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rabbit anti-fgfr1 polyclonal #gb115541 (Servicebio Inc)

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Servicebio Inc rabbit anti-fgfr1 polyclonal #gb115541
Rabbit Anti Fgfr1 Polyclonal #Gb115541, supplied by Servicebio Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/rabbit+anti-fgfr1+polyclonal/pm39037153-83-4-9?v=Servicebio+Inc
Average 90 stars, based on 1 article reviews

rabbit anti-fgfr1 polyclonal #gb115541 - by Bioz Stars, 2026-07

90/100 stars

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(A) Box plot representation of FGFR1 and Notch2 gene expression in GBM (T, red) and normal tissue (N, grey) based on tumor and normal samples from the TCGA and the GTEx databases. (B) Kaplan-Meier curve representing overall survival associated with low (blue) and high (red) gene expression of FGFR1 and Notch2 in GBM, obtained as in (A). (C) Representative images of different grades of phospho-FGFR1 expression in human primary GBM samples by immunohistochemistry. (D) Scatter plot for the visual score of images as in (C) for phospho-FGFR1 (P-FGFR1) expression from 27 human primary GBM samples. (E) Kaplan Meier plot curves showing Relapse-Free Survival (RFS) for GBM patients based on the classification as phospho-FGFR1 positive or phospho-FGFR1 negative from the immunohistochemistry samples from (D). (F) Representative immunoblot showing the effect of TMZ treatment on FGFR1 phosphorylation, Notch2 activation (N2ICD) and p53 phosphorylation in several human GBM cell lines.

Journal: bioRxiv

Article Title: FGFR1 inhibition improves therapy efficacy and prevents metabolic adaptation associated with temozolomide resistance in glioblastoma

doi: 10.1101/2025.01.11.632515

Figure Lengend Snippet: (A) Box plot representation of FGFR1 and Notch2 gene expression in GBM (T, red) and normal tissue (N, grey) based on tumor and normal samples from the TCGA and the GTEx databases. (B) Kaplan-Meier curve representing overall survival associated with low (blue) and high (red) gene expression of FGFR1 and Notch2 in GBM, obtained as in (A). (C) Representative images of different grades of phospho-FGFR1 expression in human primary GBM samples by immunohistochemistry. (D) Scatter plot for the visual score of images as in (C) for phospho-FGFR1 (P-FGFR1) expression from 27 human primary GBM samples. (E) Kaplan Meier plot curves showing Relapse-Free Survival (RFS) for GBM patients based on the classification as phospho-FGFR1 positive or phospho-FGFR1 negative from the immunohistochemistry samples from (D). (F) Representative immunoblot showing the effect of TMZ treatment on FGFR1 phosphorylation, Notch2 activation (N2ICD) and p53 phosphorylation in several human GBM cell lines.

Article Snippet: Paraffin-embedded samples were submitted to standard immunohistochemistry (IHC) protocol with rabbit anti-phospho-FGFR1 (Tyr653/Tyr654) polyclonal antibody, 1:50 (44-1140G, Thermo Scientific), mouse anti-Ki67, 1:100 (550609, BD Pharmingen), rabbit anti-cleaved Caspase 3, 1:100 (9664, Cell Signalling), and rabbit anti-phospho-ERK, 1:100 (4370; Cell Signalling).

Techniques: Expressing, Immunohistochemistry, Western Blot, Activation Assay

(A) Box plot for FGFR1 and Notch2 gene expression in low grade glioma (LGG) tumors (T, red) and normal tissue (N, grey) based on tumor and normal samples from TCGA and GTEx databases. (B, C) Box plot for FGFR2, FGFR3, and FGFR4 (B) and Notch1 (C) gene expression in GBM (T, red) and normal tissue (N, grey) analysed as in (A). (D) Survival heatmap for GBM cohort from TCGA and the GTEx datasets showing the survival contribution of the indicated genes. (E) Cell viability curves to establish TMZ IC50 for the indicated GBM cell lines. (F) Classification of GBM cell lines for the resistance to TMZ treatment according to the IC50 analysis in (E). (G) Classification of GBM cell lines according to their genetic status and the activation of FGFR1 and Notch2 receptors. MGMT unmethylated (+) and methylated (-); wildtype (WT) or mutated (MUT): low (-) and high (+) activation. (H) Scatter plot and correlation coefficient between phospho-FGFR1 (P-FGFR1) expression and TMZ IC50 in GBM cell lines. (I) mRNA levels for FGFR1 and Notch2 upon TMZ treatment in CCF cells, assessed by qPCR. (J) mRNA expression analysis for FGFR1 and Notch2 from RNA-seq clinical data from the TCGA Pan-Cancer Atlas GBM dataset. (K) Stacked bar graphs showing the percentage of cells at the different stages of cell cycle upon TMZ treatment of GBM cell lines.

Journal: bioRxiv

Article Title: FGFR1 inhibition improves therapy efficacy and prevents metabolic adaptation associated with temozolomide resistance in glioblastoma

doi: 10.1101/2025.01.11.632515

Figure Lengend Snippet: (A) Box plot for FGFR1 and Notch2 gene expression in low grade glioma (LGG) tumors (T, red) and normal tissue (N, grey) based on tumor and normal samples from TCGA and GTEx databases. (B, C) Box plot for FGFR2, FGFR3, and FGFR4 (B) and Notch1 (C) gene expression in GBM (T, red) and normal tissue (N, grey) analysed as in (A). (D) Survival heatmap for GBM cohort from TCGA and the GTEx datasets showing the survival contribution of the indicated genes. (E) Cell viability curves to establish TMZ IC50 for the indicated GBM cell lines. (F) Classification of GBM cell lines for the resistance to TMZ treatment according to the IC50 analysis in (E). (G) Classification of GBM cell lines according to their genetic status and the activation of FGFR1 and Notch2 receptors. MGMT unmethylated (+) and methylated (-); wildtype (WT) or mutated (MUT): low (-) and high (+) activation. (H) Scatter plot and correlation coefficient between phospho-FGFR1 (P-FGFR1) expression and TMZ IC50 in GBM cell lines. (I) mRNA levels for FGFR1 and Notch2 upon TMZ treatment in CCF cells, assessed by qPCR. (J) mRNA expression analysis for FGFR1 and Notch2 from RNA-seq clinical data from the TCGA Pan-Cancer Atlas GBM dataset. (K) Stacked bar graphs showing the percentage of cells at the different stages of cell cycle upon TMZ treatment of GBM cell lines.

Techniques: Expressing, Activation Assay, Methylation, RNA Sequencing Assay

(A, B, C) Percentage of dead cells estimated by trypan blue viability assay for CCF, LN18 and U87 treated with vehicle (DMSO), TMZ (100 µM) and DAPT (10µM) for 72 hours. (D) Immunoblot analysis of Notch signaling activation (N1ICD and N2ICD) in U87, CCF, LN18 treated with DAPT (10µM) for 72 hours. (E) Immunoblot for Notch2 activation levels (N2ICD) after Notch2 silencing using siRNA and treated with TMZ (100µM) for 72 hours in CCF. (F) Percentage of dead cells by trypan blue assay for CCF cells after Notch2 silencing and TMZ treatment as in (E). (G) Immunoblot of apoptotic markers (cleaved Caspase3 and cleaved PARP) in LN18 and U87 cells incubated with TMZ (100 µM) and the FGFR1i (PD173074, 4 µM) for 72 hours. (H, I) Percentage of dead cells estimated by trypan blue viability assay (H) and flow cytometry with annexin V / PI staining (I) in CCF cells treated with TMZ (100 µM) and FGFR1i (PD166866 5µM) for 72 hours. (J) Percentage of dead cells estimated by trypan blue in LN18 and U87 treated as indicated for 72 hours. (K) Immunoblot for FGFR1 expression and activity (FGFR1 phosphorylation) upon CCF treatment as described in (E). (L) DNA damage quantification of CCF cells by γH2AX expression using MetaXpress analysis upon treatment with TMZ (100 µM) and FGFR1i (PD166866 5µM) for 72 hours. (M) Immunoblot for FGFR1 activation (FGFR1 and ERK phosphorylation), and cell cycle markers (E2F1, p53 and cyclins) in CCF cells treated with TMZ (100 µM) and FGFR1i (PD166866 5µM) for 72 hours. (N) Immunoblot for FGFR1 activation and cell cycle markers in A172 treated with TMZ (100 µM) and FGFR1i (PD166866, at the indicated concentration) for 72 hours. (O) Percentage of dead cells estimated by trypan blue assay in CCF cells treated with ERK and EGFR inhibitors (Ravoxertinib and Lapatinib respectively) combined or not with TMZ for 72 hours. Graphs show mean values ±SEM (n=3 biologically independent experiments). * p < 0.05 (ANOVA post hoc Bonferroni test).

Journal: bioRxiv

Article Title: FGFR1 inhibition improves therapy efficacy and prevents metabolic adaptation associated with temozolomide resistance in glioblastoma

doi: 10.1101/2025.01.11.632515

Figure Lengend Snippet: (A, B, C) Percentage of dead cells estimated by trypan blue viability assay for CCF, LN18 and U87 treated with vehicle (DMSO), TMZ (100 µM) and DAPT (10µM) for 72 hours. (D) Immunoblot analysis of Notch signaling activation (N1ICD and N2ICD) in U87, CCF, LN18 treated with DAPT (10µM) for 72 hours. (E) Immunoblot for Notch2 activation levels (N2ICD) after Notch2 silencing using siRNA and treated with TMZ (100µM) for 72 hours in CCF. (F) Percentage of dead cells by trypan blue assay for CCF cells after Notch2 silencing and TMZ treatment as in (E). (G) Immunoblot of apoptotic markers (cleaved Caspase3 and cleaved PARP) in LN18 and U87 cells incubated with TMZ (100 µM) and the FGFR1i (PD173074, 4 µM) for 72 hours. (H, I) Percentage of dead cells estimated by trypan blue viability assay (H) and flow cytometry with annexin V / PI staining (I) in CCF cells treated with TMZ (100 µM) and FGFR1i (PD166866 5µM) for 72 hours. (J) Percentage of dead cells estimated by trypan blue in LN18 and U87 treated as indicated for 72 hours. (K) Immunoblot for FGFR1 expression and activity (FGFR1 phosphorylation) upon CCF treatment as described in (E). (L) DNA damage quantification of CCF cells by γH2AX expression using MetaXpress analysis upon treatment with TMZ (100 µM) and FGFR1i (PD166866 5µM) for 72 hours. (M) Immunoblot for FGFR1 activation (FGFR1 and ERK phosphorylation), and cell cycle markers (E2F1, p53 and cyclins) in CCF cells treated with TMZ (100 µM) and FGFR1i (PD166866 5µM) for 72 hours. (N) Immunoblot for FGFR1 activation and cell cycle markers in A172 treated with TMZ (100 µM) and FGFR1i (PD166866, at the indicated concentration) for 72 hours. (O) Percentage of dead cells estimated by trypan blue assay in CCF cells treated with ERK and EGFR inhibitors (Ravoxertinib and Lapatinib respectively) combined or not with TMZ for 72 hours. Graphs show mean values ±SEM (n=3 biologically independent experiments). * p < 0.05 (ANOVA post hoc Bonferroni test).

Techniques: Viability Assay, Western Blot, Activation Assay, Incubation, Flow Cytometry, Staining, Expressing, Activity Assay, Concentration Assay

(A, B, C) Percentage of dead cells as estimated by trypan blue viability assay for GBM cell lines treated with vehicle (DMSO), TMZ (100 µM) or FGFR1i PD173074 (4 µM) for 72 hours. (D) Representative flow cytometry dot plots of annexin V / PI staining of CCF cells treated as indicated for 72 hours. (E) Quantification of the apoptotic population shown in (D) from two biologically independent experiments. (F) Immunoblot of apoptotic markers (cleaved Caspase 3, cleaved PARP), Notch2 activity (N2ICD) and FGFR1 activation (FGFR1 phosphorylation) in CCF cells upon treatment. (G, H) Stacked bar graph (G) of cell cycle analysis by flow cytometry, and quantification (H) of S+G2/M cell percentage for the indicated conditions in CCF cells. (I) Immunoblot of FGFR1 pathway activation (FGFR1 phosphorylation and ERK phosphorylation), and key cell cycle mediators (E2F1, p53 and cyclins) after 72 hours treatment in CCF cells. (J) Percentage of dead cells estimated by trypan blue viability assay for A172 treated with vehicle (DMSO), TMZ (100 µM) and the two FGFR1 inhibitors PD173074 and PD166866 (4 µM and 0.5 µM, respectively), for 72 hours. (K) Stacked bar graph of cell cycle analysis by flow cytometry of A172 treated with PD166866 (0.5 µM) and TMZ (100 µM) for 72 hours. Graphs show mean values ±SEM (n=3 biologically independent experiments). *p < 0.05 (ANOVA post hoc Bonferroni test).

Journal: bioRxiv

Article Title: FGFR1 inhibition improves therapy efficacy and prevents metabolic adaptation associated with temozolomide resistance in glioblastoma

doi: 10.1101/2025.01.11.632515

Figure Lengend Snippet: (A, B, C) Percentage of dead cells as estimated by trypan blue viability assay for GBM cell lines treated with vehicle (DMSO), TMZ (100 µM) or FGFR1i PD173074 (4 µM) for 72 hours. (D) Representative flow cytometry dot plots of annexin V / PI staining of CCF cells treated as indicated for 72 hours. (E) Quantification of the apoptotic population shown in (D) from two biologically independent experiments. (F) Immunoblot of apoptotic markers (cleaved Caspase 3, cleaved PARP), Notch2 activity (N2ICD) and FGFR1 activation (FGFR1 phosphorylation) in CCF cells upon treatment. (G, H) Stacked bar graph (G) of cell cycle analysis by flow cytometry, and quantification (H) of S+G2/M cell percentage for the indicated conditions in CCF cells. (I) Immunoblot of FGFR1 pathway activation (FGFR1 phosphorylation and ERK phosphorylation), and key cell cycle mediators (E2F1, p53 and cyclins) after 72 hours treatment in CCF cells. (J) Percentage of dead cells estimated by trypan blue viability assay for A172 treated with vehicle (DMSO), TMZ (100 µM) and the two FGFR1 inhibitors PD173074 and PD166866 (4 µM and 0.5 µM, respectively), for 72 hours. (K) Stacked bar graph of cell cycle analysis by flow cytometry of A172 treated with PD166866 (0.5 µM) and TMZ (100 µM) for 72 hours. Graphs show mean values ±SEM (n=3 biologically independent experiments). *p < 0.05 (ANOVA post hoc Bonferroni test).

Techniques: Viability Assay, Flow Cytometry, Staining, Western Blot, Activity Assay, Activation Assay, Cell Cycle Assay

(A) Heatmap of gene expression fold change from RNA-seq analysis in CCF cells treated with TMZ (100 µM) and FGFR1 (PD166866, 5 µM). (B, C) Volcano plot from RNA-seq analysis for upregulated (red) and downregulated (blue) genes for the indicated conditions. (D, E) Gene Ontology (GO) enrichment analysis for biological processes for the up-regulated (D) and down-regulated (E) genes for the dual treatment TMZ plus FGFR1i compared to DMSO (control). (F) GSEA plots for cell cycle related hallmarks comparing gene sets from TMZ treatment and dual treatment with TMZ and FGFR1i. (G) Volcano plot for upregulated (red) and downregulated (blue) metabolism-related genes. (H) GO plot representing the metabolic pathways with dysregulated genes by the treatment with TMZ and FGFR1i. (I-L) mRNA expression levels assessed by qPCR for genes found dysregulated in the RNA-seq analysis and highlighted in (G).

Journal: bioRxiv

Article Title: FGFR1 inhibition improves therapy efficacy and prevents metabolic adaptation associated with temozolomide resistance in glioblastoma

doi: 10.1101/2025.01.11.632515

Figure Lengend Snippet: (A) Heatmap of gene expression fold change from RNA-seq analysis in CCF cells treated with TMZ (100 µM) and FGFR1 (PD166866, 5 µM). (B, C) Volcano plot from RNA-seq analysis for upregulated (red) and downregulated (blue) genes for the indicated conditions. (D, E) Gene Ontology (GO) enrichment analysis for biological processes for the up-regulated (D) and down-regulated (E) genes for the dual treatment TMZ plus FGFR1i compared to DMSO (control). (F) GSEA plots for cell cycle related hallmarks comparing gene sets from TMZ treatment and dual treatment with TMZ and FGFR1i. (G) Volcano plot for upregulated (red) and downregulated (blue) metabolism-related genes. (H) GO plot representing the metabolic pathways with dysregulated genes by the treatment with TMZ and FGFR1i. (I-L) mRNA expression levels assessed by qPCR for genes found dysregulated in the RNA-seq analysis and highlighted in (G).

Techniques: Expressing, RNA Sequencing Assay, Control

(A) Principal component analysis (PCA) plot showing clustering of the different treatments and replicates from the RNA-seq dataset. (B, C) Volcano plot of the upregulated (red) and downregulated (blue) genes for FGFR1i (B) or TMZ (C) individual treatments. (D) Venn diagram showing the overlapping genes affected upon the indicated treatments as estimated from RNA-seq analysis. (E) Genes from the MAPK signaling pathway dysregulated by FGFR1 inhibition as estimated from RNA-seq analysis. (F) GESEA plot for E2F target genes in the indicated conditions as estimated from RNA-seq analysis. (G) Metabolic genes dysregulated in the dual treatment TMZ plus FGFR1i organised by the metabolic pathway as shown in .

Journal: bioRxiv

Article Title: FGFR1 inhibition improves therapy efficacy and prevents metabolic adaptation associated with temozolomide resistance in glioblastoma

doi: 10.1101/2025.01.11.632515

Figure Lengend Snippet: (A) Principal component analysis (PCA) plot showing clustering of the different treatments and replicates from the RNA-seq dataset. (B, C) Volcano plot of the upregulated (red) and downregulated (blue) genes for FGFR1i (B) or TMZ (C) individual treatments. (D) Venn diagram showing the overlapping genes affected upon the indicated treatments as estimated from RNA-seq analysis. (E) Genes from the MAPK signaling pathway dysregulated by FGFR1 inhibition as estimated from RNA-seq analysis. (F) GESEA plot for E2F target genes in the indicated conditions as estimated from RNA-seq analysis. (G) Metabolic genes dysregulated in the dual treatment TMZ plus FGFR1i organised by the metabolic pathway as shown in .

Techniques: RNA Sequencing Assay, Inhibition

(A) Evolution of xenograft tumor volume during time in mice treated as indicated (n= 5 mice per treatment). Treatments started when tumors reached 100mm 3 . (B) Bar graph representation of tumor volume differences at endpoint between TMZ treatment and the combination of TMZ with FGFR1i. (C) Representative histological images of tumor sections from the xenograft tumors with the different treatments, stained with haematoxylin and eosin (H&E). Scale bars represent 100μm. (D) Representative images of the immunohistochemistry on sections from xenograft tumors at endpoint for the indicated markers and counterstained with haematoxylin. Scale bar represents 50μm. (E, F) Visual score analysis of images as in (D) for P-FGFR1 (E) and Ki67 (F) staining. The upper and lower limits of the boxes represent quartiles, the line within the boxes indicates the median and the whiskers show the extremes (n ≥ 15 images per treatment). (G) Immunoblot for ERK activity (ERK phosphorylation) and p53 from 3 different xenograft tumors treated as indicated. (H) Scheme of the working model representing the signaling and metabolic reprograming associated with TMZ resistance and controlled by FGFR1. was created with BioRender.com.

Journal: bioRxiv

Article Title: FGFR1 inhibition improves therapy efficacy and prevents metabolic adaptation associated with temozolomide resistance in glioblastoma

doi: 10.1101/2025.01.11.632515

Figure Lengend Snippet: (A) Evolution of xenograft tumor volume during time in mice treated as indicated (n= 5 mice per treatment). Treatments started when tumors reached 100mm 3 . (B) Bar graph representation of tumor volume differences at endpoint between TMZ treatment and the combination of TMZ with FGFR1i. (C) Representative histological images of tumor sections from the xenograft tumors with the different treatments, stained with haematoxylin and eosin (H&E). Scale bars represent 100μm. (D) Representative images of the immunohistochemistry on sections from xenograft tumors at endpoint for the indicated markers and counterstained with haematoxylin. Scale bar represents 50μm. (E, F) Visual score analysis of images as in (D) for P-FGFR1 (E) and Ki67 (F) staining. The upper and lower limits of the boxes represent quartiles, the line within the boxes indicates the median and the whiskers show the extremes (n ≥ 15 images per treatment). (G) Immunoblot for ERK activity (ERK phosphorylation) and p53 from 3 different xenograft tumors treated as indicated. (H) Scheme of the working model representing the signaling and metabolic reprograming associated with TMZ resistance and controlled by FGFR1. was created with BioRender.com.

Techniques: Staining, Immunohistochemistry, Western Blot, Activity Assay

(A) Longitudinal development of body weight of control animals (DMSO) and animals with the different treatments along the experimental period. (B) Two representative immunofluorescence images from primary astrocyte cultures stained with the astrocytic marker GFAP (red), and quantification of GFAP positive cells (n=14 images). (C) Quantification of apoptotic cells by flow cytometry analysis of annexin V/ PI staining of primary astrocyte cultures treated with vehicle (DMSO), TMZ (100 µM) and FGFR1i (PD166866, 5µM) for 72 hours. (D) Immunoblot of FGFR1 (total and phosphorylated), ERK (total and phosphorylated) and p53 in primary astrocyte cultures treated as indicated. (E) Photograph of 5 xenografts tumors observed at endpoint for each condition of treatment. (F) Lower magnification images of histological sections xenografts tumors from each condition of treatment. Scale bar represents 100 µm.

Journal: bioRxiv

Article Title: FGFR1 inhibition improves therapy efficacy and prevents metabolic adaptation associated with temozolomide resistance in glioblastoma

doi: 10.1101/2025.01.11.632515

Figure Lengend Snippet: (A) Longitudinal development of body weight of control animals (DMSO) and animals with the different treatments along the experimental period. (B) Two representative immunofluorescence images from primary astrocyte cultures stained with the astrocytic marker GFAP (red), and quantification of GFAP positive cells (n=14 images). (C) Quantification of apoptotic cells by flow cytometry analysis of annexin V/ PI staining of primary astrocyte cultures treated with vehicle (DMSO), TMZ (100 µM) and FGFR1i (PD166866, 5µM) for 72 hours. (D) Immunoblot of FGFR1 (total and phosphorylated), ERK (total and phosphorylated) and p53 in primary astrocyte cultures treated as indicated. (E) Photograph of 5 xenografts tumors observed at endpoint for each condition of treatment. (F) Lower magnification images of histological sections xenografts tumors from each condition of treatment. Scale bar represents 100 µm.

Techniques: Control, Immunofluorescence, Staining, Marker, Flow Cytometry, Western Blot

Enhanced expression of FGFR1 in human PTC. A ) Representative immunohistochemical staining of PTC tumors (n=3) and neighboring healthy thyroid samples (n=3). B,C ) Quantitative PCR by RT-qPCR of FGFR1 mRNA ( B ) and immunoblots of FGFR1 protein expression ( C ) in PTC tumors (n=32) and neighboring healthy thyroid samples (n=32). D) Representative immunoblot analysis of three PTC cell lines (IHH-4, TPC-1, and SW579) and control cell line Nthy-ori3-1 to detect FGFR1 protein levels. * p <0.05.

Journal: European Journal of Histochemistry : EJH

Article Title: Identification of mechanism of the oncogenic role of FGFR1 in papillary thyroid carcinoma

doi: 10.4081/ejh.2024.4048

Figure Lengend Snippet: Enhanced expression of FGFR1 in human PTC. A ) Representative immunohistochemical staining of PTC tumors (n=3) and neighboring healthy thyroid samples (n=3). B,C ) Quantitative PCR by RT-qPCR of FGFR1 mRNA ( B ) and immunoblots of FGFR1 protein expression ( C ) in PTC tumors (n=32) and neighboring healthy thyroid samples (n=32). D) Representative immunoblot analysis of three PTC cell lines (IHH-4, TPC-1, and SW579) and control cell line Nthy-ori3-1 to detect FGFR1 protein levels. * p <0.05.

Article Snippet: The primary antibodies, including rabbit anti-FGFR1 polyclonal (#GB115541, 1:100; Servicebio) and mouse anti-USP7 monoclonal (#66514-1-Ig, 1:300; Proteintech), were used prior to the application of Alexa 488-labeled anti-mouse (#GB25301, 1:500; Servicebio) and Cy3-labeled anti-rabbit (#GB21303, 1:500; Servicebio) IgG secondary antibodies following the vendors’ guidelines.

Techniques: Expressing, Immunohistochemical staining, Staining, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Western Blot, Control

Regulatory functions of FGFR1 in PTC cell phenotypes. A ) Representative immunoblot showing the protein expression of FGFR1 in TPC-1 and SW579 PTC cells that were introduced with a FGFR1-siRNA (si-FGFR1) or scrambled siRNA sequence (si-NC). B ) CCK-8 cell viability analysis of TPC-1 and SW579 PTC cells transfected as in A. C ) EdU cell proliferation assay of TPC-1 and SW579 PTC cells transfected as in A. D ) Annexin V-FITC and PI staining-based cell apoptosis analysis of TPC-1 and SW579 PTC cells treated as in A. E,F ) Transwell invasiveness analysis of TPC-1 and SW579 PTC cells introduced as in A. G ) Would healing assay of TPC-1 and SW579 PTC cells introduced as in A to test cell migratory ability. * p <0.05.

Journal: European Journal of Histochemistry : EJH

Article Title: Identification of mechanism of the oncogenic role of FGFR1 in papillary thyroid carcinoma

doi: 10.4081/ejh.2024.4048

Figure Lengend Snippet: Regulatory functions of FGFR1 in PTC cell phenotypes. A ) Representative immunoblot showing the protein expression of FGFR1 in TPC-1 and SW579 PTC cells that were introduced with a FGFR1-siRNA (si-FGFR1) or scrambled siRNA sequence (si-NC). B ) CCK-8 cell viability analysis of TPC-1 and SW579 PTC cells transfected as in A. C ) EdU cell proliferation assay of TPC-1 and SW579 PTC cells transfected as in A. D ) Annexin V-FITC and PI staining-based cell apoptosis analysis of TPC-1 and SW579 PTC cells treated as in A. E,F ) Transwell invasiveness analysis of TPC-1 and SW579 PTC cells introduced as in A. G ) Would healing assay of TPC-1 and SW579 PTC cells introduced as in A to test cell migratory ability. * p <0.05.

Techniques: Western Blot, Expressing, Sequencing, CCK-8 Assay, Transfection, Proliferation Assay, Staining

USP7 promotes FGFR1 deubiquitination to stabilize FGFR1 protein. A ) Ubibrowser 2.0 database predicted the USP7-FGFR1 interaction. B ) Immunoblots of si-USP7-transfected or si-NC-introduced TPC-1 and SW579 cells for evaluation of USP7 protein expression. C,D ) FGFR1 mRNA expression analysis by RT-qPCR ( C ) and FGFR1 protein level analysis by immunoblot assay ( D ) in si-USP7-transfected or si-NC-introduced TPC-1 and SW579 cells. E ) Representative immunoblotting revealing FGFR1 protein level in TPC-1 and SW579 cells after si-NC introduction, si-USP7 transfection, or si-USP7 transfection before MG132 exposure (100 nM, 24 h). F ) TPC-1 cells were co-transfected with Flag-FGFR1 plasmid and si-USP7 or sh-NC control, followed by immunoprecipitation (IP) experiment with anti-Flag antibody; the immunoprecipitates were subjected to immunoblot assay (IB) using anti-Ub antibody. G ) Representative immunofluorescence staining depicting the expression and localization of USP7 and FGFR1 in si-USP7-transfected or si-NC-introduced TPC-1 cells. * p <0.05.

Journal: European Journal of Histochemistry : EJH

Article Title: Identification of mechanism of the oncogenic role of FGFR1 in papillary thyroid carcinoma

doi: 10.4081/ejh.2024.4048

Figure Lengend Snippet: USP7 promotes FGFR1 deubiquitination to stabilize FGFR1 protein. A ) Ubibrowser 2.0 database predicted the USP7-FGFR1 interaction. B ) Immunoblots of si-USP7-transfected or si-NC-introduced TPC-1 and SW579 cells for evaluation of USP7 protein expression. C,D ) FGFR1 mRNA expression analysis by RT-qPCR ( C ) and FGFR1 protein level analysis by immunoblot assay ( D ) in si-USP7-transfected or si-NC-introduced TPC-1 and SW579 cells. E ) Representative immunoblotting revealing FGFR1 protein level in TPC-1 and SW579 cells after si-NC introduction, si-USP7 transfection, or si-USP7 transfection before MG132 exposure (100 nM, 24 h). F ) TPC-1 cells were co-transfected with Flag-FGFR1 plasmid and si-USP7 or sh-NC control, followed by immunoprecipitation (IP) experiment with anti-Flag antibody; the immunoprecipitates were subjected to immunoblot assay (IB) using anti-Ub antibody. G ) Representative immunofluorescence staining depicting the expression and localization of USP7 and FGFR1 in si-USP7-transfected or si-NC-introduced TPC-1 cells. * p <0.05.

Techniques: Western Blot, Transfection, Expressing, Quantitative RT-PCR, Plasmid Preparation, Control, Immunoprecipitation, Immunofluorescence, Staining

USP7 correlates with PTC cell malignant behaviors by stabilizing FGFR1. A ) Immunoblots of lysates of TPC-1 and SW579 PTC cells that were introduced with si-USP7, si-USP7+FGFR1 plasmid or scrambled siRNA sequence (si-NC) for evaluation of FGFR1 protein. B ) Viability analysis of TPC-1 and SW579 PTC cells transfected as in A by CCK-8 assay. C,D ) Proliferative ability evaluation of TPC-1 and SW579 PTC cells transfected as in A by EdU assay. E ) Apoptosis analysis of TPC-1 and SW579 PTC cells treated as in A by flow cytometry based Annexin V-FITC and PI staining. F,G ) Assessment of invasiveness of TPC-1 and SW579 PTC cells introduced as in A by transwell assay. H) Determination of migratory ability of TPC-1 and SW579 PTC cells introduced as in A by would healing assay. * p <0.05.

Journal: European Journal of Histochemistry : EJH

Article Title: Identification of mechanism of the oncogenic role of FGFR1 in papillary thyroid carcinoma

doi: 10.4081/ejh.2024.4048

Figure Lengend Snippet: USP7 correlates with PTC cell malignant behaviors by stabilizing FGFR1. A ) Immunoblots of lysates of TPC-1 and SW579 PTC cells that were introduced with si-USP7, si-USP7+FGFR1 plasmid or scrambled siRNA sequence (si-NC) for evaluation of FGFR1 protein. B ) Viability analysis of TPC-1 and SW579 PTC cells transfected as in A by CCK-8 assay. C,D ) Proliferative ability evaluation of TPC-1 and SW579 PTC cells transfected as in A by EdU assay. E ) Apoptosis analysis of TPC-1 and SW579 PTC cells treated as in A by flow cytometry based Annexin V-FITC and PI staining. F,G ) Assessment of invasiveness of TPC-1 and SW579 PTC cells introduced as in A by transwell assay. H) Determination of migratory ability of TPC-1 and SW579 PTC cells introduced as in A by would healing assay. * p <0.05.

Techniques: Western Blot, Plasmid Preparation, Sequencing, Transfection, CCK-8 Assay, EdU Assay, Flow Cytometry, Staining, Transwell Assay

TF YY1 can promote FGFR1 transcription. A ) Schematic of the motif of YY1, the predicted pairing sequence for YY1 in the FGFR1 promoter, the mutation in the pairing sequence. B ) ChIP experiments of chromatin of TPC-1 and SW579 cells using antibodies against YY1 and IgG, followed by DNA purification and enrichment analysis of the FGFR1 promoter. C ) Immunoblots of lysates of si-YY1- or si-NC-transfected TPC-1 and SW579 cells to assess YY1 protein expression. D,E ) The reporter construct WT-FGFR1 or MUT-FGFR1 was introduced into TPC-1 and SW579 cells along with si-YY1 or si-NC control, followed by analysis of luciferase activity. F) Representative immunoblotting showing FGFR1 protein level in si-YY1- or si-NC-introduced TPC-1 and SW579 cells. * p <0.05.

Journal: European Journal of Histochemistry : EJH

Article Title: Identification of mechanism of the oncogenic role of FGFR1 in papillary thyroid carcinoma

doi: 10.4081/ejh.2024.4048

Figure Lengend Snippet: TF YY1 can promote FGFR1 transcription. A ) Schematic of the motif of YY1, the predicted pairing sequence for YY1 in the FGFR1 promoter, the mutation in the pairing sequence. B ) ChIP experiments of chromatin of TPC-1 and SW579 cells using antibodies against YY1 and IgG, followed by DNA purification and enrichment analysis of the FGFR1 promoter. C ) Immunoblots of lysates of si-YY1- or si-NC-transfected TPC-1 and SW579 cells to assess YY1 protein expression. D,E ) The reporter construct WT-FGFR1 or MUT-FGFR1 was introduced into TPC-1 and SW579 cells along with si-YY1 or si-NC control, followed by analysis of luciferase activity. F) Representative immunoblotting showing FGFR1 protein level in si-YY1- or si-NC-introduced TPC-1 and SW579 cells. * p <0.05.

Techniques: Sequencing, Mutagenesis, DNA Purification, Western Blot, Transfection, Expressing, Construct, Control, Luciferase, Activity Assay

Reduction of USP7 prevents xenograft growth by downregulating FGFR1. A,B ) Xenograft growth curve ( A ) and weight ( B ) in BALB/c nude mice after injection of sh-NC lentivirus-infected SW579 cells, sh-USP7 lentivirus-transduced SW579 cells with or without intratumor injection of FGFR1 expression plasmid. C ) Immunoblots of sh-NC SW579 xenografts, sh-USP7 SW579 xenografts and shUSP7+FGFR1 xenografts to evaluate FGFR1 protein expression. D ) Representative immunohistochemical staining of xenografts shown in C for evaluation of FGFR1 expression and the Ki67-positive cells. * p <0.05.

Journal: European Journal of Histochemistry : EJH

Article Title: Identification of mechanism of the oncogenic role of FGFR1 in papillary thyroid carcinoma

doi: 10.4081/ejh.2024.4048

Figure Lengend Snippet: Reduction of USP7 prevents xenograft growth by downregulating FGFR1. A,B ) Xenograft growth curve ( A ) and weight ( B ) in BALB/c nude mice after injection of sh-NC lentivirus-infected SW579 cells, sh-USP7 lentivirus-transduced SW579 cells with or without intratumor injection of FGFR1 expression plasmid. C ) Immunoblots of sh-NC SW579 xenografts, sh-USP7 SW579 xenografts and shUSP7+FGFR1 xenografts to evaluate FGFR1 protein expression. D ) Representative immunohistochemical staining of xenografts shown in C for evaluation of FGFR1 expression and the Ki67-positive cells. * p <0.05.

Techniques: Injection, Infection, Expressing, Plasmid Preparation, Western Blot, Immunohistochemical staining, Staining

Schematic of the USP7/FGFR1 and YY1/FGFR1 cascades in PTC progression. In PTC cells, the TF YY1 promotes the transcription of FGFR1 and the deubiquitinating enzyme USP7 stabilizes FGFR1, thereby contributing PTC progression

Journal: European Journal of Histochemistry : EJH

Article Title: Identification of mechanism of the oncogenic role of FGFR1 in papillary thyroid carcinoma

doi: 10.4081/ejh.2024.4048

Figure Lengend Snippet: Schematic of the USP7/FGFR1 and YY1/FGFR1 cascades in PTC progression. In PTC cells, the TF YY1 promotes the transcription of FGFR1 and the deubiquitinating enzyme USP7 stabilizes FGFR1, thereby contributing PTC progression

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