mouse fibronectin elisa kit  (Novus Biologicals)

Journal: Molecular Cancer

Article Title: c-Rel drives pancreatic cancer metastasis through fibronectin-integrin signaling-induced isolation stress resistance and EMT

doi: 10.1186/s12943-025-02486-5

Figure Lengend Snippet: A Representative images of Masson's trichrome (p<0.0001) and Picosirius-red stained tumors and their quantification (p=0.0248) B Representative FN1-IHC images (p=0.0186). GCKP-1 reflects fibrillar FN1 deposition around cancer cells individually. GCKP-2 reflects the perinuclear FN1 signal intracellularly, as shown with arrowheads. C Western blot for FN1 in bulk tumors and isolated cancer cell lysates. The expression is normalized to HSP90 (tissues p=0.0002, cells n.s.) D Mouse serum FN1 ELISA results (One-way ANOVA for a linear trend p=0.0366) E Fibronectin adhesion assay. The number of cells attached to the FN1-coated wells was normalized to the seeding number (One-way ANOVA test for a linear trend p=0.0242) F Heatmap of the differentially expressed genes in the RNA-seq analysis of CCKP-CKP-GCKP cells. G Principal component analysis (PCA) plot of the cells used for the RNAseq analysis. H Venn diagrams illustrating the number of common genes up- or down-regulated in the given comparison pairs. I GSEA of the DEGs between the given comparison pairs. The red stars indicate enrichments related to ECM remodeling, whereas the blue stars indicate EMT-related pathways. Unless otherwise indicated, for all analyses, ordinary one-way ANOVA was used. ANOVA p values are given in the figure legends. Tukey's multiple comparison tests are shown in the figures

Article Snippet: The serum samples were diluted 1:8000 and analyzed with a Mouse Fibronectin ELISA Kit (Novus, NBP2-60517).

Techniques: Staining, Western Blot, Isolation, Expressing, Enzyme-linked Immunosorbent Assay, Cell Adhesion Assay, RNA Sequencing, Comparison

Journal: Molecular Cancer

Article Title: c-Rel drives pancreatic cancer metastasis through fibronectin-integrin signaling-induced isolation stress resistance and EMT

doi: 10.1186/s12943-025-02486-5

Figure Lengend Snippet: A Colony-forming frequency was assessed by the ability of cells to form an organoid in Matrigel (one-way ANOVA, p=0.0015). Tukey's multiple comparisons test results are shown in the figure. B Representative microscopy images of spheroids formed under nonadherent conditions. The average spheroid diameter was quantified and analyzed (genotype factor p=0.0227). C Representative spheroid images and their diameter quantification. The spheroid medium was supplemented with either human plasma fibronectin (pFN1) or cellular fibronectin with EDB domain + type II domains 8−14 (EDB cFN1.3) (treatment factor p= n.s.) D Surface expression of selected proteins on spheroids as assessed by flow cytometry analysis (one-way ANOVA test for CD61 p=0.0244, CD133, EpCAM, CD44, CXCR4, Sca1 p= n.s.). Tukey's multiple comparisons test results are shown in the figure. E Representative macroscopic and microscopic images of the transplanted mouse lungs. The number of cell lines used per genotype are CKP=5, GCKP=5 and FNGCKP=4. Each cell line was injected two times to two individual mice. Nested one-way ANOVA was used for both analyses. Tukey's multiple comparisons test results are shown in the figure. Unless otherwise indicated, for all analyses, two-way ANOVA was used. ANOVA p values are given in the figure or their legends. Šídák's multiple comparison tests between genotypes are shown in the figures. F Schematic depicting the function of c-Rel in PDAC pathophysiology. c-Rel is an oncogenic factor involved in PDAC survival and metastasis. Increased c-Rel expression remodels the ECM by converting the collagen-rich stroma to a fibronectin-rich stroma. Cancer cells undergo epithelial-to-mesenchymal transition, increasing EMP by reducing the surface expression of E-cadherin and contractility via Src and Stat3 phosphorylation. Once isolation stress is induced under nonadherent conditions, c-Rel induces a niche enriched with fibronectin, coupled with increased Itgb3, Itga5 and Itgav expression. These changes are also supported by EMP, where c-Rel directly induces EMT-TFs such as Snai1, Snai2, Zeb2, and Tgfb . Increased tolerance to isolation stress ultimately drives metastasis. Created in BioRender. Kabacaoglu, D. (2025)

Article Snippet: The serum samples were diluted 1:8000 and analyzed with a Mouse Fibronectin ELISA Kit (Novus, NBP2-60517).

Techniques: Microscopy, Clinical Proteomics, Expressing, Flow Cytometry, Injection, Comparison, Phospho-proteomics, Isolation

Journal: International journal of molecular sciences

Article Title: Heart Failure Promotes Cancer Progression in an Integrin β1-Dependent Manner.

doi: 10.3390/ijms242417367

Figure Lengend Snippet: Figure 1. TAC-operation promotes LLC cancer cell growth in periostin KO mice. (A) Serum levels of B6 (green) and POSTN(−/−) (red) mice (n = 3 per group) were obtained by ELISA for Periostin. (B) Schematic experimental timeline for the Lewis lung carcinoma (LLC) cell model implanted in Periostin KO (POSTN(−/−)) male mice. (C) POSTN(−/−) mice were subcutaneously implanted into the flanks with LLC cells (0.5 × 106 cells per mouse) (n = 7). Mice were divided into 2 groups: TAC-operated group (red, n = 3), and non-opereted group (black, n = 4). Tumors were monitored over time and tumor volume was calculated using the formula: Width × Length × 0.5. (D) Tumor weight at sacrifice. Each dot represents one mouse. Data are presented as mean ± SE. Two-way repeated measures ANOVA followed by the Bonferroni post-test (C), and Student’s t-test (A,D). * p < 0.05, *** p < 0.001, **** p < 0.0001.

Article Snippet: The quantification of Periostin and Fibronectin in the serum was performed using the mouse Periostin/OSF-2 Quantikine ELISA kit (R&D systems Inc., Minneapolis, MN, USA) and mouse Fibronectin ELISA kit (E-EL-M0506, Elabscience, Houston, TX, USA), according to the manufacturer’s instructions.

Techniques: Enzyme-linked Immunosorbent Assay

Journal: International journal of molecular sciences

Article Title: Heart Failure Promotes Cancer Progression in an Integrin β1-Dependent Manner.

doi: 10.3390/ijms242417367

Figure Lengend Snippet: Figure 2. Tumor-promotion phenotype in the serum derived from POSTN(−/−) mice is mediated by multiple secreted factors. The proliferation of (A) polyoma middle T breast cancer cells (PyMT) or (B) Lewis lung carcinoma (LLC) cells under different growth conditions in the presence of the indicated murine serums; n = 4 plates per treatment for each time point. (C) Pooled serum from POSTN(−/−) or C57Bl/6 male mice (n = 3 per pool) was used to probe the proteome cytokine array. For each protein, the serum levels are presented as a fold change in the serum derived from POSTN(−/−) relative to the control C57Bl/6 serum. (D) Fibronectin (FN) serum levels measured by ELISA (n = 3 per group; C57Bl/6 in green, POSTN(−/−) in red). Data are presented as mean ± SE. One-way ANOVA followed by Tukey’s post-test (A,B), and Student’s t-test (D). * p < 0.05, ** p < 0.01.

Article Snippet: The quantification of Periostin and Fibronectin in the serum was performed using the mouse Periostin/OSF-2 Quantikine ELISA kit (R&D systems Inc., Minneapolis, MN, USA) and mouse Fibronectin ELISA kit (E-EL-M0506, Elabscience, Houston, TX, USA), according to the manufacturer’s instructions.

Techniques: Derivative Assay, Control, Enzyme-linked Immunosorbent Assay