-expressing plasmid delivered via the gDAM method. Scale bar, 100 μm. (C) An astrocyte expressing tdTomato with characteristic endfoot structures. Scale bar, 20 μm. (D) gDAM-induced primary glioma observed at five months, showing immunostaining for Ki67 (green), VCAM1 (purple), and mCherry + tumor cells (red). Scale bar, 2 mm. (E) SOX2-expressing mCherry + tumor cells in a five-month-old primary glioma, indicated by yellow arrows. Scale bar, 20 μm. (F) Expression patterns of VCAM1, SOX2 and tumor cells in GC and TSM. GC, glioma core; TSM, tumor substantial margins. Scale bar, 20 μm. (G) The proportion of SOX2 + mCherry + cells relative to the total mCherry + cells in the GC and the TSM. * p = 0.0313. Data are presented as mean ± SEM (n = 6 randomly selected fields derived from 3 mice per group). Statistical significance was determined by unpaired two-tailed Student’s t-test. (H) Relative fluorescence intensity of VCAM1 in the GC and TSM, based on randomly selected 200 μm × 200 μm regions. n.s. p = 0.1563. Data are presented as mean ± SEM (n = 6 randomly selected fields derived from 3 mice per group). Statistical significance was determined by unpaired two-tailed Student’s t-test.

Techniques Used: In Vivo, Injection, Plasmid Preparation, Labeling, Expressing, Immunostaining, Derivative Assay, Two Tailed Test, Fluorescence

VCAM1 is expressed in a subset of GLAST+ astrocytes in glioma-bearing mice. (A) Experimental timeline for glioma cell implantation in GLAST-CreER::Ai14 mice. Mice received daily intraperitoneal injections of tamoxifen (TAM) for one week, followed by a one-week resting period. On day 1, 5,000-6,000 eGFP + 73C or GL261-luc glioma cells were implanted beneath the hippocampus. Tumor-bearing mice were harvested on day 10 (eGFP + 73C) or day 20 (GL261-luc). (B) Immunofluorescence staining of VCAM1 in eGFP + 73C gliomas at day 10 post-implantation of GLAST-CreER::Ai14 mice. Scale bars: (B) 1 mm; (a), 500 μm; (a’, b’), 100μm. (C) Immunofluorescence staining of VCAM1 in GL261-luc gliomas at day 20 post-implantation of GLAST-CreER::Ai14 mice. Scale bars: (C) 1 mm; (a), 500 μm; (a’), 100 μm.
Figure Legend Snippet: VCAM1 is expressed in a subset of GLAST+ astrocytes in glioma-bearing mice. (A) Experimental timeline for glioma cell implantation in GLAST-CreER::Ai14 mice. Mice received daily intraperitoneal injections of tamoxifen (TAM) for one week, followed by a one-week resting period. On day 1, 5,000-6,000 eGFP + 73C or GL261-luc glioma cells were implanted beneath the hippocampus. Tumor-bearing mice were harvested on day 10 (eGFP + 73C) or day 20 (GL261-luc). (B) Immunofluorescence staining of VCAM1 in eGFP + 73C gliomas at day 10 post-implantation of GLAST-CreER::Ai14 mice. Scale bars: (B) 1 mm; (a), 500 μm; (a’, b’), 100μm. (C) Immunofluorescence staining of VCAM1 in GL261-luc gliomas at day 20 post-implantation of GLAST-CreER::Ai14 mice. Scale bars: (C) 1 mm; (a), 500 μm; (a’), 100 μm.

Techniques Used: Immunofluorescence, Staining

Knockout of VCAM1 in GLAST+ cells prolongs mouse survival. (A) Experimental timeline for glioma cell implantation in GLAST-CreER::VCAM1 fl/fl and control mice. Mice received daily intraperitoneal injections of tamoxifen (TAM) for one week, followed by a one-week waiting period. On day 1, 5,000-6,000 tumor cells were injected into the cortex or below the hippocampus. Live imaging analysis was conducted at the predetermined points. (B) Kaplan-Meier survival curves of mice implanted with eGFP+ 73C tumor cells below the hippocampus. Control group (n = 6), GLAST-CreER::VCAM1fl/fl group (n = 6). p-value calculated using the log-rank Mantel-Cox test. Control vs GLAST-CreER::VCAM1fl/fl, “ns” indicates no statistical significance ( p > 0.05). Here, p = 0.1209. (C) Kaplan-Meier survival curves of mice implanted with eGFP+ 73C tumor cells in the cortex. Control group (n = 6), GLAST-CreER::VCAM1fl/fl group (n = 6). p-value calculated using the log-rank Mantel-Cox test. Control vs GLAST-CreER::VCAM1fl/fl, ** p = 0.0053. (D) Live imaging analysis of GL261-luc-bearing mice in hippocampus GLAST-CreER::VCAM1 fl/fl and control groups at days 9, 28 and 50. (E) Kaplan-Meier survival curves of mice implanted with GL261-luc tumor cells below the hippocampus. Control group (n = 7), GLAST-CreER::VCAM1 fl/fl group (n = 6). p -value calculated using the log-rank Mantel-Cox test. Control vs. GLAST-CreER::VCAM1 fl/fl , * p = 0.0223. (F) Longitudinal quantification of tumor burden by bioluminescence imaging (Total Flux) in the Hippocampus GL261-luc models. Data are presented as mean ± SEM. Statistical significance was evaluated using Two-way repeated measures ANOVA. The asterisks indicate a significant interaction effect between time and genotype, ** p = 0.0082. Data are presented as mean ± SEM (n = 6–7 mice per group). Statistical significance was evaluated using two-way repeated measures ANOVA. (G) Live imaging analysis of GL261-luc-bearing mice in cortex from the GLAST-CreER::VCAM1 fl/fl and control groups at days 20, 40, 60. (H) Kaplan-Meier survival curves of mice implanted with GL261-luc tumor cells in the cortex. Control group (n = 7), GLAST-CreER::VCAM1 fl/fl group (n = 6). p -value calculated using the log-rank Mantel-Cox test. Control vs. GLAST-CreER::VCAM1 fl/fl , * p = 0.0465. (I) Longitudinal quantification of tumor burden by bioluminescence imaging (Total Flux) in the Cortex GL261-luc models. Data are presented as mean ± SEM. Statistical significance was evaluated using Two-way repeated measures ANOVA. The asterisks indicate a significant interaction effect between time and genotype, * p = 0.0106. Data are presented as mean ± SEM (n = 6–7 mice per group). Statistical significance was evaluated using two-way repeated measures ANOVA.
Figure Legend Snippet: Knockout of VCAM1 in GLAST+ cells prolongs mouse survival. (A) Experimental timeline for glioma cell implantation in GLAST-CreER::VCAM1 fl/fl and control mice. Mice received daily intraperitoneal injections of tamoxifen (TAM) for one week, followed by a one-week waiting period. On day 1, 5,000-6,000 tumor cells were injected into the cortex or below the hippocampus. Live imaging analysis was conducted at the predetermined points. (B) Kaplan-Meier survival curves of mice implanted with eGFP+ 73C tumor cells below the hippocampus. Control group (n = 6), GLAST-CreER::VCAM1fl/fl group (n = 6). p-value calculated using the log-rank Mantel-Cox test. Control vs GLAST-CreER::VCAM1fl/fl, “ns” indicates no statistical significance ( p > 0.05). Here, p = 0.1209. (C) Kaplan-Meier survival curves of mice implanted with eGFP+ 73C tumor cells in the cortex. Control group (n = 6), GLAST-CreER::VCAM1fl/fl group (n = 6). p-value calculated using the log-rank Mantel-Cox test. Control vs GLAST-CreER::VCAM1fl/fl, ** p = 0.0053. (D) Live imaging analysis of GL261-luc-bearing mice in hippocampus GLAST-CreER::VCAM1 fl/fl and control groups at days 9, 28 and 50. (E) Kaplan-Meier survival curves of mice implanted with GL261-luc tumor cells below the hippocampus. Control group (n = 7), GLAST-CreER::VCAM1 fl/fl group (n = 6). p -value calculated using the log-rank Mantel-Cox test. Control vs. GLAST-CreER::VCAM1 fl/fl , * p = 0.0223. (F) Longitudinal quantification of tumor burden by bioluminescence imaging (Total Flux) in the Hippocampus GL261-luc models. Data are presented as mean ± SEM. Statistical significance was evaluated using Two-way repeated measures ANOVA. The asterisks indicate a significant interaction effect between time and genotype, ** p = 0.0082. Data are presented as mean ± SEM (n = 6–7 mice per group). Statistical significance was evaluated using two-way repeated measures ANOVA. (G) Live imaging analysis of GL261-luc-bearing mice in cortex from the GLAST-CreER::VCAM1 fl/fl and control groups at days 20, 40, 60. (H) Kaplan-Meier survival curves of mice implanted with GL261-luc tumor cells in the cortex. Control group (n = 7), GLAST-CreER::VCAM1 fl/fl group (n = 6). p -value calculated using the log-rank Mantel-Cox test. Control vs. GLAST-CreER::VCAM1 fl/fl , * p = 0.0465. (I) Longitudinal quantification of tumor burden by bioluminescence imaging (Total Flux) in the Cortex GL261-luc models. Data are presented as mean ± SEM. Statistical significance was evaluated using Two-way repeated measures ANOVA. The asterisks indicate a significant interaction effect between time and genotype, * p = 0.0106. Data are presented as mean ± SEM (n = 6–7 mice per group). Statistical significance was evaluated using two-way repeated measures ANOVA.

Techniques Used: Knock-Out, Control, Injection, Imaging

The RNA-seq reveals the changes of TME following astrocytic VCAM1 deletion. (A) The protocol of RNA-seq on tumor associated VCAM1-deficient GLAST positive astrocytes. n = 6 biological replicates per group (derived from 3 mice per group, 2 independent samples per mouse) were analyzed. (B) Differentially expressed genes in astrocytic VCAM1-deficient TME. (C, F) The KEGG and GO enrichment analysis of our inhouse dataset. (D, E, G, H) The GSEA analysis of differentially expressed genes identified several functional pathways, antigen processing and presentation, cell adhesion, oxidative phosphorylation, and cholesterol efflux.
Figure Legend Snippet: The RNA-seq reveals the changes of TME following astrocytic VCAM1 deletion. (A) The protocol of RNA-seq on tumor associated VCAM1-deficient GLAST positive astrocytes. n = 6 biological replicates per group (derived from 3 mice per group, 2 independent samples per mouse) were analyzed. (B) Differentially expressed genes in astrocytic VCAM1-deficient TME. (C, F) The KEGG and GO enrichment analysis of our inhouse dataset. (D, E, G, H) The GSEA analysis of differentially expressed genes identified several functional pathways, antigen processing and presentation, cell adhesion, oxidative phosphorylation, and cholesterol efflux.

Techniques Used: RNA Sequencing, Derivative Assay, Functional Assay, Phospho-proteomics

Clinical relevance of VCAM1 expression in human gliomas based on public database analysis. (A) Kaplan-Meier survival curve of patients with lower grade glioma and glioblastoma (GBMLGG) with different expression levels of VCAM1 in TCGA. The p-value was calculated using log-rank test (Mantel-Cox test). VCAM1>=9.605 (n=351) vs VCAM1<9.605 (n=343) *** p = 0.000001255. (B) Kaplan-Meier survival curve of patients with lower grade glioma (LGG) with different expression levels of VCAM1 in TCGA. The p-value was calculated using Mantel-Cox test. VCAM1>=9.243 (n=265) vs VCAM1<9.243 (n=263) ** p = 0.001199. (C) Kaplan-Meier survival curve of patients with glioblastoma (GBM) with different expression levels of VCAM1 in TCGA. The p-value was calculated using Mantel-Cox test. VCAM1>=10.25 (n=86) vs VCAM1<10.25 (n=80) ns p = 0.8022. (D) A 32-year-old female with moderate staining intensity of VCAM1 protein expression in LGG. Images were obtained from the Human Protein Atlas (HPA) database.
Figure Legend Snippet: Clinical relevance of VCAM1 expression in human gliomas based on public database analysis. (A) Kaplan-Meier survival curve of patients with lower grade glioma and glioblastoma (GBMLGG) with different expression levels of VCAM1 in TCGA. The p-value was calculated using log-rank test (Mantel-Cox test). VCAM1>=9.605 (n=351) vs VCAM1<9.605 (n=343) *** p = 0.000001255. (B) Kaplan-Meier survival curve of patients with lower grade glioma (LGG) with different expression levels of VCAM1 in TCGA. The p-value was calculated using Mantel-Cox test. VCAM1>=9.243 (n=265) vs VCAM1<9.243 (n=263) ** p = 0.001199. (C) Kaplan-Meier survival curve of patients with glioblastoma (GBM) with different expression levels of VCAM1 in TCGA. The p-value was calculated using Mantel-Cox test. VCAM1>=10.25 (n=86) vs VCAM1<10.25 (n=80) ns p = 0.8022. (D) A 32-year-old female with moderate staining intensity of VCAM1 protein expression in LGG. Images were obtained from the Human Protein Atlas (HPA) database.

Techniques Used: Expressing, Staining



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<t>VCAM1</t> is expressed in glioma stem cells of eGFP+ 73C and eGFP+ GL261-luc tumor models in vivo. (A) Schematic timeline illustrating glioma cell implantation and acute cell staining. Gliomas were induced by intracranial implantation of 5,000–6,000 eGFP + 73C or eGFP + GL261-luc tumor cells in C57BL/6J mice. Acute cell staining was performed on day 12 post-implantation for eGFP + 73C and on day 20 for eGFP + GL261-luc. (B) Co-staining of VCAM1 with other glioma stem cell markers (SOX2, CD133, Nestin) and Ki-67 in acutely isolated eGFP + 73C glioma at 12 days post-implantation. Scale bar, 10 μm. (C) Co-staining of VCAM1 with other glioma stem cell markers (SOX2, CD133, Nestin) and Ki-67 in acutely isolated eGFP + GL261-luc glioma at 20 days post-implantation. Scale bar, 10 μm. (D) Quantitative analysis of the percentage of VCAM1-expressing cells in different glioma stem cell type populations in eGFP + 73C glioma. Data represent mean ± SEM (n = 6 biological replicates). Six randomly selected 500 × 500 μm regions were analyzed per sample. (E) Quantitative analysis of the percentage of VCAM1-expressing cells in different glioma stem cell type populations in eGFP + GL261-luc glioma. Data represent mean ± SEM, n = 6 repeats. Six 500 μm×500 μm regions were randomly selected.
Vcam1 Protein Expression, supplied by Human Protein Atlas, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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VCAM1 is expressed in glioma stem cells of eGFP+ 73C and eGFP+ GL261-luc tumor models in vivo. (A) Schematic timeline illustrating glioma cell implantation and acute cell staining. Gliomas were induced by intracranial implantation of 5,000–6,000 eGFP + 73C or eGFP + GL261-luc tumor cells in C57BL/6J mice. Acute cell staining was performed on day 12 post-implantation for eGFP + 73C and on day 20 for eGFP + GL261-luc. (B) Co-staining of VCAM1 with other glioma stem cell markers (SOX2, CD133, Nestin) and Ki-67 in acutely isolated eGFP + 73C glioma at 12 days post-implantation. Scale bar, 10 μm. (C) Co-staining of VCAM1 with other glioma stem cell markers (SOX2, CD133, Nestin) and Ki-67 in acutely isolated eGFP + GL261-luc glioma at 20 days post-implantation. Scale bar, 10 μm. (D) Quantitative analysis of the percentage of VCAM1-expressing cells in different glioma stem cell type populations in eGFP + 73C glioma. Data represent mean ± SEM (n = 6 biological replicates). Six randomly selected 500 × 500 μm regions were analyzed per sample. (E) Quantitative analysis of the percentage of VCAM1-expressing cells in different glioma stem cell type populations in eGFP + GL261-luc glioma. Data represent mean ± SEM, n = 6 repeats. Six 500 μm×500 μm regions were randomly selected.

Journal: Frontiers in Oncology

Article Title: Glia-derived VCAM1 promotes glioma progression

doi: 10.3389/fonc.2026.1802953

Figure Lengend Snippet: VCAM1 is expressed in glioma stem cells of eGFP+ 73C and eGFP+ GL261-luc tumor models in vivo. (A) Schematic timeline illustrating glioma cell implantation and acute cell staining. Gliomas were induced by intracranial implantation of 5,000–6,000 eGFP + 73C or eGFP + GL261-luc tumor cells in C57BL/6J mice. Acute cell staining was performed on day 12 post-implantation for eGFP + 73C and on day 20 for eGFP + GL261-luc. (B) Co-staining of VCAM1 with other glioma stem cell markers (SOX2, CD133, Nestin) and Ki-67 in acutely isolated eGFP + 73C glioma at 12 days post-implantation. Scale bar, 10 μm. (C) Co-staining of VCAM1 with other glioma stem cell markers (SOX2, CD133, Nestin) and Ki-67 in acutely isolated eGFP + GL261-luc glioma at 20 days post-implantation. Scale bar, 10 μm. (D) Quantitative analysis of the percentage of VCAM1-expressing cells in different glioma stem cell type populations in eGFP + 73C glioma. Data represent mean ± SEM (n = 6 biological replicates). Six randomly selected 500 × 500 μm regions were analyzed per sample. (E) Quantitative analysis of the percentage of VCAM1-expressing cells in different glioma stem cell type populations in eGFP + GL261-luc glioma. Data represent mean ± SEM, n = 6 repeats. Six 500 μm×500 μm regions were randomly selected.

Article Snippet: Furthermore, evaluation of VCAM1 protein expression via The Human Protein Atlas (HPA) revealed variable staining intensities among glioma patients ( ).

Techniques: In Vivo, Staining, Isolation, Expressing

VCAM1 is expressed in glioma stem cell-like cells of gDAM-induced primary glioma in vivo . (A) Schematic timeline for the application of the gDAM method in C57BL/6J mice, involving the injection of a plasmid combination and proline mixture for gliomagenesis. (B) Labeling of tdTomato-expressing astrocytes in the brain of Ai14 mice using a Cre-expressing plasmid delivered via the gDAM method. Scale bar, 100 μm. (C) An astrocyte expressing tdTomato with characteristic endfoot structures. Scale bar, 20 μm. (D) gDAM-induced primary glioma observed at five months, showing immunostaining for Ki67 (green), VCAM1 (purple), and mCherry + tumor cells (red). Scale bar, 2 mm. (E) SOX2-expressing mCherry + tumor cells in a five-month-old primary glioma, indicated by yellow arrows. Scale bar, 20 μm. (F) Expression patterns of VCAM1, SOX2 and tumor cells in GC and TSM. GC, glioma core; TSM, tumor substantial margins. Scale bar, 20 μm. (G) The proportion of SOX2 + mCherry + cells relative to the total mCherry + cells in the GC and the TSM. * p = 0.0313. Data are presented as mean ± SEM (n = 6 randomly selected fields derived from 3 mice per group). Statistical significance was determined by unpaired two-tailed Student’s t-test. (H) Relative fluorescence intensity of VCAM1 in the GC and TSM, based on randomly selected 200 μm × 200 μm regions. n.s. p = 0.1563. Data are presented as mean ± SEM (n = 6 randomly selected fields derived from 3 mice per group). Statistical significance was determined by unpaired two-tailed Student’s t-test.

Journal: Frontiers in Oncology

Article Title: Glia-derived VCAM1 promotes glioma progression

doi: 10.3389/fonc.2026.1802953

Figure Lengend Snippet: VCAM1 is expressed in glioma stem cell-like cells of gDAM-induced primary glioma in vivo . (A) Schematic timeline for the application of the gDAM method in C57BL/6J mice, involving the injection of a plasmid combination and proline mixture for gliomagenesis. (B) Labeling of tdTomato-expressing astrocytes in the brain of Ai14 mice using a Cre-expressing plasmid delivered via the gDAM method. Scale bar, 100 μm. (C) An astrocyte expressing tdTomato with characteristic endfoot structures. Scale bar, 20 μm. (D) gDAM-induced primary glioma observed at five months, showing immunostaining for Ki67 (green), VCAM1 (purple), and mCherry + tumor cells (red). Scale bar, 2 mm. (E) SOX2-expressing mCherry + tumor cells in a five-month-old primary glioma, indicated by yellow arrows. Scale bar, 20 μm. (F) Expression patterns of VCAM1, SOX2 and tumor cells in GC and TSM. GC, glioma core; TSM, tumor substantial margins. Scale bar, 20 μm. (G) The proportion of SOX2 + mCherry + cells relative to the total mCherry + cells in the GC and the TSM. * p = 0.0313. Data are presented as mean ± SEM (n = 6 randomly selected fields derived from 3 mice per group). Statistical significance was determined by unpaired two-tailed Student’s t-test. (H) Relative fluorescence intensity of VCAM1 in the GC and TSM, based on randomly selected 200 μm × 200 μm regions. n.s. p = 0.1563. Data are presented as mean ± SEM (n = 6 randomly selected fields derived from 3 mice per group). Statistical significance was determined by unpaired two-tailed Student’s t-test.

Article Snippet: Furthermore, evaluation of VCAM1 protein expression via The Human Protein Atlas (HPA) revealed variable staining intensities among glioma patients ( ).

Techniques: In Vivo, Injection, Plasmid Preparation, Labeling, Expressing, Immunostaining, Derivative Assay, Two Tailed Test, Fluorescence

VCAM1 is expressed in a subset of GLAST+ astrocytes in glioma-bearing mice. (A) Experimental timeline for glioma cell implantation in GLAST-CreER::Ai14 mice. Mice received daily intraperitoneal injections of tamoxifen (TAM) for one week, followed by a one-week resting period. On day 1, 5,000-6,000 eGFP + 73C or GL261-luc glioma cells were implanted beneath the hippocampus. Tumor-bearing mice were harvested on day 10 (eGFP + 73C) or day 20 (GL261-luc). (B) Immunofluorescence staining of VCAM1 in eGFP + 73C gliomas at day 10 post-implantation of GLAST-CreER::Ai14 mice. Scale bars: (B) 1 mm; (a), 500 μm; (a’, b’), 100μm. (C) Immunofluorescence staining of VCAM1 in GL261-luc gliomas at day 20 post-implantation of GLAST-CreER::Ai14 mice. Scale bars: (C) 1 mm; (a), 500 μm; (a’), 100 μm.

Journal: Frontiers in Oncology

Article Title: Glia-derived VCAM1 promotes glioma progression

doi: 10.3389/fonc.2026.1802953

Figure Lengend Snippet: VCAM1 is expressed in a subset of GLAST+ astrocytes in glioma-bearing mice. (A) Experimental timeline for glioma cell implantation in GLAST-CreER::Ai14 mice. Mice received daily intraperitoneal injections of tamoxifen (TAM) for one week, followed by a one-week resting period. On day 1, 5,000-6,000 eGFP + 73C or GL261-luc glioma cells were implanted beneath the hippocampus. Tumor-bearing mice were harvested on day 10 (eGFP + 73C) or day 20 (GL261-luc). (B) Immunofluorescence staining of VCAM1 in eGFP + 73C gliomas at day 10 post-implantation of GLAST-CreER::Ai14 mice. Scale bars: (B) 1 mm; (a), 500 μm; (a’, b’), 100μm. (C) Immunofluorescence staining of VCAM1 in GL261-luc gliomas at day 20 post-implantation of GLAST-CreER::Ai14 mice. Scale bars: (C) 1 mm; (a), 500 μm; (a’), 100 μm.

Article Snippet: Furthermore, evaluation of VCAM1 protein expression via The Human Protein Atlas (HPA) revealed variable staining intensities among glioma patients ( ).

Techniques: Immunofluorescence, Staining

Knockout of VCAM1 in GLAST+ cells prolongs mouse survival. (A) Experimental timeline for glioma cell implantation in GLAST-CreER::VCAM1 fl/fl and control mice. Mice received daily intraperitoneal injections of tamoxifen (TAM) for one week, followed by a one-week waiting period. On day 1, 5,000-6,000 tumor cells were injected into the cortex or below the hippocampus. Live imaging analysis was conducted at the predetermined points. (B) Kaplan-Meier survival curves of mice implanted with eGFP+ 73C tumor cells below the hippocampus. Control group (n = 6), GLAST-CreER::VCAM1fl/fl group (n = 6). p-value calculated using the log-rank Mantel-Cox test. Control vs GLAST-CreER::VCAM1fl/fl, “ns” indicates no statistical significance ( p > 0.05). Here, p = 0.1209. (C) Kaplan-Meier survival curves of mice implanted with eGFP+ 73C tumor cells in the cortex. Control group (n = 6), GLAST-CreER::VCAM1fl/fl group (n = 6). p-value calculated using the log-rank Mantel-Cox test. Control vs GLAST-CreER::VCAM1fl/fl, ** p = 0.0053. (D) Live imaging analysis of GL261-luc-bearing mice in hippocampus GLAST-CreER::VCAM1 fl/fl and control groups at days 9, 28 and 50. (E) Kaplan-Meier survival curves of mice implanted with GL261-luc tumor cells below the hippocampus. Control group (n = 7), GLAST-CreER::VCAM1 fl/fl group (n = 6). p -value calculated using the log-rank Mantel-Cox test. Control vs. GLAST-CreER::VCAM1 fl/fl , * p = 0.0223. (F) Longitudinal quantification of tumor burden by bioluminescence imaging (Total Flux) in the Hippocampus GL261-luc models. Data are presented as mean ± SEM. Statistical significance was evaluated using Two-way repeated measures ANOVA. The asterisks indicate a significant interaction effect between time and genotype, ** p = 0.0082. Data are presented as mean ± SEM (n = 6–7 mice per group). Statistical significance was evaluated using two-way repeated measures ANOVA. (G) Live imaging analysis of GL261-luc-bearing mice in cortex from the GLAST-CreER::VCAM1 fl/fl and control groups at days 20, 40, 60. (H) Kaplan-Meier survival curves of mice implanted with GL261-luc tumor cells in the cortex. Control group (n = 7), GLAST-CreER::VCAM1 fl/fl group (n = 6). p -value calculated using the log-rank Mantel-Cox test. Control vs. GLAST-CreER::VCAM1 fl/fl , * p = 0.0465. (I) Longitudinal quantification of tumor burden by bioluminescence imaging (Total Flux) in the Cortex GL261-luc models. Data are presented as mean ± SEM. Statistical significance was evaluated using Two-way repeated measures ANOVA. The asterisks indicate a significant interaction effect between time and genotype, * p = 0.0106. Data are presented as mean ± SEM (n = 6–7 mice per group). Statistical significance was evaluated using two-way repeated measures ANOVA.

Journal: Frontiers in Oncology

Article Title: Glia-derived VCAM1 promotes glioma progression

doi: 10.3389/fonc.2026.1802953

Figure Lengend Snippet: Knockout of VCAM1 in GLAST+ cells prolongs mouse survival. (A) Experimental timeline for glioma cell implantation in GLAST-CreER::VCAM1 fl/fl and control mice. Mice received daily intraperitoneal injections of tamoxifen (TAM) for one week, followed by a one-week waiting period. On day 1, 5,000-6,000 tumor cells were injected into the cortex or below the hippocampus. Live imaging analysis was conducted at the predetermined points. (B) Kaplan-Meier survival curves of mice implanted with eGFP+ 73C tumor cells below the hippocampus. Control group (n = 6), GLAST-CreER::VCAM1fl/fl group (n = 6). p-value calculated using the log-rank Mantel-Cox test. Control vs GLAST-CreER::VCAM1fl/fl, “ns” indicates no statistical significance ( p > 0.05). Here, p = 0.1209. (C) Kaplan-Meier survival curves of mice implanted with eGFP+ 73C tumor cells in the cortex. Control group (n = 6), GLAST-CreER::VCAM1fl/fl group (n = 6). p-value calculated using the log-rank Mantel-Cox test. Control vs GLAST-CreER::VCAM1fl/fl, ** p = 0.0053. (D) Live imaging analysis of GL261-luc-bearing mice in hippocampus GLAST-CreER::VCAM1 fl/fl and control groups at days 9, 28 and 50. (E) Kaplan-Meier survival curves of mice implanted with GL261-luc tumor cells below the hippocampus. Control group (n = 7), GLAST-CreER::VCAM1 fl/fl group (n = 6). p -value calculated using the log-rank Mantel-Cox test. Control vs. GLAST-CreER::VCAM1 fl/fl , * p = 0.0223. (F) Longitudinal quantification of tumor burden by bioluminescence imaging (Total Flux) in the Hippocampus GL261-luc models. Data are presented as mean ± SEM. Statistical significance was evaluated using Two-way repeated measures ANOVA. The asterisks indicate a significant interaction effect between time and genotype, ** p = 0.0082. Data are presented as mean ± SEM (n = 6–7 mice per group). Statistical significance was evaluated using two-way repeated measures ANOVA. (G) Live imaging analysis of GL261-luc-bearing mice in cortex from the GLAST-CreER::VCAM1 fl/fl and control groups at days 20, 40, 60. (H) Kaplan-Meier survival curves of mice implanted with GL261-luc tumor cells in the cortex. Control group (n = 7), GLAST-CreER::VCAM1 fl/fl group (n = 6). p -value calculated using the log-rank Mantel-Cox test. Control vs. GLAST-CreER::VCAM1 fl/fl , * p = 0.0465. (I) Longitudinal quantification of tumor burden by bioluminescence imaging (Total Flux) in the Cortex GL261-luc models. Data are presented as mean ± SEM. Statistical significance was evaluated using Two-way repeated measures ANOVA. The asterisks indicate a significant interaction effect between time and genotype, * p = 0.0106. Data are presented as mean ± SEM (n = 6–7 mice per group). Statistical significance was evaluated using two-way repeated measures ANOVA.

Article Snippet: Furthermore, evaluation of VCAM1 protein expression via The Human Protein Atlas (HPA) revealed variable staining intensities among glioma patients ( ).

Techniques: Knock-Out, Control, Injection, Imaging

The RNA-seq reveals the changes of TME following astrocytic VCAM1 deletion. (A) The protocol of RNA-seq on tumor associated VCAM1-deficient GLAST positive astrocytes. n = 6 biological replicates per group (derived from 3 mice per group, 2 independent samples per mouse) were analyzed. (B) Differentially expressed genes in astrocytic VCAM1-deficient TME. (C, F) The KEGG and GO enrichment analysis of our inhouse dataset. (D, E, G, H) The GSEA analysis of differentially expressed genes identified several functional pathways, antigen processing and presentation, cell adhesion, oxidative phosphorylation, and cholesterol efflux.

Journal: Frontiers in Oncology

Article Title: Glia-derived VCAM1 promotes glioma progression

doi: 10.3389/fonc.2026.1802953

Figure Lengend Snippet: The RNA-seq reveals the changes of TME following astrocytic VCAM1 deletion. (A) The protocol of RNA-seq on tumor associated VCAM1-deficient GLAST positive astrocytes. n = 6 biological replicates per group (derived from 3 mice per group, 2 independent samples per mouse) were analyzed. (B) Differentially expressed genes in astrocytic VCAM1-deficient TME. (C, F) The KEGG and GO enrichment analysis of our inhouse dataset. (D, E, G, H) The GSEA analysis of differentially expressed genes identified several functional pathways, antigen processing and presentation, cell adhesion, oxidative phosphorylation, and cholesterol efflux.

Article Snippet: Furthermore, evaluation of VCAM1 protein expression via The Human Protein Atlas (HPA) revealed variable staining intensities among glioma patients ( ).

Techniques: RNA Sequencing, Derivative Assay, Functional Assay, Phospho-proteomics

Clinical relevance of VCAM1 expression in human gliomas based on public database analysis. (A) Kaplan-Meier survival curve of patients with lower grade glioma and glioblastoma (GBMLGG) with different expression levels of VCAM1 in TCGA. The p-value was calculated using log-rank test (Mantel-Cox test). VCAM1>=9.605 (n=351) vs VCAM1<9.605 (n=343) *** p = 0.000001255. (B) Kaplan-Meier survival curve of patients with lower grade glioma (LGG) with different expression levels of VCAM1 in TCGA. The p-value was calculated using Mantel-Cox test. VCAM1>=9.243 (n=265) vs VCAM1<9.243 (n=263) ** p = 0.001199. (C) Kaplan-Meier survival curve of patients with glioblastoma (GBM) with different expression levels of VCAM1 in TCGA. The p-value was calculated using Mantel-Cox test. VCAM1>=10.25 (n=86) vs VCAM1<10.25 (n=80) ns p = 0.8022. (D) A 32-year-old female with moderate staining intensity of VCAM1 protein expression in LGG. Images were obtained from the Human Protein Atlas (HPA) database.

Journal: Frontiers in Oncology

Article Title: Glia-derived VCAM1 promotes glioma progression

doi: 10.3389/fonc.2026.1802953

Figure Lengend Snippet: Clinical relevance of VCAM1 expression in human gliomas based on public database analysis. (A) Kaplan-Meier survival curve of patients with lower grade glioma and glioblastoma (GBMLGG) with different expression levels of VCAM1 in TCGA. The p-value was calculated using log-rank test (Mantel-Cox test). VCAM1>=9.605 (n=351) vs VCAM1<9.605 (n=343) *** p = 0.000001255. (B) Kaplan-Meier survival curve of patients with lower grade glioma (LGG) with different expression levels of VCAM1 in TCGA. The p-value was calculated using Mantel-Cox test. VCAM1>=9.243 (n=265) vs VCAM1<9.243 (n=263) ** p = 0.001199. (C) Kaplan-Meier survival curve of patients with glioblastoma (GBM) with different expression levels of VCAM1 in TCGA. The p-value was calculated using Mantel-Cox test. VCAM1>=10.25 (n=86) vs VCAM1<10.25 (n=80) ns p = 0.8022. (D) A 32-year-old female with moderate staining intensity of VCAM1 protein expression in LGG. Images were obtained from the Human Protein Atlas (HPA) database.

Article Snippet: Furthermore, evaluation of VCAM1 protein expression via The Human Protein Atlas (HPA) revealed variable staining intensities among glioma patients ( ).

Techniques: Expressing, Staining