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Proteintech rabbit monoclonal anti fgf1 pa5 79249
Rabbit Monoclonal Anti Fgf1 Pa5 79249, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 12 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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rabbit monoclonal anti fgf1 pa5 79249 - by Bioz Stars, 2026-05

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FGF1 reduces hepatic steatosis and acutely induces ApoB. (A) Hepatic TG in high-fat diet-fed adipose-specific Fgfr1 -/- mice treated with FGF1 every 3 days for 5 weeks (Mann-Whitney U test; ∗∗ p < 0.01). (B) Plasma free fatty acid levels, (C) plasma TG, and (D) total cholesterol levels 24 h after an FGF1 injection in chow-fed ob/ob mice (Mann-Whitney U test; ∗ p < 0.05). (E) Volcano plot of significantly (red) and non-significantly (green) affected plasma proteins in chow-fed ob/ob mice after 24 h FGF1 treatment as determined by untargeted proteomics. Arrow highlights ApoB. (F) Profiling of apolipoproteins in plasma of chow-fed ob/ob mice after 24 h of FGF1 treatment using a targeted proteomics strategy (Mann-Whitney U test; ∗∗ p < 0.01). All panels n = 6-8. TG, triglyceride.

Journal: JHEP Reports

Article Title: FGF1 ameliorates hepatic steatosis through acute activation of the unfolded protein response and VLDL production

doi: 10.1016/j.jhepr.2025.101660

Figure Lengend Snippet: FGF1 reduces hepatic steatosis and acutely induces ApoB. (A) Hepatic TG in high-fat diet-fed adipose-specific Fgfr1 -/- mice treated with FGF1 every 3 days for 5 weeks (Mann-Whitney U test; ∗∗ p < 0.01). (B) Plasma free fatty acid levels, (C) plasma TG, and (D) total cholesterol levels 24 h after an FGF1 injection in chow-fed ob/ob mice (Mann-Whitney U test; ∗ p < 0.05). (E) Volcano plot of significantly (red) and non-significantly (green) affected plasma proteins in chow-fed ob/ob mice after 24 h FGF1 treatment as determined by untargeted proteomics. Arrow highlights ApoB. (F) Profiling of apolipoproteins in plasma of chow-fed ob/ob mice after 24 h of FGF1 treatment using a targeted proteomics strategy (Mann-Whitney U test; ∗∗ p < 0.01). All panels n = 6-8. TG, triglyceride.

Article Snippet: Mice were treated with vehicle (PBS), recombinant FGF1 (0.5 mg/kg, R&D Systems) or the FGF1 K133E variant (kind gift by Birgitte Andersen, Novo Nordisk, Bagsværd Denmark) by intraperitoneal (i.p.) injection.

Techniques: MANN-WHITNEY, Clinical Proteomics, Injection, Targeted Proteomics

$FGF1 acutely and transiently stimulates VLDL production in ob/ob mice. (A) Temporal dynamics of plasma TG in ob/ob mice upon FGF1 injection (Mann-Whitney U test; ∗∗ p < 0.01). (B) TG levels in FPLC fractions from plasma of ob/ob mice, 24 h after FGF1 injection. Inset: ApoB in FPLC fractions 7, 9, 11 and 13 corresponding to VLDL. (C) Plasma TG/ApoB ratios 24 h after an FGF1 injection in ob/ob. (D) Left panel: plasma TG levels upon LPL inhibition by poloxamer in 14 h FGF1-stimulated ob/ob and right panel: calculated production rate from the curves. (E) Plasma TG in ob/ob mice 24 h after FGF1 K133E administration (Mann-Whitney U test; ∗∗ p < 0.01). All panels n = 6-8. FPLC, fast protein liquid chromatography; TG, triglyceride.$

Journal: JHEP Reports

Article Title: FGF1 ameliorates hepatic steatosis through acute activation of the unfolded protein response and VLDL production

doi: 10.1016/j.jhepr.2025.101660

Figure Lengend Snippet: FGF1 acutely and transiently stimulates VLDL production in ob/ob mice. (A) Temporal dynamics of plasma TG in ob/ob mice upon FGF1 injection (Mann-Whitney U test; ∗∗ p < 0.01). (B) TG levels in FPLC fractions from plasma of ob/ob mice, 24 h after FGF1 injection. Inset: ApoB in FPLC fractions 7, 9, 11 and 13 corresponding to VLDL. (C) Plasma TG/ApoB ratios 24 h after an FGF1 injection in ob/ob. (D) Left panel: plasma TG levels upon LPL inhibition by poloxamer in 14 h FGF1-stimulated ob/ob and right panel: calculated production rate from the curves. (E) Plasma TG in ob/ob mice 24 h after FGF1 K133E administration (Mann-Whitney U test; ∗∗ p < 0.01). All panels n = 6-8. FPLC, fast protein liquid chromatography; TG, triglyceride.

Techniques: Clinical Proteomics, Injection, MANN-WHITNEY, Inhibition, Fast Protein Liquid Chromatography

Anti-steatotic FGF1 effects are not associated with adipose lipolysis, hepatic lipogenesis or β-oxidation. (A) Fatty acid synthesis and elongation rates of most common fatty acids using 13 C-acetate in ob/ob mouse livers during 24 h of FGF1 treatment. (B) Hepatic levels of lipogenesis proteins ACC and FAS, as well as phosphorylation of ACC in ob/ob mice 14 h after FGF1 injection. (C) Hepatic long-chain (C14–C18) acylcarnitines and (D) plasma acylcarnitines of 14 h FGF1-treated ob/ob mice. (E) Respiratory exchange ratios of FGF1-treated (at arrow) ob/ob mice. Mann-Whitney U test; ∗ p < 0.05, ∗∗ p < 0.01; n = 6-8.

Journal: JHEP Reports

Article Title: FGF1 ameliorates hepatic steatosis through acute activation of the unfolded protein response and VLDL production

doi: 10.1016/j.jhepr.2025.101660

Figure Lengend Snippet: Anti-steatotic FGF1 effects are not associated with adipose lipolysis, hepatic lipogenesis or β-oxidation. (A) Fatty acid synthesis and elongation rates of most common fatty acids using 13 C-acetate in ob/ob mouse livers during 24 h of FGF1 treatment. (B) Hepatic levels of lipogenesis proteins ACC and FAS, as well as phosphorylation of ACC in ob/ob mice 14 h after FGF1 injection. (C) Hepatic long-chain (C14–C18) acylcarnitines and (D) plasma acylcarnitines of 14 h FGF1-treated ob/ob mice. (E) Respiratory exchange ratios of FGF1-treated (at arrow) ob/ob mice. Mann-Whitney U test; ∗ p < 0.05, ∗∗ p < 0.01; n = 6-8.

Techniques: Phospho-proteomics, Injection, Clinical Proteomics, MANN-WHITNEY

FGF1 hyperactivates the UPR in the liver and hepatocytes. (A) Hepatic protein levels of the three UPR branch markers XBP1s, ATF6 (ATF6-U: unspliced & ATF6-N nuclear) and Perk phosphorylation 14 h after FGF1 injection of ob/ob showing UPR activation. In addition, XBP1s and ATF6 in nuclear extracts from these livers. (B) Hepatic expression levels of UPR chaperones ( Grp78 , Erp72 , Erdj3 , Grp94 , and Pdi ), ER-associated protein degradation genes ( Edem and Herp ), and PERK–ATF4–CHOP pathway genes ( Chop and Gadd34 ) in ob/ob mouse liver (Mann-Whitney U test; ∗ p < 0.05, ∗∗ p < 0.01). (C) Hepatic protein levels of Grp78, Grp94, Erp72, Erp57, Pdi and Chop 14 h after FGF1 injection of ob/ob mice. (D) Effect of 3 or 6 h FGF1 on UPR sensors in glucosamine-stressed HepG2 cells, showing Xbp1 mRNA (uXBP1: unspliced & sXBP: spliced), Ire1 and Perk phosphorylation, XBP1s and Atf6 protein levels (unspliced & nuclear) (E) Hyperactivation of UPR chaperone expression levels but not ERAD genes by 6 h FGF1 treatment in glucosamine-stressed (2 h) primary rat hepatocytes. ∗ p < 0.05 glucosamine vs. control, # p < 0.05 glucosamine vs. glucosamine + FGF1 (Kruskal-Wallis test). (F) UPR chaperone protein induction after FGF1 treatment in HepG2 cells with and without glucosamine pre-treatment. UPR, unfolded protein response.

Journal: JHEP Reports

Article Title: FGF1 ameliorates hepatic steatosis through acute activation of the unfolded protein response and VLDL production

doi: 10.1016/j.jhepr.2025.101660

Figure Lengend Snippet: FGF1 hyperactivates the UPR in the liver and hepatocytes. (A) Hepatic protein levels of the three UPR branch markers XBP1s, ATF6 (ATF6-U: unspliced & ATF6-N nuclear) and Perk phosphorylation 14 h after FGF1 injection of ob/ob showing UPR activation. In addition, XBP1s and ATF6 in nuclear extracts from these livers. (B) Hepatic expression levels of UPR chaperones ( Grp78 , Erp72 , Erdj3 , Grp94 , and Pdi ), ER-associated protein degradation genes ( Edem and Herp ), and PERK–ATF4–CHOP pathway genes ( Chop and Gadd34 ) in ob/ob mouse liver (Mann-Whitney U test; ∗ p < 0.05, ∗∗ p < 0.01). (C) Hepatic protein levels of Grp78, Grp94, Erp72, Erp57, Pdi and Chop 14 h after FGF1 injection of ob/ob mice. (D) Effect of 3 or 6 h FGF1 on UPR sensors in glucosamine-stressed HepG2 cells, showing Xbp1 mRNA (uXBP1: unspliced & sXBP: spliced), Ire1 and Perk phosphorylation, XBP1s and Atf6 protein levels (unspliced & nuclear) (E) Hyperactivation of UPR chaperone expression levels but not ERAD genes by 6 h FGF1 treatment in glucosamine-stressed (2 h) primary rat hepatocytes. ∗ p < 0.05 glucosamine vs. control, # p < 0.05 glucosamine vs. glucosamine + FGF1 (Kruskal-Wallis test). (F) UPR chaperone protein induction after FGF1 treatment in HepG2 cells with and without glucosamine pre-treatment. UPR, unfolded protein response.

Techniques: Phospho-proteomics, Injection, Activation Assay, Expressing, MANN-WHITNEY, Control

FGF1 stimulates major regulators of protein synthesis that link to the UPR. (A) Temporal phosphorylation dynamics of signaling pathways in FGF1-stimulated HepG2 cells and primary rat hepatocytes: RSK, mTOR and downstream targets, 4E-BP1, P70S6K, eF2K and S6. (B) Phosphorylation of FRS2α, 4E-BP1, P70S6K, RSK, and S6 in livers of DIO mice 15 min after FGF1 stimulation. (C) Suppression of FGF1-induced UPR hyperactivation by inhibition of PI3K, mTOR, protein translation, ER protein import and a chemical protein folding chaperone in HepG2 cells (Kruskal-Wallis-test). ∗ p < 0.05 ER stress vs. ER stress + FGF1, # p < 0.05 ER stress + FGF1 vs. ER stress + FGF1 + inhibitor. DIO, diet-induced obese; ER, endoplasmic reticulum; UPR, unfolded protein response.

Journal: JHEP Reports

Article Title: FGF1 ameliorates hepatic steatosis through acute activation of the unfolded protein response and VLDL production

doi: 10.1016/j.jhepr.2025.101660

Figure Lengend Snippet: FGF1 stimulates major regulators of protein synthesis that link to the UPR. (A) Temporal phosphorylation dynamics of signaling pathways in FGF1-stimulated HepG2 cells and primary rat hepatocytes: RSK, mTOR and downstream targets, 4E-BP1, P70S6K, eF2K and S6. (B) Phosphorylation of FRS2α, 4E-BP1, P70S6K, RSK, and S6 in livers of DIO mice 15 min after FGF1 stimulation. (C) Suppression of FGF1-induced UPR hyperactivation by inhibition of PI3K, mTOR, protein translation, ER protein import and a chemical protein folding chaperone in HepG2 cells (Kruskal-Wallis-test). ∗ p < 0.05 ER stress vs. ER stress + FGF1, # p < 0.05 ER stress + FGF1 vs. ER stress + FGF1 + inhibitor. DIO, diet-induced obese; ER, endoplasmic reticulum; UPR, unfolded protein response.

Techniques: Phospho-proteomics, Protein-Protein interactions, Inhibition

FGF1-induced hepatic TG clearance requires pre-existing ER stress. Temporal dynamics of plasma TG upon an FGF1 injection in (A) wild-type mice, (B) wild-type mice pre-treated with tunicamycin (Mann-Whitney U test; ∗ p < 0.05, ∗∗ p < 0.01). (C) Plasma ALT levels after tunicamycin pre-treatment showing no liver damage and (D) after 3-days of phenylbutyrate pre-treatment in DIO mice showing ER liver damage reduction (Mann-Whitney U test; ∗∗∗ p < 0.001). (E) Temporal dynamics of plasma TG upon an FGF1 injection in DIO mice with or without pre-treatment for 3 days with the ER chaperone phenylbutyrate (Kruskal-Wallis-test; ∗∗∗ p < 0.001 FGF1 vs. PBS, ### p < 0.001 FGF1 vs. PHB, $ p < 0.05 FGF1 vs. PHB+FGF1). (F) Albumin levels in ob/ob and wild-type mice 24 h after FGF1 injection (Mann-Whitney U test; ∗∗∗ p < 0.01). (G) Temporal dynamics of plasma ALT in ob/ob mice after a single FGF1 injection showing a transient reduction in liver damage (Mann-Whitney U test; ∗ p < 0.05, ∗∗ p < 0.01). (H) Model summarizing the underlying mechanism of FGF1-induced clearance of hepatic steatosis; in blue, the elements of the signaling pathways and UPR that are affected downstream of FGF1 binding and the subsequent secretory output. n = 5-6, n = 11 for panel E. ∗ p < 0.05, ∗∗ p < 0.01. ALT, alanine aminotransferase; DIO, diet-induced obese; ER, endoplasmic reticulum; TG, triglyceride; UPR, unfolded protein response.

Journal: JHEP Reports

Article Title: FGF1 ameliorates hepatic steatosis through acute activation of the unfolded protein response and VLDL production

doi: 10.1016/j.jhepr.2025.101660

Figure Lengend Snippet: FGF1-induced hepatic TG clearance requires pre-existing ER stress. Temporal dynamics of plasma TG upon an FGF1 injection in (A) wild-type mice, (B) wild-type mice pre-treated with tunicamycin (Mann-Whitney U test; ∗ p < 0.05, ∗∗ p < 0.01). (C) Plasma ALT levels after tunicamycin pre-treatment showing no liver damage and (D) after 3-days of phenylbutyrate pre-treatment in DIO mice showing ER liver damage reduction (Mann-Whitney U test; ∗∗∗ p < 0.001). (E) Temporal dynamics of plasma TG upon an FGF1 injection in DIO mice with or without pre-treatment for 3 days with the ER chaperone phenylbutyrate (Kruskal-Wallis-test; ∗∗∗ p < 0.001 FGF1 vs. PBS, ### p < 0.001 FGF1 vs. PHB, $ p < 0.05 FGF1 vs. PHB+FGF1). (F) Albumin levels in ob/ob and wild-type mice 24 h after FGF1 injection (Mann-Whitney U test; ∗∗∗ p < 0.01). (G) Temporal dynamics of plasma ALT in ob/ob mice after a single FGF1 injection showing a transient reduction in liver damage (Mann-Whitney U test; ∗ p < 0.05, ∗∗ p < 0.01). (H) Model summarizing the underlying mechanism of FGF1-induced clearance of hepatic steatosis; in blue, the elements of the signaling pathways and UPR that are affected downstream of FGF1 binding and the subsequent secretory output. n = 5-6, n = 11 for panel E. ∗ p < 0.05, ∗∗ p < 0.01. ALT, alanine aminotransferase; DIO, diet-induced obese; ER, endoplasmic reticulum; TG, triglyceride; UPR, unfolded protein response.

Techniques: Clinical Proteomics, Injection, MANN-WHITNEY, Protein-Protein interactions, Binding Assay

(A) ETV4 expression in breast tumors and paired normal breast tissue from people with breast cancer. Data obtained from tnmplot.com. Mann-Whitney test determined significance. (B) High ETV4 expression (RNA seq) associates with lower overall survival for people with breast cancer. HR=1.44 (1.14-1.82). (C) Tumors with high ETV4 expression (mRNA z-score >1.5) are more likely to be ER-negative than ER-positive. Chi-squared test q-value <0.0001. (D) High ETV4 expression (RNA seq) associates with lower overall survival for patients with ER-positive breast cancer. HR=1.39 (1.05-1.85). (E) High ETV4 expression (array) associates with lower recurrence-free survival for patients with lymph node-positive ER-positive breast cancer. HR=1.3 (1.031-1.628). (F) ETV4 expression in ER-positive breast tumors stratified by pathologic complete response after aromatase inhibitors using data from ROCplotter.com. (G) ETV4 expression in ER-positive tumors stratified by pathologic complete response to any chemotherapy using data from ROCplotter.com. Mann-Whitney test determined significance for f and g . (H) ETV4 expression (RNA seq) in UCD12 PDX tumors from lean or obese female mice. (I) ETV4 expression (array) in tumors from patients with ER-positive breast cancer (data from GSE24185). (J) Pearson correlation between ETV4 and FGF1 expression in tumors from patients classified as obese, overweight, or lean based on BMI (data from GSE24185). (K) Expression of ETV4 in ER-positive breast cancer cells with or without FGF1 treatment. MCF7 Parental (M7P) or TAMR (M7T); UCD12 (U12). (L) Representative western blot showing ETV4 expression in ER-positive breast cancer cells with or without FGF1 treatment.

Journal: bioRxiv

Article Title: The Ets transcription factor ETV4 regulates FGF1-dependent proliferation and glycolysis in ER-positive breast cancer

doi: 10.64898/2026.01.13.699240

Figure Lengend Snippet: (A) ETV4 expression in breast tumors and paired normal breast tissue from people with breast cancer. Data obtained from tnmplot.com. Mann-Whitney test determined significance. (B) High ETV4 expression (RNA seq) associates with lower overall survival for people with breast cancer. HR=1.44 (1.14-1.82). (C) Tumors with high ETV4 expression (mRNA z-score >1.5) are more likely to be ER-negative than ER-positive. Chi-squared test q-value <0.0001. (D) High ETV4 expression (RNA seq) associates with lower overall survival for patients with ER-positive breast cancer. HR=1.39 (1.05-1.85). (E) High ETV4 expression (array) associates with lower recurrence-free survival for patients with lymph node-positive ER-positive breast cancer. HR=1.3 (1.031-1.628). (F) ETV4 expression in ER-positive breast tumors stratified by pathologic complete response after aromatase inhibitors using data from ROCplotter.com. (G) ETV4 expression in ER-positive tumors stratified by pathologic complete response to any chemotherapy using data from ROCplotter.com. Mann-Whitney test determined significance for f and g . (H) ETV4 expression (RNA seq) in UCD12 PDX tumors from lean or obese female mice. (I) ETV4 expression (array) in tumors from patients with ER-positive breast cancer (data from GSE24185). (J) Pearson correlation between ETV4 and FGF1 expression in tumors from patients classified as obese, overweight, or lean based on BMI (data from GSE24185). (K) Expression of ETV4 in ER-positive breast cancer cells with or without FGF1 treatment. MCF7 Parental (M7P) or TAMR (M7T); UCD12 (U12). (L) Representative western blot showing ETV4 expression in ER-positive breast cancer cells with or without FGF1 treatment.

Article Snippet: Recombinant human FGF1 was purchased from R&D Systems and was diluted in 0.01% bovine serum albumin (BSA) in PBS and used at a final concentration of 5 ng/mL.

Techniques: Expressing, MANN-WHITNEY, RNA Sequencing, Western Blot

(A) Q-PCR ( left ) and immunoblot ( right ) analysis of ETV4 in MCF7-P cells. (B) Q-PCR ( left ) and immunoblot ( right ) analysis of ETV4 in MCF7-TAMR cells. (C) Representative images of the final timepoint (left) and growth rates (right) of MCF7-P control or ETV4-knockdown cells treated with vehicle or FGF1. (D) Area confluence relative to control vehicle time 0 of cells at the final timepoint following treatment of MCF7-P cells. Two-way ANOVA testing for main effects of ETV4 knockdown or FGF1 treatment or interaction was performed. P-values indicate post-hoc multiple testing for specific differences between pre-defined comparisons. (E) Representative images of the final timepoint (left) and growth rates (right) of MCF7-TAMR control or ETV4-knockdown cells treated with vehicle or FGF1. (F) Area confluence relative to control vehicle time 0 of cells at the final timepoint following treatment of MCF7-TAMR cells. Two-way ANOVA testing for main effects of ETV4 knockdown or FGF1 treatment or interaction was performed. P-values indicate post-hoc multiple testing for specific differences between pre-defined comparisons. (G) Dose-response curve and interpolated IC 50 values of tamoxifen treatment in MCF7-P control and ETV4 knockdown cells following treatment with or without FGF1. (H) Dose-response curve and interpolated IC 50 values of tamoxifen treatment in MCF7-TAMR control and ETV4 knockdown cells following treatment with or without FGF1.

Journal: bioRxiv

Article Title: The Ets transcription factor ETV4 regulates FGF1-dependent proliferation and glycolysis in ER-positive breast cancer

doi: 10.64898/2026.01.13.699240

Figure Lengend Snippet: (A) Q-PCR ( left ) and immunoblot ( right ) analysis of ETV4 in MCF7-P cells. (B) Q-PCR ( left ) and immunoblot ( right ) analysis of ETV4 in MCF7-TAMR cells. (C) Representative images of the final timepoint (left) and growth rates (right) of MCF7-P control or ETV4-knockdown cells treated with vehicle or FGF1. (D) Area confluence relative to control vehicle time 0 of cells at the final timepoint following treatment of MCF7-P cells. Two-way ANOVA testing for main effects of ETV4 knockdown or FGF1 treatment or interaction was performed. P-values indicate post-hoc multiple testing for specific differences between pre-defined comparisons. (E) Representative images of the final timepoint (left) and growth rates (right) of MCF7-TAMR control or ETV4-knockdown cells treated with vehicle or FGF1. (F) Area confluence relative to control vehicle time 0 of cells at the final timepoint following treatment of MCF7-TAMR cells. Two-way ANOVA testing for main effects of ETV4 knockdown or FGF1 treatment or interaction was performed. P-values indicate post-hoc multiple testing for specific differences between pre-defined comparisons. (G) Dose-response curve and interpolated IC 50 values of tamoxifen treatment in MCF7-P control and ETV4 knockdown cells following treatment with or without FGF1. (H) Dose-response curve and interpolated IC 50 values of tamoxifen treatment in MCF7-TAMR control and ETV4 knockdown cells following treatment with or without FGF1.

Article Snippet: Recombinant human FGF1 was purchased from R&D Systems and was diluted in 0.01% bovine serum albumin (BSA) in PBS and used at a final concentration of 5 ng/mL.

Techniques: Western Blot, Control, Knockdown

(A) Expression of ETV4 gene ( left ) and protein ( right ) following knockdown in MCF7-P cells. (B) Expression of ETV4 gene ( left ) and protein ( right ) following knockdown in MCF7-TAMR cells. (C) Representative images of the final timepoint (left) and growth rates (right) of MCF7-P control or ETV4-overexpressing cells treated with vehicle or FGF1. (D) Area confluence relative to control vehicle time 0 of cells at the final timepoint following treatment of MCF7-P cells. Two-way ANOVA testing for main effects of ETV4 overexpression or FGF1 treatment or interaction was performed. P-values indicate post-hoc multiple testing for specific differences between pre-defined comparisons. (E) Representative images of the final timepoint (left) and growth rates (right) of MCF7-TAMR control or ETV4-overexpressing cells treated with vehicle or FGF1. (F) Area confluence relative to control vehicle time 0 of cells at the final timepoint following treatment of MCF7-TAMR cells. Two-way ANOVA testing for main effects of ETV4 overexpression or FGF1 treatment or interaction was performed. P-values indicate post-hoc multiple testing for specific differences between pre-defined comparisons. (G) Dose-response curve and interpolated IC 50 values of tamoxifen treatment in MCF7-P control and ETV4 overexpressing cells following treatment with or without FGF1. (H) Dose-response curve and interpolated IC 50 values of tamoxifen treatment in MCF7-TAMR control and ETV4 overexpressing cells following treatment with or without FGF1. (I) Dose-response curve and interpolated IC 50 values of BGJ398 treatment in MCF7-P and MCF7-TAMR control and ETV4 overexpressing cells.

Journal: bioRxiv

Article Title: The Ets transcription factor ETV4 regulates FGF1-dependent proliferation and glycolysis in ER-positive breast cancer

doi: 10.64898/2026.01.13.699240

Figure Lengend Snippet: (A) Expression of ETV4 gene ( left ) and protein ( right ) following knockdown in MCF7-P cells. (B) Expression of ETV4 gene ( left ) and protein ( right ) following knockdown in MCF7-TAMR cells. (C) Representative images of the final timepoint (left) and growth rates (right) of MCF7-P control or ETV4-overexpressing cells treated with vehicle or FGF1. (D) Area confluence relative to control vehicle time 0 of cells at the final timepoint following treatment of MCF7-P cells. Two-way ANOVA testing for main effects of ETV4 overexpression or FGF1 treatment or interaction was performed. P-values indicate post-hoc multiple testing for specific differences between pre-defined comparisons. (E) Representative images of the final timepoint (left) and growth rates (right) of MCF7-TAMR control or ETV4-overexpressing cells treated with vehicle or FGF1. (F) Area confluence relative to control vehicle time 0 of cells at the final timepoint following treatment of MCF7-TAMR cells. Two-way ANOVA testing for main effects of ETV4 overexpression or FGF1 treatment or interaction was performed. P-values indicate post-hoc multiple testing for specific differences between pre-defined comparisons. (G) Dose-response curve and interpolated IC 50 values of tamoxifen treatment in MCF7-P control and ETV4 overexpressing cells following treatment with or without FGF1. (H) Dose-response curve and interpolated IC 50 values of tamoxifen treatment in MCF7-TAMR control and ETV4 overexpressing cells following treatment with or without FGF1. (I) Dose-response curve and interpolated IC 50 values of BGJ398 treatment in MCF7-P and MCF7-TAMR control and ETV4 overexpressing cells.

Article Snippet: Recombinant human FGF1 was purchased from R&D Systems and was diluted in 0.01% bovine serum albumin (BSA) in PBS and used at a final concentration of 5 ng/mL.

Techniques: Expressing, Knockdown, Control, Over Expression

(A) Bubble plot of gene set enrichment analysis (GSEA) showing enriched pathways in MCF7-TAMR control, ETV4 knockdown, and ETV4-overexpressing cells with or without FGF1 stimulation. (B) Hallmarks of Cancer enrichment plot illustrating the pathways represented by genes that are downregulated by ≥2-fold (adjusted p-value) in ETV4 knockdown compared with control vehicle-treated MCF7-TAMR cells. Bar height reflects −log10 adjusted p-value, with dashed circles indicating significance thresholds. (C) Volcano plot comparing ETV4 knockdown versus control vehicle-treated MCF7-TAMR cells, highlighting downregulated genes involved in reprogramming energy metabolism. Blue points denote significantly downregulated genes. Blue points denote significantly downregulated genes that correspond to the significant cancer hallmarks. (D) Hallmarks of Cancer enrichment plot illustrating the pathways represented by genes that are upregulated by ≥1.58-fold (adjusted p-value) in MCF7-TAMR ETV4 overexpressing cells treated with FGF1 vs vehicle controls. Bar height reflects −log10 adjusted p-value, with dashed circles indicating significance thresholds, including sustaining proliferative signaling. (E) Volcano plot comparing genes significantly altered in MCF7-TAMR ETV4 overexpressing cells treated with or without FGF1. Red points denote significantly upregulated genes that correspond to the significant cancer hallmarks.

Journal: bioRxiv

Article Title: The Ets transcription factor ETV4 regulates FGF1-dependent proliferation and glycolysis in ER-positive breast cancer

doi: 10.64898/2026.01.13.699240

Figure Lengend Snippet: (A) Bubble plot of gene set enrichment analysis (GSEA) showing enriched pathways in MCF7-TAMR control, ETV4 knockdown, and ETV4-overexpressing cells with or without FGF1 stimulation. (B) Hallmarks of Cancer enrichment plot illustrating the pathways represented by genes that are downregulated by ≥2-fold (adjusted p-value) in ETV4 knockdown compared with control vehicle-treated MCF7-TAMR cells. Bar height reflects −log10 adjusted p-value, with dashed circles indicating significance thresholds. (C) Volcano plot comparing ETV4 knockdown versus control vehicle-treated MCF7-TAMR cells, highlighting downregulated genes involved in reprogramming energy metabolism. Blue points denote significantly downregulated genes. Blue points denote significantly downregulated genes that correspond to the significant cancer hallmarks. (D) Hallmarks of Cancer enrichment plot illustrating the pathways represented by genes that are upregulated by ≥1.58-fold (adjusted p-value) in MCF7-TAMR ETV4 overexpressing cells treated with FGF1 vs vehicle controls. Bar height reflects −log10 adjusted p-value, with dashed circles indicating significance thresholds, including sustaining proliferative signaling. (E) Volcano plot comparing genes significantly altered in MCF7-TAMR ETV4 overexpressing cells treated with or without FGF1. Red points denote significantly upregulated genes that correspond to the significant cancer hallmarks.

Article Snippet: Recombinant human FGF1 was purchased from R&D Systems and was diluted in 0.01% bovine serum albumin (BSA) in PBS and used at a final concentration of 5 ng/mL.

Techniques: Control, Knockdown

(A-B) Heatmaps showing mRNA expression levels of glycolytic pathway genes (HK2, PFKP, PGK1, ENO1, and LDHA) under vehicle and FGF1-treated conditions in MCF7-P ( a ) and MCF7-TAMR ( b ) control and ETV4 knockdown cells, respectively. Data are expressed as fold change versus the average of vehicle treated cells for each gene, showing 3 replicates per group. (C) Seahorse metabolic flux analysis showing the kinetic graph of oxygen consumption rate (OCR) in MCF7-P cells. (D-G) Metabolic parameters including basal respiration ( d ), maximal respiration ( e ), ATP-production coupled respiration ( f ), and ECAR ( g ) in control and ETV4 knockdown MCF7-P cells, upon vehicle and FGF1 stimulation. Data analyzed using a 2-way ANOVA testing for main effects of ETV4 or FGF1 treatment or interactions. P-values denote post-hoc analysis of specific comparisons. (H) Seahorse metabolic flux analysis showing the kinetic graph of oxygen consumption rate (OCR) in MCF7-TAMR cells. (I-L) Metabolic parameters including basal respiration ( i ), maximal respiration ( j ), ATP-production coupled respiration ( k ), and ECAR ( l ) in control and ETV4 knockdown MCF7-TAMR cells, upon vehicle and FGF1 stimulation. Data were analyzed using a 2-way ANOVA testing for main effects of ETV4 or FGF1 treatment or interactions. P-values denote post-hoc analysis of specific comparisons. All Seahorse data were normalized to total protein in each well. N=16-24 replicates per measure.

Journal: bioRxiv

Article Title: The Ets transcription factor ETV4 regulates FGF1-dependent proliferation and glycolysis in ER-positive breast cancer

doi: 10.64898/2026.01.13.699240

Figure Lengend Snippet: (A-B) Heatmaps showing mRNA expression levels of glycolytic pathway genes (HK2, PFKP, PGK1, ENO1, and LDHA) under vehicle and FGF1-treated conditions in MCF7-P ( a ) and MCF7-TAMR ( b ) control and ETV4 knockdown cells, respectively. Data are expressed as fold change versus the average of vehicle treated cells for each gene, showing 3 replicates per group. (C) Seahorse metabolic flux analysis showing the kinetic graph of oxygen consumption rate (OCR) in MCF7-P cells. (D-G) Metabolic parameters including basal respiration ( d ), maximal respiration ( e ), ATP-production coupled respiration ( f ), and ECAR ( g ) in control and ETV4 knockdown MCF7-P cells, upon vehicle and FGF1 stimulation. Data analyzed using a 2-way ANOVA testing for main effects of ETV4 or FGF1 treatment or interactions. P-values denote post-hoc analysis of specific comparisons. (H) Seahorse metabolic flux analysis showing the kinetic graph of oxygen consumption rate (OCR) in MCF7-TAMR cells. (I-L) Metabolic parameters including basal respiration ( i ), maximal respiration ( j ), ATP-production coupled respiration ( k ), and ECAR ( l ) in control and ETV4 knockdown MCF7-TAMR cells, upon vehicle and FGF1 stimulation. Data were analyzed using a 2-way ANOVA testing for main effects of ETV4 or FGF1 treatment or interactions. P-values denote post-hoc analysis of specific comparisons. All Seahorse data were normalized to total protein in each well. N=16-24 replicates per measure.

Article Snippet: Recombinant human FGF1 was purchased from R&D Systems and was diluted in 0.01% bovine serum albumin (BSA) in PBS and used at a final concentration of 5 ng/mL.

Techniques: Expressing, Control, Knockdown

Journal: bioRxiv

Article Title: The Ets transcription factor ETV4 regulates FGF1-dependent proliferation and glycolysis in ER-positive breast cancer

doi: 10.64898/2026.01.13.699240

Figure Lengend Snippet: (A-B) Heatmaps showing mRNA expression levels of glycolytic pathway genes (HK2, PFKP, PGK1, ENO1, and LDHA) under vehicle and FGF1-treated conditions in MCF7-P ( a ) and MCF7-TAMR ( b ) control and ETV4 overexpressing cells, respectively. Data are expressed as fold change versus the average of vehicle treated cells for each gene, showing 3 replicates per group. (C) Seahorse metabolic flux analysis showing the kinetic graph of oxygen consumption rate (OCR) in MCF7-P cells. (D-G) Metabolic parameters including basal respiration ( d ), maximal respiration ( e ), ATP-production coupled respiration ( f ), and ECAR ( g ) in control and ETV4 overexpressing MCF7-P cells upon vehicle and FGF1 stimulation. Data were analyzed using a 2-way ANOVA testing for main effects of ETV4 or FGF1 treatment or interactions. P-values denote post-hoc analysis of specific comparisons. (H) Seahorse metabolic flux analysis showing the kinetic graph of oxygen consumption rate (OCR) in MCF7-TAMR cells. (I-L) Metabolic parameters including basal respiration ( i ), maximal respiration ( j ), ATP-production coupled respiration ( k ), and ECAR ( l ) in control and ETV4 knockdown MCF7-TAMR cells, upon vehicle and FGF1 stimulation. Data were analyzed using a 2-way ANOVA testing for main effects of ETV4 or FGF1 treatment or interactions. P-values denote post-hoc analysis of specific comparisons. All Seahorse data were normalized to total protein in each well. N=16-24 replicates per measure.

Article Snippet: Recombinant human FGF1 was purchased from R&D Systems and was diluted in 0.01% bovine serum albumin (BSA) in PBS and used at a final concentration of 5 ng/mL.

Techniques: Expressing, Control, Knockdown

Effect of introducing point mutations on the biological activity of FGF1. a Serum-starved NIH 3T3 cells were treated with 10 ng/mL FGF1 variants for 15 min in the presence of heparin (10 U/mL). Activation of the downstream cascade was detected by immunoblotting using the following antibodies: anti-phospho-FRS2 (pFRS2) and anti-phospho-ERK1/2 (pERK1/2). Anti-ERK1/2 and anti-vinculin antibodies were used to confirm equal loading. Representative results are shown (n ≥ 3). The vertical lines in the last WB panel show the deleted wells. The original membranes, together with the method of trimming, are presented in Fig. S2. Densitometric analysis of pERK/ERK is presented in Fig. S3. b Effect of 20-h FGF1 variants stimulation (20 ng/mL) in the presence of 10 U/mL heparin on glucose uptake by 3T3-L1 adipocytes. Data are presented as mean ± SEM, n = 4. Statistical significance: * p ≤ 0.05; ** p ≤ 0.01 and *** p ≤ 0.001

Journal: Molecular Biomedicine

Article Title: Engineered fibroblast growth factor 1 variants uncouple glucose-lowering effects from mitogenic activity with therapeutic potential for type 2 diabetes

doi: 10.1186/s43556-025-00398-w

Figure Lengend Snippet: Effect of introducing point mutations on the biological activity of FGF1. a Serum-starved NIH 3T3 cells were treated with 10 ng/mL FGF1 variants for 15 min in the presence of heparin (10 U/mL). Activation of the downstream cascade was detected by immunoblotting using the following antibodies: anti-phospho-FRS2 (pFRS2) and anti-phospho-ERK1/2 (pERK1/2). Anti-ERK1/2 and anti-vinculin antibodies were used to confirm equal loading. Representative results are shown (n ≥ 3). The vertical lines in the last WB panel show the deleted wells. The original membranes, together with the method of trimming, are presented in Fig. S2. Densitometric analysis of pERK/ERK is presented in Fig. S3. b Effect of 20-h FGF1 variants stimulation (20 ng/mL) in the presence of 10 U/mL heparin on glucose uptake by 3T3-L1 adipocytes. Data are presented as mean ± SEM, n = 4. Statistical significance: * p ≤ 0.05; ** p ≤ 0.01 and *** p ≤ 0.001

Article Snippet: Human FGF1 ELISA Kit was purchased from R&D Systems (#DFA00B).

Techniques: Activity Assay, Activation Assay, Western Blot

Impaired activation of signaling pathways by FGF1 variants due to reduced affinity for the FGFR1 (IIIc) receptor. a Serum-starved NIH 3T3 cells were stimulated with 10 ng/mL FGF1 variants in the presence of heparin (10 U/mL) for 15 min, and activation of downstream signaling cascades was detected by immunoblotting using the following antibodies: anti-phospho-FGFR (pFGFR), anti-phospho-PLCγ (pPLCγ), anti-phosphoFRS2 (pFRS2), anti-phospho-ERK1/2 (pERK1/2). Anti-ERK1/2, anti-FGFR1, anti-PLCγ and anti-γTubulin antibodies were used to confirm equal loading. Representative results are shown. Densitometric analysis is presented as mean ± SEM, n = 3/4. Statistical significance: * p ≤ 0.05; ** p ≤ 0.01 and *** p ≤ 0.001. b BLI analysis of the affinity of FGF1 variants for FGFR1-Fc (IIIc isoform). FGFR1-Fc was immobilized on a Protein A sensor and its interactions (association and dissociation) with selected FGF1 mutants were analyzed in the concentration range of 100–800 nM. Curves obtained by global fitting are marked in red. Representative results are shown (n ≥ 3). The equilibrium dissociation constant (K D ) was calculated from the saturation binding curve

Journal: Molecular Biomedicine

Article Title: Engineered fibroblast growth factor 1 variants uncouple glucose-lowering effects from mitogenic activity with therapeutic potential for type 2 diabetes

doi: 10.1186/s43556-025-00398-w

Figure Lengend Snippet: Impaired activation of signaling pathways by FGF1 variants due to reduced affinity for the FGFR1 (IIIc) receptor. a Serum-starved NIH 3T3 cells were stimulated with 10 ng/mL FGF1 variants in the presence of heparin (10 U/mL) for 15 min, and activation of downstream signaling cascades was detected by immunoblotting using the following antibodies: anti-phospho-FGFR (pFGFR), anti-phospho-PLCγ (pPLCγ), anti-phosphoFRS2 (pFRS2), anti-phospho-ERK1/2 (pERK1/2). Anti-ERK1/2, anti-FGFR1, anti-PLCγ and anti-γTubulin antibodies were used to confirm equal loading. Representative results are shown. Densitometric analysis is presented as mean ± SEM, n = 3/4. Statistical significance: * p ≤ 0.05; ** p ≤ 0.01 and *** p ≤ 0.001. b BLI analysis of the affinity of FGF1 variants for FGFR1-Fc (IIIc isoform). FGFR1-Fc was immobilized on a Protein A sensor and its interactions (association and dissociation) with selected FGF1 mutants were analyzed in the concentration range of 100–800 nM. Curves obtained by global fitting are marked in red. Representative results are shown (n ≥ 3). The equilibrium dissociation constant (K D ) was calculated from the saturation binding curve

Article Snippet: Human FGF1 ELISA Kit was purchased from R&D Systems (#DFA00B).

Techniques: Activation Assay, Protein-Protein interactions, Western Blot, Concentration Assay, Binding Assay

Effect of introduced mutations on the long-term activity of FGF1. a Induction of Glut1 expression after stimulation with FGF1 variants. 3T3-L1 cells were treated with 100 ng/mL FGF1 muteins in the presence of 10 U/mL heparin for 24 h, followed by WB analysis with anti-Glut1 and anti-γTubulin antibodies, data are presented as mean ± SEM, n = 6. Statistical significance: * p ≤ 0.05; ** p ≤ 0.01 and *** p ≤ 0.001. b Normalized thermal denaturation curves of FGF1 variants monitored by ellipticity changes (λ = 227 nm). c Degradation of FGF1 variants in the presence of adipocytes. Serum-starved 3T3-L1 adipocytes were incubated with 1 µg/mL FGF1 variants. The progress of proteolysis on subsequent days was monitored by immunoblotting with anti-FGF1 antibody. Representative results are shown ( n = 5). Densitometric analysis of proteolysis of FGF1 variants is presented as the ratio the intensity of the upper band to the intensity of the whole amount of protein. Mean ± SEM are shown, n = 5. Statistical significance: * p ≤ 0.05; ** p ≤ 0.01 and *** p ≤ 0.001

Journal: Molecular Biomedicine

Article Title: Engineered fibroblast growth factor 1 variants uncouple glucose-lowering effects from mitogenic activity with therapeutic potential for type 2 diabetes

doi: 10.1186/s43556-025-00398-w

Figure Lengend Snippet: Effect of introduced mutations on the long-term activity of FGF1. a Induction of Glut1 expression after stimulation with FGF1 variants. 3T3-L1 cells were treated with 100 ng/mL FGF1 muteins in the presence of 10 U/mL heparin for 24 h, followed by WB analysis with anti-Glut1 and anti-γTubulin antibodies, data are presented as mean ± SEM, n = 6. Statistical significance: * p ≤ 0.05; ** p ≤ 0.01 and *** p ≤ 0.001. b Normalized thermal denaturation curves of FGF1 variants monitored by ellipticity changes (λ = 227 nm). c Degradation of FGF1 variants in the presence of adipocytes. Serum-starved 3T3-L1 adipocytes were incubated with 1 µg/mL FGF1 variants. The progress of proteolysis on subsequent days was monitored by immunoblotting with anti-FGF1 antibody. Representative results are shown ( n = 5). Densitometric analysis of proteolysis of FGF1 variants is presented as the ratio the intensity of the upper band to the intensity of the whole amount of protein. Mean ± SEM are shown, n = 5. Statistical significance: * p ≤ 0.05; ** p ≤ 0.01 and *** p ≤ 0.001

Article Snippet: Human FGF1 ELISA Kit was purchased from R&D Systems (#DFA00B).

Techniques: Activity Assay, Expressing, Incubation, Western Blot

Mitogenic activity of selected FGF1 variants in different cell types. Mitogenic activity of selected FGF1 variants was assessed by stimulating serum-starved C2C12, MCF7 or 4MBr-5 cells with FGF1 mutants in the concentration range 0.1–100 ng/ml in the presence of 10 U/ml heparin for 48 h, 72 h or 96 h, respectively. Cell viability was assessed by PrestoBlue cell viability assay a or by CellTiter-Fluor cell viability assay b . Cell number was determined by counting NucBlue-stained nuclei using an Opera Phenix Plus High-Content Screening System c . Data are presented as mean ± SEM, n = 3. Multiple t-test; statistical significance: * p ≤ 0.05; ** p ≤ 0.01 and *** p ≤ 0.001

Journal: Molecular Biomedicine

Article Title: Engineered fibroblast growth factor 1 variants uncouple glucose-lowering effects from mitogenic activity with therapeutic potential for type 2 diabetes

doi: 10.1186/s43556-025-00398-w

Figure Lengend Snippet: Mitogenic activity of selected FGF1 variants in different cell types. Mitogenic activity of selected FGF1 variants was assessed by stimulating serum-starved C2C12, MCF7 or 4MBr-5 cells with FGF1 mutants in the concentration range 0.1–100 ng/ml in the presence of 10 U/ml heparin for 48 h, 72 h or 96 h, respectively. Cell viability was assessed by PrestoBlue cell viability assay a or by CellTiter-Fluor cell viability assay b . Cell number was determined by counting NucBlue-stained nuclei using an Opera Phenix Plus High-Content Screening System c . Data are presented as mean ± SEM, n = 3. Multiple t-test; statistical significance: * p ≤ 0.05; ** p ≤ 0.01 and *** p ≤ 0.001

Article Snippet: Human FGF1 ELISA Kit was purchased from R&D Systems (#DFA00B).

Techniques: Activity Assay, Concentration Assay, Viability Assay, Staining, High Content Screening

Metabolic activity of FGF1 variants in vivo. a , b Change in blood glucose levels in db/db mice after a single administration of FGF1 variants (measurements at 0, 6, 18, 24, 30, 48, 72, 96 and 168 h after protein administration). FGF1 variants were administered at a dose of 1 mg/kg body weight. Data were normalized to glucose levels before protein administration and presented as mean ± SEM, n = 7/6. Statistical significance * p ≤ 0.05; ** p ≤ 0.01 and *** p ≤ 0.001; (*) indicates comparison with vehicle; (#) indicates comparison with wild-type protein. c Analysis of mouse body weight 96 h after administration. d Pharmacokinetics of FGF1 variants after a single subcutaneous administration in Wistar Han rats. FGF1 variants were administered subcutaneously at a dose 0.5 mg/kg, and blood samples were collected before injection and at 5 min, 15 min, 30 min and 1, 2, 4, 7, 12, 24, 48 h after injection and protein levels were analyzed by ELISA. Data are presented as mean ± SEM, n = 5

Journal: Molecular Biomedicine

Article Title: Engineered fibroblast growth factor 1 variants uncouple glucose-lowering effects from mitogenic activity with therapeutic potential for type 2 diabetes

doi: 10.1186/s43556-025-00398-w

Figure Lengend Snippet: Metabolic activity of FGF1 variants in vivo. a , b Change in blood glucose levels in db/db mice after a single administration of FGF1 variants (measurements at 0, 6, 18, 24, 30, 48, 72, 96 and 168 h after protein administration). FGF1 variants were administered at a dose of 1 mg/kg body weight. Data were normalized to glucose levels before protein administration and presented as mean ± SEM, n = 7/6. Statistical significance * p ≤ 0.05; ** p ≤ 0.01 and *** p ≤ 0.001; (*) indicates comparison with vehicle; (#) indicates comparison with wild-type protein. c Analysis of mouse body weight 96 h after administration. d Pharmacokinetics of FGF1 variants after a single subcutaneous administration in Wistar Han rats. FGF1 variants were administered subcutaneously at a dose 0.5 mg/kg, and blood samples were collected before injection and at 5 min, 15 min, 30 min and 1, 2, 4, 7, 12, 24, 48 h after injection and protein levels were analyzed by ELISA. Data are presented as mean ± SEM, n = 5

Article Snippet: Human FGF1 ELISA Kit was purchased from R&D Systems (#DFA00B).

Techniques: Activity Assay, In Vivo, Comparison, Drug discovery, Injection, Enzyme-linked Immunosorbent Assay

Journal: Molecular Biomedicine

Article Title: Engineered fibroblast growth factor 1 variants uncouple glucose-lowering effects from mitogenic activity with therapeutic potential for type 2 diabetes

doi: 10.1186/s43556-025-00398-w

Article Snippet: The following primary antibodies were used: anti-phospho-FGFR (Tyr653/Tyr654) (pFGFR) (#06–1433) from Millipore, anti-tubulin (#T6557) from Sigma-Aldrich, anti-FGFR1 (FGFR1) (#9740), anti-phospho-p44/42 (Thr202/Tyr204) MAP kinase (pERK1/2) (#9101), anti-p44/42 MAP kinase (ERK1/2) (#9102), anti-phospho-FRS2α (Tyr196) (pFRS2) (#3864), anti-vinculin (#13901), anti-phospho-PLCγ1 (Tyr783) (pPLCγ) (#14,008), anti-PLCγ1 (#5690), anti-Glut1 (#73,015) and anti-FGF1 (#3139) from Cell Signaling Technology.

Techniques: Activity Assay, Expressing, Incubation, Western Blot

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