Journal: Cells

Article Title: Regulation of Transplanted Cell Homing by FGF1 and PDGFB after Doxorubicin Myocardial Injury

doi: 10.3390/cells10112998

Figure Lengend Snippet: Doxorubicin increases FGF-1 and PDGF-B protein levels in adult heart ventricular cells. Mice were given intraperitoneal injections of saline (S) or doxorubicin (D) and their hearts were harvested after 24 h (Day 1) or 72 h (Day 3). Using Western blotting, lysates containing equal amounts of total protein from the ventricular tissue of the differently treated animals were tested for FGF-1 and PDGF-B protein levels. When standardized against GAPDH, the level of both proteins (FGF-1 and PDGF-B) was found to be significantly higher in the Dox-treated ventricles than in the saline treated ventricles by Day 3. * p < 0.05 vs. saline (S), One-way ANOVA with Tukey’s multiple comparisons test, N = 3 independent experiments for each group.

Article Snippet: For the analysis of growth factor effects, the wells contained 1% FBS (Low Serum) DMEM and 40 ng/mL of FGF-1 (rMuFGF1 TM , Gold Biotechnology, St. Louis, MO, USA), its neutralizing antibody (Santa Cruz sc-7910, 100 ng/mL), or both.

Techniques: Western Blot

Journal: Cells

Article Title: Regulation of Transplanted Cell Homing by FGF1 and PDGFB after Doxorubicin Myocardial Injury

doi: 10.3390/cells10112998

Figure Lengend Snippet: FGF-1 and PDGF-B increase embryonic ventricular cell migration, whereas their neutralizing antibodies decrease migration. 300 μL of 0.5 × 10 6 cells/mL serum-free cell suspensions were incubated for 22 h at 37 °C in polycarbonate membrane inserts with 8 μm pores, with surrounding wells containing 1% FBS DMEM and FGF-1, its antibody, or both ( A ) or PDGF-B, its antibody, or both ( B ). The inserts were then removed, migratory cells that had passed through the pores were washed and stained, and the cell stain was solubilized for measurement of absorbance. * p < 0.05 vs. all other groups; # p < 0.05 vs. all other groups, One-way ANOVA with Tukey’s multiple comparisons test, N = 3 independent experiments for each group.

Article Snippet: For the analysis of growth factor effects, the wells contained 1% FBS (Low Serum) DMEM and 40 ng/mL of FGF-1 (rMuFGF1 TM , Gold Biotechnology, St. Louis, MO, USA), its neutralizing antibody (Santa Cruz sc-7910, 100 ng/mL), or both.

Techniques: Migration, Incubation, Staining

Journal: Frontiers in Oncology

Article Title: The Association of Aberrant Expression of FGF1 and mTOR-S6K1 in Colorectal Cancer

doi: 10.3389/fonc.2021.706838

Figure Lengend Snippet: Expression of FGF1 in CRC and paired normal tissues. (A) FGF1 mRNA levels in CRC and normal tissues in Skrzypczak’s datasets. (B) Comparison of FGF1 mRNA expression in CRC and normal tissues across 16 Oncomine datasets. (C) Representative IHC images showing in situ FGF1 expression in CRC and normal tissues (scale bar = 100μm). (D) IHC scores of FGF1 in CRC vs normal tissues. (E) OS of FGF1(+) and FGF1(-) in CRC patients in TCGA dataset searched via GEPIA platform. (F) OS of FGF1(+) and FGF1(-) in CRC patients. *** P < 0.001.

Article Snippet: After blocking with 5% non-fat milk for 1h, the membranes were probed overnight with FGF1 (1:1000, BOSTER, China), p-mTOR (1:1000, Cell Signaling Technology, USA), mTOR (1:1000, Bioss, China), p-S6K1 (1:1000, Cell Signaling Technology, USA), and S6K1 (1:1000, Bioss, China) and β-Actin (1:5000, BOSTER, China) antibodies at 4°C with gentle shaking, followed by horseradish peroxidase-conjugated secondary antibodies.

Techniques: Expressing, Comparison, In Situ

Journal: Frontiers in Oncology

Article Title: The Association of Aberrant Expression of FGF1 and mTOR-S6K1 in Colorectal Cancer

doi: 10.3389/fonc.2021.706838

Figure Lengend Snippet: Statistics of FGF1 expression in 135 CRC tissues and adjacent normal tissue.

Article Snippet: After blocking with 5% non-fat milk for 1h, the membranes were probed overnight with FGF1 (1:1000, BOSTER, China), p-mTOR (1:1000, Cell Signaling Technology, USA), mTOR (1:1000, Bioss, China), p-S6K1 (1:1000, Cell Signaling Technology, USA), and S6K1 (1:1000, Bioss, China) and β-Actin (1:5000, BOSTER, China) antibodies at 4°C with gentle shaking, followed by horseradish peroxidase-conjugated secondary antibodies.

Techniques: Expressing

Journal: Frontiers in Oncology

Article Title: The Association of Aberrant Expression of FGF1 and mTOR-S6K1 in Colorectal Cancer

doi: 10.3389/fonc.2021.706838

Figure Lengend Snippet: Relationship between FGF1 and clinic-pathological factors in CRC patients.

Article Snippet: After blocking with 5% non-fat milk for 1h, the membranes were probed overnight with FGF1 (1:1000, BOSTER, China), p-mTOR (1:1000, Cell Signaling Technology, USA), mTOR (1:1000, Bioss, China), p-S6K1 (1:1000, Cell Signaling Technology, USA), and S6K1 (1:1000, Bioss, China) and β-Actin (1:5000, BOSTER, China) antibodies at 4°C with gentle shaking, followed by horseradish peroxidase-conjugated secondary antibodies.

Techniques:

Journal: Frontiers in Oncology

Article Title: The Association of Aberrant Expression of FGF1 and mTOR-S6K1 in Colorectal Cancer

doi: 10.3389/fonc.2021.706838

Figure Lengend Snippet: Results of univariate and multivariate analyses of underwent gastrectomy patients’ survival by Cox’s proportional hazard model.

Article Snippet: After blocking with 5% non-fat milk for 1h, the membranes were probed overnight with FGF1 (1:1000, BOSTER, China), p-mTOR (1:1000, Cell Signaling Technology, USA), mTOR (1:1000, Bioss, China), p-S6K1 (1:1000, Cell Signaling Technology, USA), and S6K1 (1:1000, Bioss, China) and β-Actin (1:5000, BOSTER, China) antibodies at 4°C with gentle shaking, followed by horseradish peroxidase-conjugated secondary antibodies.

Techniques: Expressing

Journal: Frontiers in Oncology

Article Title: The Association of Aberrant Expression of FGF1 and mTOR-S6K1 in Colorectal Cancer

doi: 10.3389/fonc.2021.706838

Figure Lengend Snippet: Effect of FGF1 on survival. (A) IHC images showing in situ FGF1 expression in CRC tissues (scale bar = 100μm). Negative (a), Weak (b), Moderate (c), Strong (d). (B) IHC scores of FGF1 in TNM stage I-II vs stage III-IV. (C) IHC scores of FGF1 in nLNM vs LNM. (D, E) OS of FGF1(+) and FGF1(-) CRC patients with TNM staging (D) I-II and (E) III-IV. nLNM, no lymph node metastasis; LNM, lymph node metastasis. ** P < 0.01.

Article Snippet: After blocking with 5% non-fat milk for 1h, the membranes were probed overnight with FGF1 (1:1000, BOSTER, China), p-mTOR (1:1000, Cell Signaling Technology, USA), mTOR (1:1000, Bioss, China), p-S6K1 (1:1000, Cell Signaling Technology, USA), and S6K1 (1:1000, Bioss, China) and β-Actin (1:5000, BOSTER, China) antibodies at 4°C with gentle shaking, followed by horseradish peroxidase-conjugated secondary antibodies.

Techniques: In Situ, Expressing

Journal: Frontiers in Oncology

Article Title: The Association of Aberrant Expression of FGF1 and mTOR-S6K1 in Colorectal Cancer

doi: 10.3389/fonc.2021.706838

Figure Lengend Snippet: Subgroup analysis for the influence factor of survival duration of CRC patients according to FGF1 expression. * P < 0.05.

Article Snippet: After blocking with 5% non-fat milk for 1h, the membranes were probed overnight with FGF1 (1:1000, BOSTER, China), p-mTOR (1:1000, Cell Signaling Technology, USA), mTOR (1:1000, Bioss, China), p-S6K1 (1:1000, Cell Signaling Technology, USA), and S6K1 (1:1000, Bioss, China) and β-Actin (1:5000, BOSTER, China) antibodies at 4°C with gentle shaking, followed by horseradish peroxidase-conjugated secondary antibodies.

Techniques: Expressing

Journal: Frontiers in Oncology

Article Title: The Association of Aberrant Expression of FGF1 and mTOR-S6K1 in Colorectal Cancer

doi: 10.3389/fonc.2021.706838

Figure Lengend Snippet: The relationship between FGF1 and p-S6K1.Nomograms to predict survival of CRC patients. (A) Correlation analysis of FGF1 and S6K1 at gene level in CRC tissues from TCGA datasets by GEPIA platform. (B) Representative IHC images showing in situ p-S6K1 expression in CRC and normal tissues (scale bar = 100μm). (C) IHC scores of p-S6K1 in CRC vs normal tissues. (D–G) Correlation between FGF1 and p-S6K1 at protein level in (D) CRC tissue, (E) normal tissue, (F) TNM stage I-II tissue and (G) TNM stage III-IV tissue. (H) Stratification of 135 pairs of CRC and normal tissues into cluster 1 and cluster 2 according to FGF1 and p-S6K1 IHC scores. *** P < 0.001.

Article Snippet: After blocking with 5% non-fat milk for 1h, the membranes were probed overnight with FGF1 (1:1000, BOSTER, China), p-mTOR (1:1000, Cell Signaling Technology, USA), mTOR (1:1000, Bioss, China), p-S6K1 (1:1000, Cell Signaling Technology, USA), and S6K1 (1:1000, Bioss, China) and β-Actin (1:5000, BOSTER, China) antibodies at 4°C with gentle shaking, followed by horseradish peroxidase-conjugated secondary antibodies.

Techniques: In Situ, Expressing

Journal: Frontiers in Oncology

Article Title: The Association of Aberrant Expression of FGF1 and mTOR-S6K1 in Colorectal Cancer

doi: 10.3389/fonc.2021.706838

Figure Lengend Snippet: FGF1 regulates CRC cell growth in an mTOR-S6K1 pathway dependent manner. (A) Immunoblot showing FGF1, p-mTOR, mTOR, p-S6K1 and S6K1, β-Actin protein levels in CRC cells transfected with FGF1-shRNA. (B) Immunoblot result of FGF1/β-Actin, p-mTOR/mTOR and p-S6K1/S6K1 were semi-quantified by ImageJ. Data are presented as mean ± SD. NC, negative control; KD, FGF1-shRNA. * P < 0.05, ** P < 0.01.

Article Snippet: After blocking with 5% non-fat milk for 1h, the membranes were probed overnight with FGF1 (1:1000, BOSTER, China), p-mTOR (1:1000, Cell Signaling Technology, USA), mTOR (1:1000, Bioss, China), p-S6K1 (1:1000, Cell Signaling Technology, USA), and S6K1 (1:1000, Bioss, China) and β-Actin (1:5000, BOSTER, China) antibodies at 4°C with gentle shaking, followed by horseradish peroxidase-conjugated secondary antibodies.

Techniques: Western Blot, Transfection, shRNA, Negative Control

Journal: Frontiers in Oncology

Article Title: The Association of Aberrant Expression of FGF1 and mTOR-S6K1 in Colorectal Cancer

doi: 10.3389/fonc.2021.706838

Figure Lengend Snippet: FGF1 promotes proliferation and migration ability of CRC cells. (A, B) Colony formation capacity (A) and migration rates (B) of FGF1-KD CRC cells. CRC, colorectal cancer. (C) Wound healing assays were carried out at 24h after transfection in 6-well plates. The gap width was measured using Open Lab software. (D) The wound rate was calculated and displayed graphically according to the measured results by Open Lab software. NC, negative control; KD, FGF1-shRNA. Data are presented as mean ± SD (n=3). Ns, no significance, * P < 0.05.

Article Snippet: After blocking with 5% non-fat milk for 1h, the membranes were probed overnight with FGF1 (1:1000, BOSTER, China), p-mTOR (1:1000, Cell Signaling Technology, USA), mTOR (1:1000, Bioss, China), p-S6K1 (1:1000, Cell Signaling Technology, USA), and S6K1 (1:1000, Bioss, China) and β-Actin (1:5000, BOSTER, China) antibodies at 4°C with gentle shaking, followed by horseradish peroxidase-conjugated secondary antibodies.

Techniques: Migration, Transfection, Software, Negative Control, shRNA

Journal: Frontiers in Oncology

Article Title: The Association of Aberrant Expression of FGF1 and mTOR-S6K1 in Colorectal Cancer

doi: 10.3389/fonc.2021.706838

Figure Lengend Snippet: FGF1 induces CRC tumor growth in vivo . (A, B) Total body weight (A) and tumor volume (B) of the mice during the experiment. (C) Representative pictures of subcutaneous tumors harvested from NC and FGF1-KD group. (D) The weights of tumor masses. (E) Net body weight after subtracting the respective tumor weights. (F) Relative FGF1 mRNA levels in the tumors and the tumor weight correlation. (G) Stratification of mice into cluster 1 (blue) and cluster 2 (grey) according to tumor weight and FGF mRNA levels. (H) Percentage of NC and FGF1-KD mice in each cluster. Data are presented as mean ± SD (n=5). CRC, colorectal cancer. NC, negative control; KD, FGF1-shRNA. * P < 0.05.

Article Snippet: After blocking with 5% non-fat milk for 1h, the membranes were probed overnight with FGF1 (1:1000, BOSTER, China), p-mTOR (1:1000, Cell Signaling Technology, USA), mTOR (1:1000, Bioss, China), p-S6K1 (1:1000, Cell Signaling Technology, USA), and S6K1 (1:1000, Bioss, China) and β-Actin (1:5000, BOSTER, China) antibodies at 4°C with gentle shaking, followed by horseradish peroxidase-conjugated secondary antibodies.

Techniques: In Vivo, Negative Control, shRNA

Journal: BMC oral health

Article Title: Preparation and characterization of bovine dental pulp-derived extracellular matrix hydrogel for regenerative endodontic applications: an in vitro study.

doi: 10.1186/s12903-024-05004-z

Figure Lengend Snippet: Fig. 6 Growth factor content; (a) Comparison between P-ECM & P-ECM + HA hydrogels regarding TGF-β1 release showing increased release in P-ECM + HA at 0,14 and 28 days ; (b) bFGF release showing higher release in P-ECM + HA group in 1,5 and 14 days ; (c) BMP2 release showing nearly indetectable concentration in P -ECM + HA while detectable in P-ECM; (d) VEGF release showing increased release of P-ECM at 7 days timepoint (e, f, g&h) bar graph showing comparison between P-ECM pre-gel and zero time point hydrogel after gelation

Article Snippet: The levels of TGF-β1, bFGF, BMP-2, and VEGF growth factors were assayed in supernatants of P-ECM and P-ECM + HA hydrogels and in pre-gel of P-ECM, using enzyme-linked immunosorbent assay (ELISA) kits according to the manufacturer’s instructions [human bone morphogenetic protein 2 (BMP-2) immunoassay, R&D Systems Inc, USA]; [Transforming growth factor beta 1 (TGF-β1 ) immunoassay, Cloud Clones Corp, USA]; [ bovine basic fibroblast growth factor (bFGF) and bovine vascular endothelial growth factor (VEGF), BTlab, China].

Techniques: Comparison, Concentration Assay

Journal: Aging (Albany NY)

Article Title: Loss of AKR1B10 promotes colorectal cancer cells proliferation and migration via regulating FGF1-dependent pathway

doi: 10.18632/aging.103393

Figure Lengend Snippet: Correlation between AKR1B10 and FGF1 in CRC tissues. ( A ) Correlation analysis of AKR1B10 and FGF1 levels in CRC tissues from TCGA datasets by GEPIA platform. ( B ) FGF1 mRNA levels in 27 paired CRC and normal tissues. ( C ) Correlation between AKR1B10 and FGF1 levels in the above. ( D ) Representative IHC images showing in situ FGF1 expression in CRC and normal tissues (scale bar = 100μm) and ( E ) corresponding IHC scores. ( F ) OS of 135 CRC patients demarcated by FGF1 expression levels. ( G ) Stratification of 135 pairs of CRC and normal tissues into cluster 1 (red) and cluster 2 (green) according to AKR1B10 and FGF1 IHC scores. ( H ) Percentage of tumor and normal samples in each cluster. CRC, colorectal cancer. OS, overall survival. *** P < 0.001.

Article Snippet: The processed sections were then blocked with 10% goat serum for 30 min, and incubated overnight with 1:200 diluted polyclonal anti-human AKR1B10 (BOSTER, Wuhan, China) or anti-human FGF1 (BOSTER, Wuhan, China) at 4°C.

Techniques: In Situ, Expressing

Journal: Aging (Albany NY)

Article Title: Loss of AKR1B10 promotes colorectal cancer cells proliferation and migration via regulating FGF1-dependent pathway

doi: 10.18632/aging.103393

Figure Lengend Snippet: AKR1B10 knockdown suppresses CRC tumor growth in vivo . ( A – B ) Total body weight ( A ) and tumor volume ( B ) of the mice during the experiment. ( C ) Representative pictures of subcutaneous tumors harvested from NC and AKR1B10-KD group. ( D ) The weights of tumor masses. ( E ) Net body weight after subtracting the respective tumor weights. ( F – G ) Relative AKR1B10 ( F ) and FGF1 ( G ) mRNA levels in the tumors and their ( H ) correlation. ( I ) Stratification of mice into cluster 1 (grey) and cluster 2 (blue) according to body weight, tumor volume, tumor weight and AKR1B10 and FGF1 mRNA levels. ( J ) Percentage of NC and AKR1B10-KD mice in each cluster. Data are presented as mean ± SD. CRC, colorectal cancer. NC, negative control; KD, AKR1B10-shRNA. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: The processed sections were then blocked with 10% goat serum for 30 min, and incubated overnight with 1:200 diluted polyclonal anti-human AKR1B10 (BOSTER, Wuhan, China) or anti-human FGF1 (BOSTER, Wuhan, China) at 4°C.

Techniques: Knockdown, In Vivo, Negative Control, shRNA

Journal: Aging (Albany NY)

Article Title: Loss of AKR1B10 promotes colorectal cancer cells proliferation and migration via regulating FGF1-dependent pathway

doi: 10.18632/aging.103393

Figure Lengend Snippet: AKR1B10 inhibits CRC cell growth in an FGF1-dependent manner. ( A ) Immunoblot showing AKR1B10, FGF1 and GAPDH protein levels in HT29 cells transfected with AKR1B10-shRNA and in HCT116 cells transfected with AKR1B10 overexpression plasmid. ( B ) Immunoblot showing AKR1B10, FGF1 and GAPDH protein levels in HT29 transfected with FGF1-shRNA alone or in combination with AKR1B10-shRNA. ( C – E ) Proliferation rates ( C ), colony forming capacity ( D ) and migration rates ( E ) of the HT29 cells transfected as above. Data are presented as mean ± SD. NC, negative control; KD, AKR1B10-shRNA; VEC, vector; OE, AKR1B10 overexpression plasmid. “-”, control-shRNA. “+”, AKR1B10 or FGF1 shRNA. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: The processed sections were then blocked with 10% goat serum for 30 min, and incubated overnight with 1:200 diluted polyclonal anti-human AKR1B10 (BOSTER, Wuhan, China) or anti-human FGF1 (BOSTER, Wuhan, China) at 4°C.

Techniques: Western Blot, Transfection, shRNA, Over Expression, Plasmid Preparation, Migration, Negative Control, Control