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anti postn  (Boster Bio)


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    Structured Review

    Boster Bio anti postn
    Anti Postn, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti postn/product/Boster Bio
    Average 93 stars, based on 2 article reviews
    anti postn - by Bioz Stars, 2026-03
    93/100 stars

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    Fibroblast-derived <t>POSTN</t> is highly expressed in obesity-related CRC. A . Differential expression analysis of POSTN in colorectal adenocarcinoma (COAD) samples versus normal samples from TCGA. B . Differential expression analysis of POSTN between paired adjacent normal and COAD tumor tissues from TCGA-COAD patients. C . Expression analysis of POSTN across different disease stages (I–IV) in TCGA-COAD patients. D . Survival analysis of TCGA-COAD patients by POSTN expression (low, n = 225; high, n = 225). The log-rank test was used for significance. E . Correlation analysis between POSTN expression and stromal scores in TCGA-COAD, assessed by Pearson correlation. F . Differential expression analysis of POSTN in WT-LF versus WT-HF groups from the GSE46843 dataset. G . Differential expression analysis of POSTN in APC (min/+) RD versus APC (min/+) HFD groups from the GSE278785 dataset. H . Representative IHC images of POSTN in normal colorectal tissues and COAD tumor tissues from obesity-associated CRC patients, with staining intensity categorized as weak or strong. Scale bars, 50 µm. The right panel quantifies the percentage of positive POSTN staining in normal, weak, and strong staining groups.I-L. scRNA-seq analysis of GSE231559 . ( I ) UMAP plot showing cell subtypes in the dataset: tumor cells, T cells, B cells, myeloid cells, fibroblasts, and endothelial cells. ( J ) Violin plot of POSTN expression across different cell subtypes (tumor cells, T cells, B cells, myeloid cells, fibroblasts, endothelial cells) in normal and tumor tissues. ( K ) UMAP plot showing fibroblast subtypes: fibroblasts, myCAFs, and iCAFs. ( L ) Violin plot of POSTN expression in fibroblast subtypes (fibroblasts, myCAFs, iCAFs) in normal and tumor tissues. M . Representative immunofluorescence co-staining of POSTN (green) and α-SMA (red) in normal and tumor tissues; Nuclei were counterstained with DAPI (blue). Scale bars, 50 µm. The right panels show intensity profiles of α-SMA and POSTN across lines drawn through the images for normal and tumor tissues.The data are means ± SD, for all panels: * P < 0.05; ** P < 0.01
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    Fibroblast-derived <t>POSTN</t> is highly expressed in obesity-related CRC. A . Differential expression analysis of POSTN in colorectal adenocarcinoma (COAD) samples versus normal samples from TCGA. B . Differential expression analysis of POSTN between paired adjacent normal and COAD tumor tissues from TCGA-COAD patients. C . Expression analysis of POSTN across different disease stages (I–IV) in TCGA-COAD patients. D . Survival analysis of TCGA-COAD patients by POSTN expression (low, n = 225; high, n = 225). The log-rank test was used for significance. E . Correlation analysis between POSTN expression and stromal scores in TCGA-COAD, assessed by Pearson correlation. F . Differential expression analysis of POSTN in WT-LF versus WT-HF groups from the GSE46843 dataset. G . Differential expression analysis of POSTN in APC (min/+) RD versus APC (min/+) HFD groups from the GSE278785 dataset. H . Representative IHC images of POSTN in normal colorectal tissues and COAD tumor tissues from obesity-associated CRC patients, with staining intensity categorized as weak or strong. Scale bars, 50 µm. The right panel quantifies the percentage of positive POSTN staining in normal, weak, and strong staining groups.I-L. scRNA-seq analysis of GSE231559 . ( I ) UMAP plot showing cell subtypes in the dataset: tumor cells, T cells, B cells, myeloid cells, fibroblasts, and endothelial cells. ( J ) Violin plot of POSTN expression across different cell subtypes (tumor cells, T cells, B cells, myeloid cells, fibroblasts, endothelial cells) in normal and tumor tissues. ( K ) UMAP plot showing fibroblast subtypes: fibroblasts, myCAFs, and iCAFs. ( L ) Violin plot of POSTN expression in fibroblast subtypes (fibroblasts, myCAFs, iCAFs) in normal and tumor tissues. M . Representative immunofluorescence co-staining of POSTN (green) and α-SMA (red) in normal and tumor tissues; Nuclei were counterstained with DAPI (blue). Scale bars, 50 µm. The right panels show intensity profiles of α-SMA and POSTN across lines drawn through the images for normal and tumor tissues.The data are means ± SD, for all panels: * P < 0.05; ** P < 0.01
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    Boster Bio anti postn
    Fibroblast-derived <t>POSTN</t> is highly expressed in obesity-related CRC. A . Differential expression analysis of POSTN in colorectal adenocarcinoma (COAD) samples versus normal samples from TCGA. B . Differential expression analysis of POSTN between paired adjacent normal and COAD tumor tissues from TCGA-COAD patients. C . Expression analysis of POSTN across different disease stages (I–IV) in TCGA-COAD patients. D . Survival analysis of TCGA-COAD patients by POSTN expression (low, n = 225; high, n = 225). The log-rank test was used for significance. E . Correlation analysis between POSTN expression and stromal scores in TCGA-COAD, assessed by Pearson correlation. F . Differential expression analysis of POSTN in WT-LF versus WT-HF groups from the GSE46843 dataset. G . Differential expression analysis of POSTN in APC (min/+) RD versus APC (min/+) HFD groups from the GSE278785 dataset. H . Representative IHC images of POSTN in normal colorectal tissues and COAD tumor tissues from obesity-associated CRC patients, with staining intensity categorized as weak or strong. Scale bars, 50 µm. The right panel quantifies the percentage of positive POSTN staining in normal, weak, and strong staining groups.I-L. scRNA-seq analysis of GSE231559 . ( I ) UMAP plot showing cell subtypes in the dataset: tumor cells, T cells, B cells, myeloid cells, fibroblasts, and endothelial cells. ( J ) Violin plot of POSTN expression across different cell subtypes (tumor cells, T cells, B cells, myeloid cells, fibroblasts, endothelial cells) in normal and tumor tissues. ( K ) UMAP plot showing fibroblast subtypes: fibroblasts, myCAFs, and iCAFs. ( L ) Violin plot of POSTN expression in fibroblast subtypes (fibroblasts, myCAFs, iCAFs) in normal and tumor tissues. M . Representative immunofluorescence co-staining of POSTN (green) and α-SMA (red) in normal and tumor tissues; Nuclei were counterstained with DAPI (blue). Scale bars, 50 µm. The right panels show intensity profiles of α-SMA and POSTN across lines drawn through the images for normal and tumor tissues.The data are means ± SD, for all panels: * P < 0.05; ** P < 0.01
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    Thermo Fisher gene exp postn cf02680557 m1
    Immunohistochemistry for <t>POSTN.</t> Positive cytoplasmic reaction in neoplastic cells of LCTs ( A ), SCTs ( B ), SEM ( C ) (400X). DAB immunohistochemistry, Mayer’s Hematoxylin counterstain, BAR 20 μm
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    Image Search Results


    Fibroblast-derived POSTN is highly expressed in obesity-related CRC. A . Differential expression analysis of POSTN in colorectal adenocarcinoma (COAD) samples versus normal samples from TCGA. B . Differential expression analysis of POSTN between paired adjacent normal and COAD tumor tissues from TCGA-COAD patients. C . Expression analysis of POSTN across different disease stages (I–IV) in TCGA-COAD patients. D . Survival analysis of TCGA-COAD patients by POSTN expression (low, n = 225; high, n = 225). The log-rank test was used for significance. E . Correlation analysis between POSTN expression and stromal scores in TCGA-COAD, assessed by Pearson correlation. F . Differential expression analysis of POSTN in WT-LF versus WT-HF groups from the GSE46843 dataset. G . Differential expression analysis of POSTN in APC (min/+) RD versus APC (min/+) HFD groups from the GSE278785 dataset. H . Representative IHC images of POSTN in normal colorectal tissues and COAD tumor tissues from obesity-associated CRC patients, with staining intensity categorized as weak or strong. Scale bars, 50 µm. The right panel quantifies the percentage of positive POSTN staining in normal, weak, and strong staining groups.I-L. scRNA-seq analysis of GSE231559 . ( I ) UMAP plot showing cell subtypes in the dataset: tumor cells, T cells, B cells, myeloid cells, fibroblasts, and endothelial cells. ( J ) Violin plot of POSTN expression across different cell subtypes (tumor cells, T cells, B cells, myeloid cells, fibroblasts, endothelial cells) in normal and tumor tissues. ( K ) UMAP plot showing fibroblast subtypes: fibroblasts, myCAFs, and iCAFs. ( L ) Violin plot of POSTN expression in fibroblast subtypes (fibroblasts, myCAFs, iCAFs) in normal and tumor tissues. M . Representative immunofluorescence co-staining of POSTN (green) and α-SMA (red) in normal and tumor tissues; Nuclei were counterstained with DAPI (blue). Scale bars, 50 µm. The right panels show intensity profiles of α-SMA and POSTN across lines drawn through the images for normal and tumor tissues.The data are means ± SD, for all panels: * P < 0.05; ** P < 0.01

    Journal: Cell Communication and Signaling : CCS

    Article Title: Fibroblast-derived POSTN promotes colorectal cancer progression under high-fat diet by reprogramming fatty acid metabolism in tumor cell

    doi: 10.1186/s12964-025-02618-w

    Figure Lengend Snippet: Fibroblast-derived POSTN is highly expressed in obesity-related CRC. A . Differential expression analysis of POSTN in colorectal adenocarcinoma (COAD) samples versus normal samples from TCGA. B . Differential expression analysis of POSTN between paired adjacent normal and COAD tumor tissues from TCGA-COAD patients. C . Expression analysis of POSTN across different disease stages (I–IV) in TCGA-COAD patients. D . Survival analysis of TCGA-COAD patients by POSTN expression (low, n = 225; high, n = 225). The log-rank test was used for significance. E . Correlation analysis between POSTN expression and stromal scores in TCGA-COAD, assessed by Pearson correlation. F . Differential expression analysis of POSTN in WT-LF versus WT-HF groups from the GSE46843 dataset. G . Differential expression analysis of POSTN in APC (min/+) RD versus APC (min/+) HFD groups from the GSE278785 dataset. H . Representative IHC images of POSTN in normal colorectal tissues and COAD tumor tissues from obesity-associated CRC patients, with staining intensity categorized as weak or strong. Scale bars, 50 µm. The right panel quantifies the percentage of positive POSTN staining in normal, weak, and strong staining groups.I-L. scRNA-seq analysis of GSE231559 . ( I ) UMAP plot showing cell subtypes in the dataset: tumor cells, T cells, B cells, myeloid cells, fibroblasts, and endothelial cells. ( J ) Violin plot of POSTN expression across different cell subtypes (tumor cells, T cells, B cells, myeloid cells, fibroblasts, endothelial cells) in normal and tumor tissues. ( K ) UMAP plot showing fibroblast subtypes: fibroblasts, myCAFs, and iCAFs. ( L ) Violin plot of POSTN expression in fibroblast subtypes (fibroblasts, myCAFs, iCAFs) in normal and tumor tissues. M . Representative immunofluorescence co-staining of POSTN (green) and α-SMA (red) in normal and tumor tissues; Nuclei were counterstained with DAPI (blue). Scale bars, 50 µm. The right panels show intensity profiles of α-SMA and POSTN across lines drawn through the images for normal and tumor tissues.The data are means ± SD, for all panels: * P < 0.05; ** P < 0.01

    Article Snippet: The recombinant protein POSTN (100 ng/mL, 10299-H08H, Sinobiological), AKT inhibitor LY294002 (20 μM, L832989-10 mg, Macklin), ERK inhibitor PD98059 (10μM, P832941-5 mg, Macklin), Cilengitide (10 μM, BD628662, Bidepharm) was applied to HCT116 and HT29 cells for 24 h. MC38 cells were treated with CM.

    Techniques: Derivative Assay, Quantitative Proteomics, Expressing, Staining, Immunofluorescence

    POSTN promotes CRC occurrence and progression under high-fat diet. A . HFD-AOM-DSS induced CRC tumorigenesis protocol in WT (n = 10) and POSTN-KO (n=10) mice. Mice were fed HFD until sacrifice, injected with AOM (12.5mg/kg), followed by three cycles of 2% DSS (5 days per cycle, with 14-day intervals between cycles), and sacrificed at 72 days after the first DSS treatment. B . Representative images of colons from WT and POSTN-KO mice following HFD-AOM-DSS treatment. Scale bars, 1 cm. C . Quantification of body weight, colorectal length, tumor number, and tumor size in WT and POSTN-KO mice following HFD-AOM-DSS induction. D . Representative HE and Ki67 IHC images of colon tissues from WT and POSTN-KO mice after HFD-AOM-DSS treatment. Scale bars, 50 µm. E .Schematic diagram of the mice transplanted tumor model. Mice were fed RD or HFD for 12 weeks, then injected subcutaneously with mouse colorectal cancer cell line MC38, and sacrificed 21 days after injection. F . The volumes of subcutaneous transplanted tumors from the WT group and POSTN-KO group fed RD or HFD. G . Representative images of subcutaneous transplanted tumors from the WT group (n = 5) and POSTN-KO group (n= 5) fed RD or HFD. H .The size and weights of subcutaneous transplanted tumors in the WT group and POSTN-KO group fed RD or HFD. I . Representative HE and Ki67 IHC images of transplanted tissues from WT and POSTN-KO mice fed RD or HFD. Scale bars, 50 µm. J . Representative IHC images of POSTN, α-SMA and Collagen Ⅰ in colon tissues from WT and POSTN-KO mice induced by HFD-AOM-DSS. Scale bars, 50 µm. K . Representative IHC images of α-SMA and Collagen I in t subcutaneous transplanted tumors from WT and POSTN-KO mice fed RD or HFD. Scale bars, 50 µm. The data are means ± SD, for all panels: * P < 0.05; ** P < 0.01

    Journal: Cell Communication and Signaling : CCS

    Article Title: Fibroblast-derived POSTN promotes colorectal cancer progression under high-fat diet by reprogramming fatty acid metabolism in tumor cell

    doi: 10.1186/s12964-025-02618-w

    Figure Lengend Snippet: POSTN promotes CRC occurrence and progression under high-fat diet. A . HFD-AOM-DSS induced CRC tumorigenesis protocol in WT (n = 10) and POSTN-KO (n=10) mice. Mice were fed HFD until sacrifice, injected with AOM (12.5mg/kg), followed by three cycles of 2% DSS (5 days per cycle, with 14-day intervals between cycles), and sacrificed at 72 days after the first DSS treatment. B . Representative images of colons from WT and POSTN-KO mice following HFD-AOM-DSS treatment. Scale bars, 1 cm. C . Quantification of body weight, colorectal length, tumor number, and tumor size in WT and POSTN-KO mice following HFD-AOM-DSS induction. D . Representative HE and Ki67 IHC images of colon tissues from WT and POSTN-KO mice after HFD-AOM-DSS treatment. Scale bars, 50 µm. E .Schematic diagram of the mice transplanted tumor model. Mice were fed RD or HFD for 12 weeks, then injected subcutaneously with mouse colorectal cancer cell line MC38, and sacrificed 21 days after injection. F . The volumes of subcutaneous transplanted tumors from the WT group and POSTN-KO group fed RD or HFD. G . Representative images of subcutaneous transplanted tumors from the WT group (n = 5) and POSTN-KO group (n= 5) fed RD or HFD. H .The size and weights of subcutaneous transplanted tumors in the WT group and POSTN-KO group fed RD or HFD. I . Representative HE and Ki67 IHC images of transplanted tissues from WT and POSTN-KO mice fed RD or HFD. Scale bars, 50 µm. J . Representative IHC images of POSTN, α-SMA and Collagen Ⅰ in colon tissues from WT and POSTN-KO mice induced by HFD-AOM-DSS. Scale bars, 50 µm. K . Representative IHC images of α-SMA and Collagen I in t subcutaneous transplanted tumors from WT and POSTN-KO mice fed RD or HFD. Scale bars, 50 µm. The data are means ± SD, for all panels: * P < 0.05; ** P < 0.01

    Article Snippet: The recombinant protein POSTN (100 ng/mL, 10299-H08H, Sinobiological), AKT inhibitor LY294002 (20 μM, L832989-10 mg, Macklin), ERK inhibitor PD98059 (10μM, P832941-5 mg, Macklin), Cilengitide (10 μM, BD628662, Bidepharm) was applied to HCT116 and HT29 cells for 24 h. MC38 cells were treated with CM.

    Techniques: Injection

    POSTN promotes fibroblast activation and promotes CRC development under high-fat diet. A . Representative IF images of biomarkers in primary WT and POSTN-KO fibroblasts. The merged images represent the overlay of DAPI (blue) with POSTN (red), α-SMA (red) and Collagen Ⅰ (red) respectively. Scale bars, 50 µm. B . Western blot analysis of POSTN, α-SMA, and Collagen Ⅰ expression levels in primary fibroblasts. Quantification of relative protein levels is shown adjacent to the blot images. C . Schematic diagram illustrating the mouse transplanted tumor model. Primary fibroblasts were isolated. Mice were fed a HFD for 12 weeks, then subcutaneously co-inoculated with MC38 cells along with WT or POSTN-KO primary fibroblasts to establish transplanted tumors. Mice were euthanized on day 21 post-inoculation for tumor harvest and analysis. D . Growth curves of subcutaneous transplanted tumors volumes in the MC38 + WT NFs group, and MC38 + POSTN-KO NFs group over 21 days. E . Representative images of subcutaneous transplanted tumors from the MC38+WT NFs group (n = 5) and MC38+KO NFs group (n = 5). Scale bar, 1 cm. F . Quantification of subcutaneous transplanted tumors size (left) and weight (right) in the MC38 + WT NFs group, and MC38 + POSTN-KO NFs group. G . Representative IHC images of α-SMA and Collagen I in subcutaneous transplanted tumors from the MC38+WT NFs group and MC38+POSTN-KO NFs group. Scale bars, 50 µm. Quantification of the percentage of positive staining for α-SMA and Collagen Ⅰ is shown adjacent to the IHC images. H .Western blot analysis and quantification of POSTN, STAT3 and p-STAT3 expression levels in WT primary fibroblasts treated with FFA. I .Western blot analysis and quantification of POSTN, STAT3, and p-STAT3 expression levels in WT primary fibroblasts treated with NSC74859, with or without FFA co-treatment.The data are means ± SD, for all panels: * P < 0.05; ** P < 0.01

    Journal: Cell Communication and Signaling : CCS

    Article Title: Fibroblast-derived POSTN promotes colorectal cancer progression under high-fat diet by reprogramming fatty acid metabolism in tumor cell

    doi: 10.1186/s12964-025-02618-w

    Figure Lengend Snippet: POSTN promotes fibroblast activation and promotes CRC development under high-fat diet. A . Representative IF images of biomarkers in primary WT and POSTN-KO fibroblasts. The merged images represent the overlay of DAPI (blue) with POSTN (red), α-SMA (red) and Collagen Ⅰ (red) respectively. Scale bars, 50 µm. B . Western blot analysis of POSTN, α-SMA, and Collagen Ⅰ expression levels in primary fibroblasts. Quantification of relative protein levels is shown adjacent to the blot images. C . Schematic diagram illustrating the mouse transplanted tumor model. Primary fibroblasts were isolated. Mice were fed a HFD for 12 weeks, then subcutaneously co-inoculated with MC38 cells along with WT or POSTN-KO primary fibroblasts to establish transplanted tumors. Mice were euthanized on day 21 post-inoculation for tumor harvest and analysis. D . Growth curves of subcutaneous transplanted tumors volumes in the MC38 + WT NFs group, and MC38 + POSTN-KO NFs group over 21 days. E . Representative images of subcutaneous transplanted tumors from the MC38+WT NFs group (n = 5) and MC38+KO NFs group (n = 5). Scale bar, 1 cm. F . Quantification of subcutaneous transplanted tumors size (left) and weight (right) in the MC38 + WT NFs group, and MC38 + POSTN-KO NFs group. G . Representative IHC images of α-SMA and Collagen I in subcutaneous transplanted tumors from the MC38+WT NFs group and MC38+POSTN-KO NFs group. Scale bars, 50 µm. Quantification of the percentage of positive staining for α-SMA and Collagen Ⅰ is shown adjacent to the IHC images. H .Western blot analysis and quantification of POSTN, STAT3 and p-STAT3 expression levels in WT primary fibroblasts treated with FFA. I .Western blot analysis and quantification of POSTN, STAT3, and p-STAT3 expression levels in WT primary fibroblasts treated with NSC74859, with or without FFA co-treatment.The data are means ± SD, for all panels: * P < 0.05; ** P < 0.01

    Article Snippet: The recombinant protein POSTN (100 ng/mL, 10299-H08H, Sinobiological), AKT inhibitor LY294002 (20 μM, L832989-10 mg, Macklin), ERK inhibitor PD98059 (10μM, P832941-5 mg, Macklin), Cilengitide (10 μM, BD628662, Bidepharm) was applied to HCT116 and HT29 cells for 24 h. MC38 cells were treated with CM.

    Techniques: Activation Assay, Western Blot, Expressing, Isolation, Staining

    POSTN promotes lipid accumulation by regulating SREBP1 and CPT1A reprogramming under high-fat diet. A .GSEA results of mitochondrial fatty acid beta oxidation signaling pathway in TCGA-COAD patients. B . In the HFD-AOM-DSS model, morphology of mitochondria under transmission electron microscopy in colon tissues of WT and POSTN-KO mice. C . In HFD-AOM-DSS model, TG and NEFA levels in serum and colorectal tissues of WT and POSTN-KO mice. D . Intracellular TG and NEFA levels in MC38 cells following co-culture with WT or POSTN-KO NFs. E . Intracellular TG and NEFA levels in MC38 cells treated with DMEM, WT-CM (conditioned medium from WT NFs), or KO-CM (conditioned medium from POSTN-KO NFs). F . Neutral lipid accumulation in MC38 cells treated with DMEM, WT-CM, or KO-CM, visualized by BODIPY staining (green, neutral lipid; blue, nuclei). Scale bars, 50 μm. G . Intracellular TG and NEFA levels in MC38 cells treated with WT-CM, KO-CM, or WT-CM plus orlistat. H . Cell viability of MC38 cells treated with WT-CM, KO-CM, or WT-CM plus orlistat. I . Neutral lipid accumulation in MC38 cells treated with WT-CM, KO-CM, or WT-CM plus orlistat, visualized by BODIPY staining. Scale bars, 50 μm. J . Western blot analysis of SREBP1 and CPT1A expression levels in MC38 cells treated with WT-CM or KO-CM when FFA was added. Quantification of relative protein levels is shown adjacent to the blot images. K . Western blot analysis of SREBP1 expression levels in MC38 cells transfected with empty vectors or SREBP1 overexpression plasmids under KO-CM treatment. Quantification of relative protein levels is shown adjacent to the blot images.Right figure: BODIPY staining of neutral lipid in cells. Scale, 50 μm. L . Western blot analysis of CPT1A expression levels in MC38 cells transfected with empty vectors or CPT1A overexpression plasmids under WT-CM treatment. Quantification of relative protein levels is shown adjacent to the blot images. Right figure: BODIPY staining of neutral lipid in cells. Scale, 50 μm.The data are means ± SD, for all panels: * P < 0.05; ** P < 0.01

    Journal: Cell Communication and Signaling : CCS

    Article Title: Fibroblast-derived POSTN promotes colorectal cancer progression under high-fat diet by reprogramming fatty acid metabolism in tumor cell

    doi: 10.1186/s12964-025-02618-w

    Figure Lengend Snippet: POSTN promotes lipid accumulation by regulating SREBP1 and CPT1A reprogramming under high-fat diet. A .GSEA results of mitochondrial fatty acid beta oxidation signaling pathway in TCGA-COAD patients. B . In the HFD-AOM-DSS model, morphology of mitochondria under transmission electron microscopy in colon tissues of WT and POSTN-KO mice. C . In HFD-AOM-DSS model, TG and NEFA levels in serum and colorectal tissues of WT and POSTN-KO mice. D . Intracellular TG and NEFA levels in MC38 cells following co-culture with WT or POSTN-KO NFs. E . Intracellular TG and NEFA levels in MC38 cells treated with DMEM, WT-CM (conditioned medium from WT NFs), or KO-CM (conditioned medium from POSTN-KO NFs). F . Neutral lipid accumulation in MC38 cells treated with DMEM, WT-CM, or KO-CM, visualized by BODIPY staining (green, neutral lipid; blue, nuclei). Scale bars, 50 μm. G . Intracellular TG and NEFA levels in MC38 cells treated with WT-CM, KO-CM, or WT-CM plus orlistat. H . Cell viability of MC38 cells treated with WT-CM, KO-CM, or WT-CM plus orlistat. I . Neutral lipid accumulation in MC38 cells treated with WT-CM, KO-CM, or WT-CM plus orlistat, visualized by BODIPY staining. Scale bars, 50 μm. J . Western blot analysis of SREBP1 and CPT1A expression levels in MC38 cells treated with WT-CM or KO-CM when FFA was added. Quantification of relative protein levels is shown adjacent to the blot images. K . Western blot analysis of SREBP1 expression levels in MC38 cells transfected with empty vectors or SREBP1 overexpression plasmids under KO-CM treatment. Quantification of relative protein levels is shown adjacent to the blot images.Right figure: BODIPY staining of neutral lipid in cells. Scale, 50 μm. L . Western blot analysis of CPT1A expression levels in MC38 cells transfected with empty vectors or CPT1A overexpression plasmids under WT-CM treatment. Quantification of relative protein levels is shown adjacent to the blot images. Right figure: BODIPY staining of neutral lipid in cells. Scale, 50 μm.The data are means ± SD, for all panels: * P < 0.05; ** P < 0.01

    Article Snippet: The recombinant protein POSTN (100 ng/mL, 10299-H08H, Sinobiological), AKT inhibitor LY294002 (20 μM, L832989-10 mg, Macklin), ERK inhibitor PD98059 (10μM, P832941-5 mg, Macklin), Cilengitide (10 μM, BD628662, Bidepharm) was applied to HCT116 and HT29 cells for 24 h. MC38 cells were treated with CM.

    Techniques: Transmission Assay, Electron Microscopy, Co-Culture Assay, Staining, Western Blot, Expressing, Transfection, Over Expression

    POSTN promotes FA synthesis via the AKT/SREBP1 signaling axis under high-fat diet. A . GSEA of the REACTOME_PI3K_AKT_SIGNALING_IN_CANCER pathway in TCGA-COAD patients. Genes are ranked by correlation with POSTN expression (red, POSTN-high; green, POSTN-low). B . Western blot analysis of AKT, p-AKT, and SREBP1 expression levels in tissues from WT and POSTN–KO mice subjected to HFD-AOM-DSS induction. Quantification of relative protein levels is shown adjacent the blot images. C .Western blot analysis of AKT and p-AKT expression levels in HCT116 and HT29 cells treated with FFA with or without recombinant POSTN supplementation. Quantification of relative protein levels is shown below the blot images. D . Western blot analysis of AKT, p-AKT, and SREBP1 expression levels in HCT116 and HT29 cells treated with FFA, with or without the AKT inhibitor LY294002 and/or recombinant POSTN supplementation. Quantification of relative protein levels is shown below to the blot image. E .Intracellular TG and NEFA levels in HCT116 and HT29 cells treated with FFA, with or without LY294002 and/or POSTN supplementation. F . Representative fluorescence microscopy images of neutral lipid accumulation (green, BODIPY staining) in HCT116 and HT29 cells treated with FFA, with or without LY294002 and/or POSTN supplementation. Nuclei are counterstained with DAPI (blue). Scale bars, 50 µm.The data are means ± SD, for all panels: * P < 0.05; ** P < 0.01

    Journal: Cell Communication and Signaling : CCS

    Article Title: Fibroblast-derived POSTN promotes colorectal cancer progression under high-fat diet by reprogramming fatty acid metabolism in tumor cell

    doi: 10.1186/s12964-025-02618-w

    Figure Lengend Snippet: POSTN promotes FA synthesis via the AKT/SREBP1 signaling axis under high-fat diet. A . GSEA of the REACTOME_PI3K_AKT_SIGNALING_IN_CANCER pathway in TCGA-COAD patients. Genes are ranked by correlation with POSTN expression (red, POSTN-high; green, POSTN-low). B . Western blot analysis of AKT, p-AKT, and SREBP1 expression levels in tissues from WT and POSTN–KO mice subjected to HFD-AOM-DSS induction. Quantification of relative protein levels is shown adjacent the blot images. C .Western blot analysis of AKT and p-AKT expression levels in HCT116 and HT29 cells treated with FFA with or without recombinant POSTN supplementation. Quantification of relative protein levels is shown below the blot images. D . Western blot analysis of AKT, p-AKT, and SREBP1 expression levels in HCT116 and HT29 cells treated with FFA, with or without the AKT inhibitor LY294002 and/or recombinant POSTN supplementation. Quantification of relative protein levels is shown below to the blot image. E .Intracellular TG and NEFA levels in HCT116 and HT29 cells treated with FFA, with or without LY294002 and/or POSTN supplementation. F . Representative fluorescence microscopy images of neutral lipid accumulation (green, BODIPY staining) in HCT116 and HT29 cells treated with FFA, with or without LY294002 and/or POSTN supplementation. Nuclei are counterstained with DAPI (blue). Scale bars, 50 µm.The data are means ± SD, for all panels: * P < 0.05; ** P < 0.01

    Article Snippet: The recombinant protein POSTN (100 ng/mL, 10299-H08H, Sinobiological), AKT inhibitor LY294002 (20 μM, L832989-10 mg, Macklin), ERK inhibitor PD98059 (10μM, P832941-5 mg, Macklin), Cilengitide (10 μM, BD628662, Bidepharm) was applied to HCT116 and HT29 cells for 24 h. MC38 cells were treated with CM.

    Techniques: Expressing, Western Blot, Recombinant, Fluorescence, Microscopy, Staining

    POSTN inhibits FAO via the ERK/CPT1A signal axis under high-fat diet. A . GSEA of the REACTOME_ONCOGENIC_MAPK_SIGNALING pathway in TCGA-COAD patients. Genes are ranked by correlation with POSTN expression (red, POSTN-high; green, POSTN-low). B .Western blot analysis of ERK, p-ERK, and CPT1A expression levels in tissues from WT and POSTN-KO mice subjected to HFD-AOM-DSS to induce. Quantification of relative protein levels is shown adjacent the blot images. C .Western blot analysis of ERK and p-ERK expression levels in HCT116 and HT29 cells treated with FFA with or without recombinant POSTN supplementation. Quantification of relative protein levels is shown below the blot images. D .Western blot analysis of ERK, p-ERK, and CPT1A expression levels in HCT116 and HT29 cells treated with FFA, with or without the ERK inhibitor PD98059 and/or recombinant POSTN supplementation. Quantification of relative protein levels is shown below to the blot image. E .Intracellular TG and NEFA levels in HCT116 and HT29 cells treated with FFA, with or without PD98059 and/or POSTN supplementation. F .Representative fluorescence microscopy images of neutral lipid accumulation (green, BODIPY staining) in HCT116 and HT29 cells treated with FFA, with or without PD98059 and/or POSTN supplementation. Nuclei are counterstained with DAPI (blue). Scale bars, 50 µm.The data are means ± SD, for all panels: * P < 0.05; ** P < 0.01

    Journal: Cell Communication and Signaling : CCS

    Article Title: Fibroblast-derived POSTN promotes colorectal cancer progression under high-fat diet by reprogramming fatty acid metabolism in tumor cell

    doi: 10.1186/s12964-025-02618-w

    Figure Lengend Snippet: POSTN inhibits FAO via the ERK/CPT1A signal axis under high-fat diet. A . GSEA of the REACTOME_ONCOGENIC_MAPK_SIGNALING pathway in TCGA-COAD patients. Genes are ranked by correlation with POSTN expression (red, POSTN-high; green, POSTN-low). B .Western blot analysis of ERK, p-ERK, and CPT1A expression levels in tissues from WT and POSTN-KO mice subjected to HFD-AOM-DSS to induce. Quantification of relative protein levels is shown adjacent the blot images. C .Western blot analysis of ERK and p-ERK expression levels in HCT116 and HT29 cells treated with FFA with or without recombinant POSTN supplementation. Quantification of relative protein levels is shown below the blot images. D .Western blot analysis of ERK, p-ERK, and CPT1A expression levels in HCT116 and HT29 cells treated with FFA, with or without the ERK inhibitor PD98059 and/or recombinant POSTN supplementation. Quantification of relative protein levels is shown below to the blot image. E .Intracellular TG and NEFA levels in HCT116 and HT29 cells treated with FFA, with or without PD98059 and/or POSTN supplementation. F .Representative fluorescence microscopy images of neutral lipid accumulation (green, BODIPY staining) in HCT116 and HT29 cells treated with FFA, with or without PD98059 and/or POSTN supplementation. Nuclei are counterstained with DAPI (blue). Scale bars, 50 µm.The data are means ± SD, for all panels: * P < 0.05; ** P < 0.01

    Article Snippet: The recombinant protein POSTN (100 ng/mL, 10299-H08H, Sinobiological), AKT inhibitor LY294002 (20 μM, L832989-10 mg, Macklin), ERK inhibitor PD98059 (10μM, P832941-5 mg, Macklin), Cilengitide (10 μM, BD628662, Bidepharm) was applied to HCT116 and HT29 cells for 24 h. MC38 cells were treated with CM.

    Techniques: Expressing, Western Blot, Recombinant, Fluorescence, Microscopy, Staining

    Cilengitide targeted therapy for CRC associated with high-fat diet. A .Western blot analysis of AKT, p-AKT, SREBP1, ERK, p-ERK, and CPT1A in HCT116 and HT29 cells treated with recombinant POSTN with or without Cilengitide. Quantification of relative protein levels is shown adjacent to the blot images. B . Intracellular TG and NEFA levels in HCT116 and HT29 cells treated with recombinant POSTN with or without Cilengitide. C . Representative fluorescence microscopy images of neutral lipid accumulation (green, BODIPY staining) in HCT116 and HT29 cells treated with recombinant POSTN with or without Cilengitide. Nuclei are counterstained with DAPI (blue). Scale bars, 50 µm. D .The volumes of subcutaneous transplanted tumors from the control group, LY294002 group, PD98059 group, Cilengitide group and Cilengitide+LY294002+PD98059 group. E . Representative images of subcutaneous transplanted tumors from control group (n = 5), LY294002 group (n = 5), PD98059 group (n = 5), Cilengitide group (n = 5), and Cilengitide+LY294002+PD98059 group (n = 5). F . The size and weights of subcutaneous transplanted tumors from the control group, LY294002 group, PD98059 group, Cilengitide group, and Cilengitide+LY294002+PD98059 group. G . Representative HE and IHC images of Ki-67 and α-SMA of subcutaneous transplanted tumors from the control group, LY294002 group, PD98059 group, Cilengitide group, and Cilengitide+LY294002+PD98059 group. Scale bars, 50 µm. H .Western blot analysis of AKT, p-AKT, SREBP1, ERK, p-ERK, and CPT1A of subcutaneous transplanted tumors from the control group, LY294002 group, PD98059 group, Cilengitide group, and Cilengitide+LY294002+PD98059 group. Quantification of relative protein levels is shown adjacent to the blot images.The data are means ± SD, for all panels: * P < 0.05; ** P < 0.01

    Journal: Cell Communication and Signaling : CCS

    Article Title: Fibroblast-derived POSTN promotes colorectal cancer progression under high-fat diet by reprogramming fatty acid metabolism in tumor cell

    doi: 10.1186/s12964-025-02618-w

    Figure Lengend Snippet: Cilengitide targeted therapy for CRC associated with high-fat diet. A .Western blot analysis of AKT, p-AKT, SREBP1, ERK, p-ERK, and CPT1A in HCT116 and HT29 cells treated with recombinant POSTN with or without Cilengitide. Quantification of relative protein levels is shown adjacent to the blot images. B . Intracellular TG and NEFA levels in HCT116 and HT29 cells treated with recombinant POSTN with or without Cilengitide. C . Representative fluorescence microscopy images of neutral lipid accumulation (green, BODIPY staining) in HCT116 and HT29 cells treated with recombinant POSTN with or without Cilengitide. Nuclei are counterstained with DAPI (blue). Scale bars, 50 µm. D .The volumes of subcutaneous transplanted tumors from the control group, LY294002 group, PD98059 group, Cilengitide group and Cilengitide+LY294002+PD98059 group. E . Representative images of subcutaneous transplanted tumors from control group (n = 5), LY294002 group (n = 5), PD98059 group (n = 5), Cilengitide group (n = 5), and Cilengitide+LY294002+PD98059 group (n = 5). F . The size and weights of subcutaneous transplanted tumors from the control group, LY294002 group, PD98059 group, Cilengitide group, and Cilengitide+LY294002+PD98059 group. G . Representative HE and IHC images of Ki-67 and α-SMA of subcutaneous transplanted tumors from the control group, LY294002 group, PD98059 group, Cilengitide group, and Cilengitide+LY294002+PD98059 group. Scale bars, 50 µm. H .Western blot analysis of AKT, p-AKT, SREBP1, ERK, p-ERK, and CPT1A of subcutaneous transplanted tumors from the control group, LY294002 group, PD98059 group, Cilengitide group, and Cilengitide+LY294002+PD98059 group. Quantification of relative protein levels is shown adjacent to the blot images.The data are means ± SD, for all panels: * P < 0.05; ** P < 0.01

    Article Snippet: The recombinant protein POSTN (100 ng/mL, 10299-H08H, Sinobiological), AKT inhibitor LY294002 (20 μM, L832989-10 mg, Macklin), ERK inhibitor PD98059 (10μM, P832941-5 mg, Macklin), Cilengitide (10 μM, BD628662, Bidepharm) was applied to HCT116 and HT29 cells for 24 h. MC38 cells were treated with CM.

    Techniques: Western Blot, Recombinant, Fluorescence, Microscopy, Staining, Control

    Schematic diagram of POSTN regulating FA metabolism in colorectal cancer cells with a high-fat diet

    Journal: Cell Communication and Signaling : CCS

    Article Title: Fibroblast-derived POSTN promotes colorectal cancer progression under high-fat diet by reprogramming fatty acid metabolism in tumor cell

    doi: 10.1186/s12964-025-02618-w

    Figure Lengend Snippet: Schematic diagram of POSTN regulating FA metabolism in colorectal cancer cells with a high-fat diet

    Article Snippet: The recombinant protein POSTN (100 ng/mL, 10299-H08H, Sinobiological), AKT inhibitor LY294002 (20 μM, L832989-10 mg, Macklin), ERK inhibitor PD98059 (10μM, P832941-5 mg, Macklin), Cilengitide (10 μM, BD628662, Bidepharm) was applied to HCT116 and HT29 cells for 24 h. MC38 cells were treated with CM.

    Techniques:

    Immunohistochemistry for POSTN. Positive cytoplasmic reaction in neoplastic cells of LCTs ( A ), SCTs ( B ), SEM ( C ) (400X). DAB immunohistochemistry, Mayer’s Hematoxylin counterstain, BAR 20 μm

    Journal: BMC Veterinary Research

    Article Title: Expression of periostin and podoplanin in canine testicular tumours

    doi: 10.1186/s12917-025-05176-y

    Figure Lengend Snippet: Immunohistochemistry for POSTN. Positive cytoplasmic reaction in neoplastic cells of LCTs ( A ), SCTs ( B ), SEM ( C ) (400X). DAB immunohistochemistry, Mayer’s Hematoxylin counterstain, BAR 20 μm

    Article Snippet: Cf02680557_m1 for POSTN, cf4931159_m1 for ACTB (Applied Biosystem) were the primers and TaqMan probes were used in the study.

    Techniques: Immunohistochemistry

    The number of samples exhibiting the expression of POSTN in LCTs, SCTs and SEMs

    Journal: BMC Veterinary Research

    Article Title: Expression of periostin and podoplanin in canine testicular tumours

    doi: 10.1186/s12917-025-05176-y

    Figure Lengend Snippet: The number of samples exhibiting the expression of POSTN in LCTs, SCTs and SEMs

    Article Snippet: Cf02680557_m1 for POSTN, cf4931159_m1 for ACTB (Applied Biosystem) were the primers and TaqMan probes were used in the study.

    Techniques: Expressing

    POSTN immunohistochemical reaction in the three types of testicular neoplasms considered. Difference between tumours has been noted in: ( A ) the number of positive cells and ( B ), the intensity of the reaction ( p < 0.0001). P-value obtained by the Kruskal-Wallis ANOVA analysis with post-hoc Dunn test: * p < 0.0001; ** p < 0.0001; *** p < 0.0001; **** p < 0.0001

    Journal: BMC Veterinary Research

    Article Title: Expression of periostin and podoplanin in canine testicular tumours

    doi: 10.1186/s12917-025-05176-y

    Figure Lengend Snippet: POSTN immunohistochemical reaction in the three types of testicular neoplasms considered. Difference between tumours has been noted in: ( A ) the number of positive cells and ( B ), the intensity of the reaction ( p < 0.0001). P-value obtained by the Kruskal-Wallis ANOVA analysis with post-hoc Dunn test: * p < 0.0001; ** p < 0.0001; *** p < 0.0001; **** p < 0.0001

    Article Snippet: Cf02680557_m1 for POSTN, cf4931159_m1 for ACTB (Applied Biosystem) were the primers and TaqMan probes were used in the study.

    Techniques: Immunohistochemical staining