Journal: International Journal of Women's Health

Article Title: Expression Levels and Significance of Gal-1 in Peripheral Blood and Placental Tissues of Pregnant Women with Fetal Growth Restriction

doi: 10.2147/IJWH.S586881

Figure Lengend Snippet: Representative immunohistochemical staining of Gal-1 in placental tissues (DAB staining). ( A ) Normal pregnancy control group. ( B ) Early-onset FGR group. ( C ) Late-onset FGR group.

Article Snippet: The primary antibody was rabbit anti-human monoclonal Gal-1 antibody (1:1000, Affinity Biosciences LTD), and the steps were strictly followed according to the kit instructions.

Techniques: Immunohistochemical staining, Staining, Control

Journal: International Journal of Women's Health

Article Title: Expression Levels and Significance of Gal-1 in Peripheral Blood and Placental Tissues of Pregnant Women with Fetal Growth Restriction

doi: 10.2147/IJWH.S586881

Figure Lengend Snippet: Scatter plot showing the negative correlation between serum Gal-1 levels and relative placental Gal-1 mRNA expression levels.

Article Snippet: The primary antibody was rabbit anti-human monoclonal Gal-1 antibody (1:1000, Affinity Biosciences LTD), and the steps were strictly followed according to the kit instructions.

Techniques: Expressing

Journal: International Journal of Women's Health

Article Title: Expression Levels and Significance of Gal-1 in Peripheral Blood and Placental Tissues of Pregnant Women with Fetal Growth Restriction

doi: 10.2147/IJWH.S586881

Figure Lengend Snippet: Receiver Operating Characteristic (ROC) curve analyzing the diagnostic performance of serum Gal-1 levels for distinguishing all FGR patients from healthy controls.

Article Snippet: The primary antibody was rabbit anti-human monoclonal Gal-1 antibody (1:1000, Affinity Biosciences LTD), and the steps were strictly followed according to the kit instructions.

Techniques: Diagnostic Assay

Journal: iScience

Article Title: GAL and F2R as immune diagnostic biomarkers for fetal growth restriction

doi: 10.1016/j.isci.2026.115228

Figure Lengend Snippet: Targeted additional analysis of the three key IR-DEGs (A) Chromosomal positions of the key IR-DEGs are presented. (B) A PCA plot illustrates the distribution of samples based on the expression profiles of the 3 key IR-DEGs. The x axis and y axis correspond to the first two principal components (PC1 and PC2), respectively, and the percentage of total variance explained by each component is indicated in parentheses adjacent to the axis labels. (C) Comparative expression levels of three crucial IR-DEGs in FGR, which integrates datasets GSE24129 , GSE100415 , and GSE147776 . (D) ROC curves were used to validate the efficacy of three crucial IR-DEGs in predicting FGR, quantifying the diagnostic performance of each gene for FGR identification. (E) A nomogram for predicting the risk of FGR is constructed based on three IR-DEGs, specifically F2R, GAL, and CXCL10. For each of these genes, a corresponding point value is assigned according to its expression level; the total point score is calculated by summing the individual gene points, and this total score is further converted to the predicted risk of developing FGR. (F) A calibration curve for the nomogram is shown, comparing the nomogram-predicted risk of FGR ( x axis) with the actually observed risk ( y axis). The diagonal line represents an ideal prediction scenario where predicted and observed risks are identical. The dashed line (“Apparent”) denotes the model’s performance before bias correction, while the solid line (“Bias-corrected”) represents performance after bias correction.

Article Snippet: IHC staining was performed according to previously established protocols using primary antibodies against GAL (Bioss, Beijing, China, catalog number: bs-0017M, RRID: AB_10855141) and F2R (Bioss, Beijing, China, catalog number: bs-0828R, RRID: AB_10857704).

Techniques: Expressing, Diagnostic Assay, Construct

Journal: iScience

Article Title: GAL and F2R as immune diagnostic biomarkers for fetal growth restriction

doi: 10.1016/j.isci.2026.115228

Figure Lengend Snippet: An evaluation focusing on immune infiltration related to two IR-DEGs (A) Stacked bar plot showing the relative abundance of 22 immune cell subtype proportions between FGR and AGA samples. (B) A boxplot is employed to visualize the differentiation in ratios of 22 immune cell types, with a specific focus on comparisons between FGR and AGA. (C) A Spearman correlation network is constructed to illustrate the correlative relationships between two IR-DEGs (namely GAL and F2R) and infiltrating immune cells in FGR. This network visualization explicitly displays how each of the four target IR-DEGs correlates with the 22 types of infiltrating immune cells, facilitating intuitive recognition of positive or negative correlation patterns between the genes and immune cell subsets. (D) Expression levels of F2R are significantly higher in FGR tissues ( n = 11) compared to AGA samples ( n = 25). Data are presented as mean ± SEM. (E) Expression levels of GAL are significantly elevated in FGR tissues ( n = 11) relative to AGA specimens ( n = 25). Data are presented as mean ± SEM. (F) qRT-PCR analysis demonstrates that F2R mRNA expression is significantly upregulated in FGR placental tissues compared to AGA controls ( p = 0.0019). Data are presented as mean ± SEM. (G) qRT-PCR analysis reveals a significant downregulation of GAL mRNA in FGR placental tissues compared to AGA controls ( p = 0.0015). Data are presented as mean ± SEM. Additionally, representative images of IHC staining for F2R and GAL in FGR and AGA patients are presented, illustrating both high and low expression levels of the two genes. All staining images are shown at magnifications of ×40 and ×200, with scale bars clearly indicated for reference. Statistical p values were calculated via the chi-square test, where ∗ p < 0.05 and ∗∗ p < 0.01.

Article Snippet: IHC staining was performed according to previously established protocols using primary antibodies against GAL (Bioss, Beijing, China, catalog number: bs-0017M, RRID: AB_10855141) and F2R (Bioss, Beijing, China, catalog number: bs-0828R, RRID: AB_10857704).

Techniques: Construct, Expressing, Quantitative RT-PCR, Immunohistochemistry, Staining

Journal: bioRxiv

Article Title: Dysplastic Epithelial Repair Propagates Chronic Pathology Through the Paracrine Transformation of Pulmonary Fibroblasts

doi: 10.64898/2026.04.02.716135

Figure Lengend Snippet: ( A ) Quantified levels of IL-1α from naïve fibroblast (Naïve fibro), inflammatory fibroblast (Inflam fibro), and ectopic basal cell (Basal) conditioned media as determined by ELISA. ( B ) Saa3 and Ccl2 gene expression by RT-qPCR for fibroblasts cultured on 0.5kPa plates and treated with a 5-fold titration of IL-1α added to control media, including the level determined in (A). ( C ) Graphic illustrating the strategy used to deplete conditioned media of endogenous IL-1α with antibodies, magnetic beads, and column-based separation. ( D ) Saa3 and Ccl2 gene expression by RT-qPCR for fibroblasts cultured on 0.5kPa plates in control or conditioned media depleted using IgG (CTRL IgG or CM IgG) or IL-1α nAb (CTRL nAB, CM nAb) and supplemented with additional IL-1α nAb after depletion (+Spike). [(B) and (D)] Data shows mean fold change ± SD and are pooled from 3 independent experiments (n=3 mice). P values were calculated using either (B) a ratio paired t -test or (D) a one-way ANOVA with post-hoc Turkey multiple comparison test: * P < 0.05, ** P < 0.01, **** P < 0.0001, ns: not significant.

Article Snippet: The working concentration for the following reagents can be found in the text and figure legends: Human IL-1RA Recombinant Protein (IL1Ra) (PeproTech®, 200-01RA), Mouse IL-1 alpha Recombinant Protein, (PeproTech®, 211-11A), Mouse IL-1α Neutralizing Antibody (Invivogen, Anti-mIL-1α-mIgG1 clone 6H7, mIL-1α-mab9-02), Recombinant Mouse IgG1 Isotype Control Antibody (Invivogen, Anti-β-Gal-mIgG1 clone T9C6, bgal-mab9-02), Human TGF-β 1 Recombinant Protein (PeproTech®, 100-21), Human GDF15 Recombinant Protein (PeproTech®, 120-28C), Human VEGF Recombinant Protein (PeproTech®, 450-32), Human OPN Recombinant Protein (PeproTech®, 120-35), Murine CXCL1 Recombinant Protein (PeproTech®, 250-11), Human IGFBP3 Recombinant Protein (PeproTech®, 100-08), Human TNFRSF11B Recombinant Protein (PeproTech®, 450-14), Murine CXCL5 Recombinant Protein (PeproTech®, 250-17), and Muring CCL20 Recombinant Protein (PeproTech®, 250-27).

Techniques: Enzyme-linked Immunosorbent Assay, Gene Expression, Quantitative RT-PCR, Cell Culture, Titration, Control, Magnetic Beads, Comparison

Journal: Cell Communication and Signaling : CCS

Article Title: The Galectin-3-binding protein promotes angiogenesis in pancreatic cancer via simultaneous upregulation of VEGFA and direct HUVEC activation mediated by and VAMP5-STAT3

doi: 10.1186/s12964-026-02801-7

Figure Lengend Snippet: Affinity matured, anti-Gal-3BP antibodies show superior in vitro efficacy for blocking PDAC cell migration and invasion. A . Schematic diagram of antibody affinity maturation of the humanized anti-Gal-3BP antibody. The #13 − 7 clone was used as a template. Two high-affinity clones, #34 and #132, were tested in further study. B . Affinity of the engineered #34 and #132 antibody clones measured by Octet (on left) and their value (Table on right). The affinity of parental clone #13 − 7 is shown at the bottom of the table. C – D . Validation of Gal-3BP binding of engineered anti-Gal-3BP antibodies (#13 − 7, #34, and #132), shown by immunoprecipitation in PDX_PC 110,621 ( C ) or PDAC PKCY ( D ). E – F . Migration and invasion of PDX_PC 115,026 treated with engineered anti-Gal-3BP antibodies (#13 − 7, #34, and #132) or hIgG (human IgG). Upper panel shows representative images, and lower graphs present analysis data. Scale bar: 200 μm. G – H . Migration and invasion of Pan02 treated with engineered anti-Gal-3BP antibodies (#13 − 7, #34, and #132) or hIgG. Upper panel shows representative images, and lower graphs present analysis data. Scale bar: 50 μm.* p < 0.05; ** p < 0.01; *** p < 0.001; ns (not significant)

Article Snippet: The immunoblotting was performed with anti-Gal-3BP antibody (AF2226, R&D systems), anti-VEGFA antibody (ab46154, Abcam), anti-p-EGFR antibody (3777, Cell Signaling Technology), anti-EGFR antibody (4267, Cell Signaling Technology), anti-p-AKT antibody (9271, Cell Signaling Technology), anti-AKT antibody (9272, Cell Signaling Technology), anti-p-STAT3 antibody (9145, Cell Signaling Technology), anti-STAT3 antibody (4904, Cell Signaling Technology), anti-β-actin antibody (Santa Cruz Biotechnology), anti-VAMP5 antibody (ab216044, Abcam), and anti-CD31 antibody (77699, Cell Signaling Technology).

Techniques: In Vitro, Blocking Assay, Migration, Clone Assay, Biomarker Discovery, Binding Assay, Immunoprecipitation

Journal: Cell Communication and Signaling : CCS

Article Title: The Galectin-3-binding protein promotes angiogenesis in pancreatic cancer via simultaneous upregulation of VEGFA and direct HUVEC activation mediated by and VAMP5-STAT3

doi: 10.1186/s12964-026-02801-7

Figure Lengend Snippet: Gal-3BP positively regulates VEGFA production in PDAC. A . Clustered heatmap of the protein expression profile for PDX_PC 110,621 treated with rhGal-3BP, rhEGF, or rhGal-3BP+rhEGF combination. Red indicates upregulated protein levels, whereas green shows downregulated cases. The bottom panel indicates the VEGFA-VEGFR2 pathway enriched in C1 cluster, as shown by WikiPathway 2021 analysis. B and C . mRNA ( B ) and protein expression ( C ) of VEGFA in PDX_PC 110,621 after Gal-3BP knockdown by shRNA. D . VEGFA secretion measured by ELISA in PDX_PC 110,621 after Gal-3BP knockdown. E . The secretion of VEGFA measured in Panc-1 cells after Gal-3BP overexpression. F . Transwell migration of HUVEC co-cultured with control PDX_PC 110,621 or with Gal-3BP knockdown. The graph on right shows relative migration rate. Scale bar: 50 μm. G – H . Expression correlation analysis between Gal-3BP and VEGFA for mRNA ( G ) or protein ( H ), using cBioportal database.* p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001; ns (not significant)

Article Snippet: The immunoblotting was performed with anti-Gal-3BP antibody (AF2226, R&D systems), anti-VEGFA antibody (ab46154, Abcam), anti-p-EGFR antibody (3777, Cell Signaling Technology), anti-EGFR antibody (4267, Cell Signaling Technology), anti-p-AKT antibody (9271, Cell Signaling Technology), anti-AKT antibody (9272, Cell Signaling Technology), anti-p-STAT3 antibody (9145, Cell Signaling Technology), anti-STAT3 antibody (4904, Cell Signaling Technology), anti-β-actin antibody (Santa Cruz Biotechnology), anti-VAMP5 antibody (ab216044, Abcam), and anti-CD31 antibody (77699, Cell Signaling Technology).

Techniques: Expressing, Knockdown, shRNA, Enzyme-linked Immunosorbent Assay, Over Expression, Migration, Cell Culture, Control

Journal: Cell Communication and Signaling : CCS

Article Title: The Galectin-3-binding protein promotes angiogenesis in pancreatic cancer via simultaneous upregulation of VEGFA and direct HUVEC activation mediated by and VAMP5-STAT3

doi: 10.1186/s12964-026-02801-7

Figure Lengend Snippet: STAT3/AKT activation mediates VEGFA production induced by Gal-3BP and is reversed by the engineered anti-Gal-3BP antibodies. A . Activation of EGFR, STAT3, and AKT in PDX_PC 110,621 with Gal-3BP knockdown, as analyzed by Western blot using phosphoantibodies. B . Activation profile of AKT and STAT3 determined by Western blot in Panc-1 stimulated with rhGal-3BP (1 µg/ml). b-actin was used as a loading control. C and D . mRNA ( C ) and secreted VEGFA levels (C and D ) in rhGal-3BP-stimulated PDX_PC 17,884 cells. E and F . Engineered Gal-3BP antibody reduces VEGFA mRNA expression ( E ) and secretion ( F ) in PDAC cell PDX_PC 17,884. G and H . The #34 or #132 Ab inactivate EGFR and STAT3 in PDX_PC 110,621. The cells were treated with 1–5 µg/ml ( G ) or 0.25–1 µg/ml ( H ) and analyzed by Western blot. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001; ns (not significant)

Article Snippet: The immunoblotting was performed with anti-Gal-3BP antibody (AF2226, R&D systems), anti-VEGFA antibody (ab46154, Abcam), anti-p-EGFR antibody (3777, Cell Signaling Technology), anti-EGFR antibody (4267, Cell Signaling Technology), anti-p-AKT antibody (9271, Cell Signaling Technology), anti-AKT antibody (9272, Cell Signaling Technology), anti-p-STAT3 antibody (9145, Cell Signaling Technology), anti-STAT3 antibody (4904, Cell Signaling Technology), anti-β-actin antibody (Santa Cruz Biotechnology), anti-VAMP5 antibody (ab216044, Abcam), and anti-CD31 antibody (77699, Cell Signaling Technology).

Techniques: Activation Assay, Knockdown, Western Blot, Control, Expressing

Journal: Cell Communication and Signaling : CCS

Article Title: The Galectin-3-binding protein promotes angiogenesis in pancreatic cancer via simultaneous upregulation of VEGFA and direct HUVEC activation mediated by and VAMP5-STAT3

doi: 10.1186/s12964-026-02801-7

Figure Lengend Snippet: Gal-3BP activates STAT3/AKT and promotes migration and tube formation of HUVEC cells. A . Increased migration of HUVEC cells treated with VEGFA (20 ng/ml) or Gal-3BP (1 µg/ml). Scale bar: 200 μm. Graph on right shows the relative migratory activity. B . Increased tube formation of HUVEC cells treated with VEGFA (20 ng/ml) or Gal-3BP (1 µg/ml). Scale bar: 200 μm. Graph on right shows number of meshes counted from the images. C and D . #132, but not anti-VEGFR2 antibody (ramucirumab), can reverse the increased migration ( C ) or tube formation ( D ) of HUVEC cells, which was induced by Gal-3BP treatment. Upper panel shows representative images, and lower graphs present analysis data. Graphs at bottom show the relative migratory activity ( C ) or the number of meshes ( D ). Scale bar: 200 μm. E . Migration assay of Gal-3BP-stimulated HUVEC cells in combination with anti-Gal-3BP antibodies (#34 and #132) or hIgG. Upper panels show representative images, and lower graphs present analysis data. Bottom graphs show relative migratory activity. Scale bar: 200 μm. F . Tube formation assay of HUVEC cells in PDX_PC 115,026-conditioned media in the presence of anti-Gal-3BP antibodies (#13 − 7, #34 and #132) or hIgG. Scale bar: 200 μm. G . Western blot analysis of p-STAT3, STAT3, p-AKT, AKT, and β-actin in VEGFA (20 ng/ml) or Gal-3BP (1 µg/ml)-stimulated HUVEC cells. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001; ns (not significant)

Article Snippet: The immunoblotting was performed with anti-Gal-3BP antibody (AF2226, R&D systems), anti-VEGFA antibody (ab46154, Abcam), anti-p-EGFR antibody (3777, Cell Signaling Technology), anti-EGFR antibody (4267, Cell Signaling Technology), anti-p-AKT antibody (9271, Cell Signaling Technology), anti-AKT antibody (9272, Cell Signaling Technology), anti-p-STAT3 antibody (9145, Cell Signaling Technology), anti-STAT3 antibody (4904, Cell Signaling Technology), anti-β-actin antibody (Santa Cruz Biotechnology), anti-VAMP5 antibody (ab216044, Abcam), and anti-CD31 antibody (77699, Cell Signaling Technology).

Techniques: Migration, Activity Assay, Tube Formation Assay, Western Blot

Journal: Cell Communication and Signaling : CCS

Article Title: The Galectin-3-binding protein promotes angiogenesis in pancreatic cancer via simultaneous upregulation of VEGFA and direct HUVEC activation mediated by and VAMP5-STAT3

doi: 10.1186/s12964-026-02801-7

Figure Lengend Snippet: VAMP5 is a mediator for the pro-angiogenic effect of Gal-3BP in HUVEC cells. A . Tube formation assay of HUVEC cells treated with Vehicle (DMSO), lapatinib (1 µM, left graph), MK-2206 (100 nM, middle graph), and S3I-201 (30 µM, right graph) in the presence of rhGal-3BP (1 µg/ml). Left panels show representative images, and graphs on right present data analysis. Scale bar: 200 μm. B . HUVEC migration assay with Vehicle, lapatinib (1 µM, left graph), MK-2206 (100 nM, middle graph), S3I-201 (30 µM, right graph) treatment in the presence of rhGal-3BP (1 µg/ml). Left panels show representative images, and graphs on right present data analysis. Scale bar: 50 μm. C . Schematic diagram for IP-LC-MS/MS analysis to identify receptor protein of secreted Gal-3BP on HUVEC cells. Engineered anti-Gal-3BP antibody #132 was used, and top 3 candidates were listed. D . MICAL2, VAMP5, and FADD mRNA levels in HUVEC cells with shRNA-mediated knockdown. E and F . Tube formation and migration assay of HUVEC cells depleted with MICAL2, VAMP5, and FADD after treatment with rhGal-3BP (1 µg/ml, marked as Gal-3BP[+]). Upper panel shows representative images, and lower graphs present data analysis. Scale bar: 200 μm (tube formation assay) and 50 μm (migration assay). G . Western blot for VAMP5, p-STAT3, STAT3, p-AKT, AKT, and β-actin in shRNA-targeted VAMP5 knockdown of HUVEC cells (left) and VAMP5 -overexpressing HUVEC cells (right). * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001; ns (not significant)

Article Snippet: The immunoblotting was performed with anti-Gal-3BP antibody (AF2226, R&D systems), anti-VEGFA antibody (ab46154, Abcam), anti-p-EGFR antibody (3777, Cell Signaling Technology), anti-EGFR antibody (4267, Cell Signaling Technology), anti-p-AKT antibody (9271, Cell Signaling Technology), anti-AKT antibody (9272, Cell Signaling Technology), anti-p-STAT3 antibody (9145, Cell Signaling Technology), anti-STAT3 antibody (4904, Cell Signaling Technology), anti-β-actin antibody (Santa Cruz Biotechnology), anti-VAMP5 antibody (ab216044, Abcam), and anti-CD31 antibody (77699, Cell Signaling Technology).

Techniques: Tube Formation Assay, Migration, Liquid Chromatography with Mass Spectroscopy, shRNA, Knockdown, Western Blot

Journal: Cell Communication and Signaling : CCS

Article Title: The Galectin-3-binding protein promotes angiogenesis in pancreatic cancer via simultaneous upregulation of VEGFA and direct HUVEC activation mediated by and VAMP5-STAT3

doi: 10.1186/s12964-026-02801-7

Figure Lengend Snippet: Engineered anti-Gal-3BP antibodies attenuate the in vivo angiogenesis of PDAC. A . Schematic representation of the PDAC orthotopic model and treatment procedure of the Gal-3BP antibodies (#34 and #132) along with live imaging schedule using IVIS. B . Luciferase assay of the PDX_PC 110,621 cells with luciferase stable expression (110621_luc). C . Body weight measurements for each group during the antibody treatment ( n = 20). D and E . A graph of a ROI value ( D ) indicating tumor progression between week 3 (start of antibody treatment) and week 5 (end of antibody treatment) along with representative IVIS images for each treatment group ( E ) from week 3 to week 5 ( n = 20). F . Images of dissected PDAC orthotopic tumors from each antibody treatment group. G . Graph showing the average tumor weight for each antibody treatment group. H . Immunohistochemistry analysis of Ki-67 and CD31 in orthotopic tumors. Representative images are shown on the left panels, and their relative signal was presented in the graphs on right. Scale bar: 200 μm (H&E and Ki-67 staining) and 50 μm (CD31 staining) ( n = 20). I . Western blot analysis of CD31, Gal 3BP, and VEGFA expression levels in harvested tumors from each group. Graphs on right presents densitometry results for VEGFA or CD31 normalized by b-actin. * p < 0.05; *** p < 0.001; ns (not significant)

Article Snippet: The immunoblotting was performed with anti-Gal-3BP antibody (AF2226, R&D systems), anti-VEGFA antibody (ab46154, Abcam), anti-p-EGFR antibody (3777, Cell Signaling Technology), anti-EGFR antibody (4267, Cell Signaling Technology), anti-p-AKT antibody (9271, Cell Signaling Technology), anti-AKT antibody (9272, Cell Signaling Technology), anti-p-STAT3 antibody (9145, Cell Signaling Technology), anti-STAT3 antibody (4904, Cell Signaling Technology), anti-β-actin antibody (Santa Cruz Biotechnology), anti-VAMP5 antibody (ab216044, Abcam), and anti-CD31 antibody (77699, Cell Signaling Technology).

Techniques: In Vivo, Imaging, Luciferase, Expressing, Immunohistochemistry, Staining, Western Blot

Journal: Cell Communication and Signaling : CCS

Article Title: The Galectin-3-binding protein promotes angiogenesis in pancreatic cancer via simultaneous upregulation of VEGFA and direct HUVEC activation mediated by and VAMP5-STAT3

doi: 10.1186/s12964-026-02801-7

Figure Lengend Snippet: Engineered anti-Gal-3BP antibodies abrogate PDAC metastasis in vivo. A . Schematic diagram of the PDAC lung metastasis experiment using a tail-vein injection of BxPC3 PDAC cells along with the treatment schedule of #13 − 7 ( n = 6), #132 ( n = 6), and control IgG ( n = 8). B . Body weight of each treatment group during the experiment period ( n = 20). C and D . Images of lungs ( C ) and their weight ( D ) at the endpoint from each treatment group. E and F . Metastasis index ( E ) or PanCK-positive area ( F ) measured by immunohistochemistry of the lungs from each treatment group. Representative images are shown on left panels, and the graphs on right show data analysis. Scale bar: 200 μm. G . Graphical summary of the study, indicating the role of extracellular Gal-3BP in promoting angiogenesis by upregulating VEGFA secretion from cancer cells (autocrine effect) or directly interacting with VAMP5 on HUVEC (paracrine effect). * p < 0.05; *** p < 0.001; **** p < 0.0001; ns (not significant)

Article Snippet: The immunoblotting was performed with anti-Gal-3BP antibody (AF2226, R&D systems), anti-VEGFA antibody (ab46154, Abcam), anti-p-EGFR antibody (3777, Cell Signaling Technology), anti-EGFR antibody (4267, Cell Signaling Technology), anti-p-AKT antibody (9271, Cell Signaling Technology), anti-AKT antibody (9272, Cell Signaling Technology), anti-p-STAT3 antibody (9145, Cell Signaling Technology), anti-STAT3 antibody (4904, Cell Signaling Technology), anti-β-actin antibody (Santa Cruz Biotechnology), anti-VAMP5 antibody (ab216044, Abcam), and anti-CD31 antibody (77699, Cell Signaling Technology).

Techniques: In Vivo, Injection, Control, Immunohistochemistry