Journal: Genes & Diseases

Article Title: IRP1/ARID3A complex promotes pancreatic cancer chemoresistance by suppressing CYGB-related ferroptosis

doi: 10.1016/j.gendis.2025.101866

Figure Lengend Snippet: IRP1 promotes pancreatic cancer GEM-resistant in vivo and in vitro. (A) IC50 curves of GEM plus erastin/hemin in IRP1-knockdown Patu-8988 cell line. (B) IC50 curves of GEM plus erastin/hemin in IRP1-overexpressing PANC-1 cell line. (C) Patu-8988 cells stably transfected with the empty vector were subcutaneously inoculated in nude mice. Afterward, the mice were subjected to injection with GEM plus PBS, GEM plus erastin, or GEM plus hemin. (D) Tumor growth curves of the three groups of nude mice (∗∗∗ P < 0.001). (E) Patu-8988 cells stably transfected with the IRP1-overexpressing lentivirus were subcutaneously inoculated in nude mice. Afterward, the mice were subjected to injection with GEM plus PBS, GEM plus erastin, or GEM plus hemin. (F) Tumor growth curves of the three groups of nude mice (ns: P > 0.05). (G, H) The expression of IRP1 was detected in tumor tissue sections from the xenografts using immunohistochemistry. (I) The results of the intersection for co-immunoprecipitation and liquid chromatography-mass spectrometry against IRP1 antibody, gene set enrichment analysis (GSEA) databases (chromatin binding, co-regulatory transcription factors), and PRO-DIA (data-independent acquisition). GEM, gemcitabine; PBS, phosphate-buffered saline.

Article Snippet: Stable knockdown or overexpression lentiviruses were provided by Shanghai Genechem Co., Ltd., China.

Techniques: In Vivo, In Vitro, Knockdown, Stable Transfection, Transfection, Plasmid Preparation, Injection, Expressing, Immunohistochemistry, Immunoprecipitation, Liquid Chromatography, Mass Spectrometry, Binding Assay, Data-independent acquisition, Saline

Journal: Genes & Diseases

Article Title: IRP1/ARID3A complex promotes pancreatic cancer chemoresistance by suppressing CYGB-related ferroptosis

doi: 10.1016/j.gendis.2025.101866

Figure Lengend Snippet: holo-IRP1/ARID3A axis promotes pancreatic cancer cells resistant to ferroptosis and chemotherapy. (A) DCFH-DA staining (green) was used to detect ROS generation in PANC-1 cells with empty vector, overexpression plasmids targeting IRP1, or overexpression plasmids targeting IRP1 and RNAi targeting ARID3A transfected. The nuclei were stained blue with Hochest33342. (B) DCFH-DA staining (green) was used to detect ROS generation in Patu-8988 cells with empty vector, overexpression plasmids targeting IRP1, or overexpression plasmids targeting IRP1 and RNAi targeting ARID3A transfected. The nuclei were stained blue with Hochest33342. (C) The oxygen consumption rates of PANC-1 cells were showed as a bar chart (∗∗∗ P < 0.001). (D) The oxygen consumption rates of Patu-8988 cells were shown as a bar chart (∗∗∗ P < 0.001, ∗∗ P < 0.01). (E) MDA levels were detected in PANC-1 cells with empty vector, overexpression plasmids targeting IRP1, or overexpression plasmids targeting IRP1 and RNAi targeting ARID3A transfected (∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001). (F) MDA levels were detected in Patu-8988 cells with empty vector, overexpression plasmids targeting IRP1, or overexpression plasmids targeting IRP1 and RNAi targeting ARID3A transfected (∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001). (G) IC50 curves of GEM plus hemin in PANC-1 cells with empty vector, overexpression plasmids targeting IRP1, or overexpression plasmids targeting IRP1 and RNAi targeting ARID3A transfected. (H) IC50 curves of GEM plus hemin in Patu-8988 cells with empty vector, overexpression plasmids targeting IRP1, or overexpression plasmids targeting IRP1 and RNAi targeting ARID3A transfected. (I) Cellular localization of IRP1 and ARID3A in PANC-1 cells transfected with vector, IRP1 WT , or IRP1 C437S lentivirus. (J) Cellular localization of IRP1 and ARID3A in Patu-8988 cells transfected with vector, IRP1 WT , or IRP1 C437S lentivirus. MDA, malondialdehyde; GEM, gemcitabine; DCFH-DA, 2′,7′-dichlorofluorescin diacetate; ROS, reactive oxygen species.

Article Snippet: Stable knockdown or overexpression lentiviruses were provided by Shanghai Genechem Co., Ltd., China.

Techniques: Staining, Plasmid Preparation, Over Expression, Transfection

Journal: Genes & Diseases

Article Title: IRP1/ARID3A complex promotes pancreatic cancer chemoresistance by suppressing CYGB-related ferroptosis

doi: 10.1016/j.gendis.2025.101866

Figure Lengend Snippet: IRP1 C437S weakens the function of holo-IRP1 in pancreatic cancer cells. (A) IC50 curves of GEM plus hemin in PANC-1 cells transfected with vector, IRP1 WT , IRP1 C437S , IRP1 C437S plus ARID3A overexpression plasmid, ARID3A overexpression plasmid, and IRP1 WT plus ARID3A overexpression plasmid. (B) IC50 curves of GEM plus hemin in Patu-8988 cells transfected with vector, IRP1 WT , IRP1 C437S , IRP1 C437S plus ARID3A overexpression plasmid, ARID3A overexpression plasmid, and IRP1 WT plus ARID3A overexpression plasmid. (C) MDA levels of PANC-1 cells transfected with vector, IRP1 WT , IRP1 C437S , IRP1 C437S plus ARID3A overexpression plasmid, ARID3A overexpression plasmid, and IRP1 WT plus ARID3A overexpression plasmid (∗∗∗ P < 0.001). (D) MDA levels of Patu-8988 cells transfected with vector, IRP1 WT , IRP1 C437S , IRP1 C437S plus ARID3A overexpression plasmid, ARID3A overexpression plasmid, and IRP1 WT plus ARID3A overexpression plasmid (∗∗ P < 0.01, ∗∗∗ P < 0.001). (E) DCFH-DA staining (green) was used to detect ROS generation in PANC-1 cells transfected with vector, IRP1 WT , IRP1 C437S , IRP1 C437S plus ARID3A overexpression plasmid, ARID3A overexpression plasmid, and IRP1 WT plus ARID3A overexpression plasmid. (F) DCFH-DA staining (green) was used to detect ROS generation in Patu-8988 cells transfected with vector, IRP1 WT , IRP1 C437S , IRP1 C437S plus ARID3A overexpression plasmid, ARID3A overexpression plasmid, and IRP1 WT plus ARID3A overexpression plasmid. (G) The oxygen consumption rates of PANC-1 cells were shown as a bar chart (∗∗ P < 0.01, ∗∗∗ P < 0.001). (H) The oxygen consumption rates of Patu-8988 cells were shown as a bar chart (∗∗ P < 0.01, ∗∗∗ P < 0.001). MDA, malondialdehyde; GEM, gemcitabine; DCFH-DA, 2′,7′-dichlorofluorescin diacetate; ROS, reactive oxygen species.

Article Snippet: Stable knockdown or overexpression lentiviruses were provided by Shanghai Genechem Co., Ltd., China.

Techniques: Transfection, Plasmid Preparation, Over Expression, Staining

Journal: Genes & Diseases

Article Title: IRP1/ARID3A complex promotes pancreatic cancer chemoresistance by suppressing CYGB-related ferroptosis

doi: 10.1016/j.gendis.2025.101866

Figure Lengend Snippet: IRP1 and ARID3A reduce the chromatin accessibility of the CYGB promoter region and inhibit CYGB expression. (A) The intersection of down-regulated peaks in ATAC sequencing, up-regulated genes in RNA sequencing, and the Ferroptosis driver database. (B) The binding peak of ARID3A and chromatin accessibility regulated by IRP1 in the promoter region of CYGB were visualized by an integrative genomics viewer (IGV). (C) CYGB mRNA expression level in ARID3A-knockdown Patu-8988 cells was detected by quantitative reverse transcription PCR (∗∗ P < 0.01, ∗∗∗ P < 0.001). (D) CYGB mRNA expression level in ARID3A-overexpressing PANC-1 cells was detected by quantitative reverse transcription PCR (∗ P < 0.05, ∗∗∗ P < 0.001). (E) ARID3A, IRP1, and CYGB protein expression levels were detected in PANC-1 and Patu-8898 cells by Western blotting to verify the relationship between ARID3A, IRP1, and CYGB under the condition of iron overload. (F) CYGB expression level was detected in Patu-8898 cells by Western blotting to verify the relationship between ARID3A, IRP1, and CYGB under the condition of iron overload (∗∗∗ P < 0.001). (G) CYGB expression level was detected in PANC-1 cells by Western blotting to verify the relationship between ARID3A, IRP1, and CYGB under the condition of iron overload (∗ P < 0.05, ∗∗∗ P < 0.001). (H, I) Chromatin immunoprecipitation assay performed with ARID3A antibody followed by detection of CYGB promoter through quantitative reverse transcription PCR in Patu-8988 and PANC-1 cells (normal condition, erastin added, hemin added; ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001). (J) DCFH-DA staining (green) was used to detect ROS generation in Patu-8988 cells transfected with control, siRNAs targeting CYGB. (K) The oxygen consumption rates of Patu-8988 cells were shown as a bar chart (∗∗∗ P < 0.001). (L) DCFH-DA staining (green) was used to detect ROS generation in PANC-1 cells transfected with the vector, overexpression plasmid targeting CYGB. (M) The oxygen consumption rates of PANC-1 cells were shown as a bar chart (∗∗∗ P < 0.001). (N) MDA levels were detected in Patu-8988 cells transfected with control, siRNAs targeting CYGB (∗∗∗ P < 0.001). (O) MDA levels were detected in PANC-1 cells transfected with the vector, overexpression plasmid targeting CYGB (∗∗∗ P < 0.001). MDA, malondialdehyde; DCFH-DA, 2′,7′-dichlorofluorescin diacetate; ROS, reactive oxygen species.

Article Snippet: Stable knockdown or overexpression lentiviruses were provided by Shanghai Genechem Co., Ltd., China.

Techniques: Expressing, Sequencing, RNA Sequencing, Binding Assay, Knockdown, Reverse Transcription, Western Blot, Chromatin Immunoprecipitation, Staining, Transfection, Control, Plasmid Preparation, Over Expression

Journal: International Dental Journal

Article Title: H19 Promotes Odontogenic Differentiation of Human Dental Pulp Cells via miR-103a-3p-Mediated PIK3R1/AKT and KLF4 Pathways

doi: 10.1016/j.identj.2026.109587

Figure Lengend Snippet: H19 promotes the odontogenic differentiation of hDPSCs in vivo . A , Schematic of subcutaneous transplantation in nude mice. B, Dentin blocks seeded with H19- or NC-transduced hDPSCs were implanted subcutaneously into nude mice for 8 weeks. C, General view of the tooth root slices before transplantation and after 8 weeks of subcutaneous transplantation. D, Fluorescence was observed under an inverted fluorescence microscope after transduction for 48 hours and mRNA levels of H19. E, mRNA levels of odontogenic genes (ALP, RUNX2, DSPP, DMP-1) were analysed by qRT-PCR. F, Representative images of H&E staining of sections from a tooth root slice. Blue arrows: odontoblast-like cells; red arrows: blood vessels; G, Representative images of Masson’s trichrome staining. H-I, Immunohistochemistry staining for odontogenic genes (DMP-1, DSPP), Blue arrows: DSPP, DMP-1 positive odontoblast-like cells. * P < .05, ** P < .01, *** P < .001.

Article Snippet: For H19 overexpression, lentiviral vectors LV-H19 and LV-NC (Obio Technology) were used to transduce hDPSCs at 40% confluence (optionally add: in the presence of 5 μg/mL polybrene).

Techniques: In Vivo, Transplantation Assay, Fluorescence, Microscopy, Transduction, Quantitative RT-PCR, Staining, Immunohistochemistry

Journal: International Dental Journal

Article Title: H19 Promotes Odontogenic Differentiation of Human Dental Pulp Cells via miR-103a-3p-Mediated PIK3R1/AKT and KLF4 Pathways

doi: 10.1016/j.identj.2026.109587

Figure Lengend Snippet: H19 functions as a ceRNA to regulate odontogenic differentiation by sponging miR-103a-3p in vitro . A, The expression levels of miR-103a-3p were measured after transduction with H19 lentivirus. B, Knockdown efficiency of miR-103a-3p and its effect on miR-140-5p levels. C, Effect of miR-103a-3p knockdown on H19 expression. D, Knockdown efficiency of miR-140-5p and its effect on miR-103a-3p levels. E, Effect of miR-140-5p knockdown on H19 expression. F, The binding site of miR-103a-3p with H19 was predicted by Starbase ( http://starbase.sysu.edu.cn/ ). G, Dual-luciferase reporter assay confirmed the direct binding. H-I, Effects of miR-103a-3p knockdown on the expression of odontogenic differentiation-related genes in hDPSCs. J and K, Relative mRNA and protein expression of mineralisation-related genes in cells co-transfected with LV-H19 and miR-103a-3p mimics after odontogenic differentiation for 14 days. L, ARS staining results in co-transfection experiments. * P < .05, ** P < .01, *** P < .001. ARS, alizarin red S; hDPSCs, human dental pulp stem cells.

Article Snippet: For H19 overexpression, lentiviral vectors LV-H19 and LV-NC (Obio Technology) were used to transduce hDPSCs at 40% confluence (optionally add: in the presence of 5 μg/mL polybrene).

Techniques: In Vitro, Expressing, Transduction, Knockdown, Binding Assay, Luciferase, Reporter Assay, Transfection, Staining, Cotransfection

Journal: International Dental Journal

Article Title: H19 Promotes Odontogenic Differentiation of Human Dental Pulp Cells via miR-103a-3p-Mediated PIK3R1/AKT and KLF4 Pathways

doi: 10.1016/j.identj.2026.109587

Figure Lengend Snippet: The mechanism diagram for H19-mediated miR-103a-3p/PIK3R1/AKT and miR-103a-3p/KLF4 pathways.

Article Snippet: For H19 overexpression, lentiviral vectors LV-H19 and LV-NC (Obio Technology) were used to transduce hDPSCs at 40% confluence (optionally add: in the presence of 5 μg/mL polybrene).

Techniques:

Journal: Bioactive Materials

Article Title: Inhalable PD-L1-engineered hybrid cellular vesicles suppress excessive neutrophil activation and restore mitochondrial homeostasis to alleviate ischemia–reperfusion lung injury and pneumonia

doi: 10.1016/j.bioactmat.2026.03.024

Figure Lengend Snippet: The schematic illustrates the nebulized inhalation of an integrated nanovesicle system (Res-PD-L1@nmEVs) alleviated inflammation, oxidative stress injury, neutrophil activation, and promote mitochondrial integrity to mitigate lung ischemia-reperfusion injury and MRSA-induced bacterial pneumonia.

Article Snippet: For assessing PD-L1 overexpression efficiency, the primary antibodies included PD-L1 (ET1701-4, HUABIO, China) and β-actin (66009-1, Proteintech, China).

Techniques: Activation Assay

Journal: Bioactive Materials

Article Title: Inhalable PD-L1-engineered hybrid cellular vesicles suppress excessive neutrophil activation and restore mitochondrial homeostasis to alleviate ischemia–reperfusion lung injury and pneumonia

doi: 10.1016/j.bioactmat.2026.03.024

Figure Lengend Snippet: Characterization of Res-PD-L1@nmEVs . (A) Schematic illustration of the Res-PD-L1@nmEVs synthesis procedure. (B-D) Representative transmission electron microscopy (TEM) images, dynamic light scattering (DLS) size distributions, and zeta potential measurements of nEVs, PD-L1@mEVs, PD-L1@nmEVs, and Res-PD-L1@nmEVs. (E) PD-L1 expression in PD-L1-overexpressing MSCs (OE-PD-L1) and negative control (NC) MSCs, and CD11b expression in HL60 cells before and after DMSO stimulation, as determined by Western blot. (F) Expression levels of neutrophil membrane markers (CD11b, CXCR2, RAGE, TLR2) and the exosomal marker CD63 in the four EV types. (G) Fluorescence co-localization images of DiO-labeled nEVs (green) and DiL-labeled PD-L1@mEVs (red) after fusion, demonstrating hybrid vesicle formation. (H) Size stability of Res-PD-L1@nmEVs stored at 4 °C and 37 °C for 7 days. (I-K) Binding and neutralization capacity of Res-PD-L1@nmEVs against inflammatory cytokines (TNF-α, IL-6, IL-1β) in vitro. ∗ vs. 0ug/ml; # vs. 100 μg/ml, p < 0.05, n = 5.

Article Snippet: For assessing PD-L1 overexpression efficiency, the primary antibodies included PD-L1 (ET1701-4, HUABIO, China) and β-actin (66009-1, Proteintech, China).

Techniques: Transmission Assay, Electron Microscopy, Zeta Potential Analyzer, Expressing, Negative Control, Western Blot, Membrane, Marker, Fluorescence, Labeling, Binding Assay, Neutralization, In Vitro

Journal: Bioactive Materials

Article Title: Inhalable PD-L1-engineered hybrid cellular vesicles suppress excessive neutrophil activation and restore mitochondrial homeostasis to alleviate ischemia–reperfusion lung injury and pneumonia

doi: 10.1016/j.bioactmat.2026.03.024

Figure Lengend Snippet: Res-PD-L1@nmEVs Attenuate Inflammation and Oxidative Damage in Lung Epithelial Cells In Vitro . (A-B) Flow cytometric analysis and quantification (B) of DiO-labeled Res-PD-L1@nmEVs uptake by BEAS-2B cells under H/R conditions after pretreatment with different endocytic inhibitors (chlorpromazine, chloroquine, and filipin) or incubation at 4 °C. (C) mRNA expression levels of IL-6, TNF-α, and IL-1β in BEAS-2B cells with or without H/R injury following pretreatment with Res, nEVs, PD-L1@mEVs, PD-L1@nmEVs, or Res-PD-L1@nmEVs. (D-E) Representative fluorescence images (D) and quantitative analysis (E) of cell proliferation assessed by BrdU incorporation (red; nuclei stained with DAPI, blue). Scale bar: 50 μm. (F-G) Apoptosis rates detected by flow cytometry (F) and flow cytometric analysis of Annexin V-positive BEAS-2B cells under the indicated conditions (G). (H–K) Fluorescence microscopy images and quantitative analysis of intracellular nitric oxide (NO, green) (H-I) and reactive oxygen species (ROS, red) (J-K). Scale bar: 100 μm. (L) Flow cytometry analysis of intracellular ROS levels. (M − O) Levels of malondialdehyde (MDA) (M), superoxide dismutase 2 (SOD2) activity (N), and glutathione (GSH) content (O) in cells. (P-Q) Cell migration ability evaluated by wound healing assay under different treatments. ∗ vs. Control; # vs. H/R; & vs. H/R + PD-L1@nmEVs, p < 0.05.

Article Snippet: For assessing PD-L1 overexpression efficiency, the primary antibodies included PD-L1 (ET1701-4, HUABIO, China) and β-actin (66009-1, Proteintech, China).

Techniques: In Vitro, Labeling, Incubation, Expressing, Fluorescence, BrdU Incorporation Assay, Staining, Flow Cytometry, Microscopy, Activity Assay, Migration, Wound Healing Assay, Control

Journal: Bioactive Materials

Article Title: Inhalable PD-L1-engineered hybrid cellular vesicles suppress excessive neutrophil activation and restore mitochondrial homeostasis to alleviate ischemia–reperfusion lung injury and pneumonia

doi: 10.1016/j.bioactmat.2026.03.024

Figure Lengend Snippet: Res-PD-L1@nmEVs Restores Mitochondrial Homeostasis and Improves Energy Metabolism BEAS-2B cells were pretreated with Res, nEVs, PD-L1@mEVs, PD-L1@nmEVs, or Res-PD-L1@nmEVs followed by H/R stimulation for subsequent analysis. (A) Representative immunofluorescence images showing the expression and localization of PINK1 (green) and the mitochondrial marker TOMM20 (red), indicating activation of mitophagy. Nuclei were stained with DAPI (blue). Scale bar: 50 μm. (B) Quantitative analysis of PINK1 fluorescence intensity. (C) Expression and localization of autophagy-related proteins LC3B and Beclin-1 detected by immunofluorescence. (D-E) Quantitative analysis of LC3B (D) and Beclin-1 (E) fluorescence intensity. (F) Mitochondrial membrane potential assessed by JC-1 staining and flow cytometry. (G) Oxygen consumption rate (OCR) profiles of lung epithelial cells under different treatments. (H-K) Key mitochondrial respiration parameters: basal respiration (H), maximal respiration (I), proton leak (J), and ATP production (K). (L) Representative confocal microscopy images of mitochondria stained with MitoTracker (green) and lysosomes stained with LysoTracker (red), demonstrating mitochondrial-lysosomal colocalization. Scale bar: 5 μm ∗ vs. Control; # vs. H/R; & vs. H/R + PD-L1@nmEVs, p < 0.05.

Article Snippet: For assessing PD-L1 overexpression efficiency, the primary antibodies included PD-L1 (ET1701-4, HUABIO, China) and β-actin (66009-1, Proteintech, China).

Techniques: Immunofluorescence, Expressing, Marker, Activation Assay, Staining, Fluorescence, Membrane, Flow Cytometry, Confocal Microscopy, Control

Journal: Bioactive Materials

Article Title: Inhalable PD-L1-engineered hybrid cellular vesicles suppress excessive neutrophil activation and restore mitochondrial homeostasis to alleviate ischemia–reperfusion lung injury and pneumonia

doi: 10.1016/j.bioactmat.2026.03.024

Figure Lengend Snippet: Res-PD-L1@nmEVs Suppresses Neutrophil Activation HL60 cells were differentiated into neutrophil-like cells using DMSO and subsequently stimulated with TNF-α to induce activation under conditions simulating IRI. The effects of Res, nEVs, PD-L1@mEVs, PD-L1@nmEVs, and Res-PD-L1@nmEVs on neutrophil activation were evaluated. (A) Cell surface PD-1 expression analyzed by flow cytometry. (B) Representative immunofluorescence images of CD206 expression (red). Nuclei were stained with DAPI (blue). Scale bar: 50 μm. (C) Flow cytometric analysis of cell surface CD206 expression. (D) Flow cytometric analysis of cell surface CD95 expression. (E-G) Levels of myeloperoxidase (MPO) (E), neutrophil elastase (NE) (F), and MMP-9 (G) in neutrophil culture supernatants, measured by ELISA. (H-J) BEAS-2B cells were co-cultured with neutrophils in the presence or absence of TNF-α stimulation. Apoptosis levels (I) and migration capacity (J) of BEAS-2B cells were assessed under different treatment conditions. ∗ vs. Control; # vs. TNF-a; & vs. TNF-a+PD-L1@nmEVs, p < 0.05.

Article Snippet: For assessing PD-L1 overexpression efficiency, the primary antibodies included PD-L1 (ET1701-4, HUABIO, China) and β-actin (66009-1, Proteintech, China).

Techniques: Activation Assay, Expressing, Flow Cytometry, Immunofluorescence, Staining, Enzyme-linked Immunosorbent Assay, Cell Culture, Migration, Control

Journal: Bioactive Materials

Article Title: Inhalable PD-L1-engineered hybrid cellular vesicles suppress excessive neutrophil activation and restore mitochondrial homeostasis to alleviate ischemia–reperfusion lung injury and pneumonia

doi: 10.1016/j.bioactmat.2026.03.024

Figure Lengend Snippet: Nebulized Res-PD-L1@nmEVs Target and Attenuate Lung Ischemia-Reperfusion Injury (A) Experimental timeline: rats undergoing lung IRI received nebulized treatments (Res, nEVs, PD-L1@mEVs, PD-L1@nmEVs, or Res-PD-L1@nmEVs) before ischemia and after reperfusion, with sample collection 2 h post-reperfusion. (B) Ex vivo organ fluorescence imaging 24 h after intravenous or bronchial nebulization of DiR-labeled Res-PD-L1@nmEVs. (C) In vivo lung distribution of nebulized DiL-labeled PD-L1@mEVs and PD-L1@nmEVs evaluated using a small animal dynamic imaging system. Blue: CD31 (vascular marker), Red: DiL. (D-E) Quantitative fluorescence intensity in ex vivo organs (heart, liver, spleen, lungs, kidneys) at 0–24 h after bronchial nebulization of DiR-labeled Res-PD-L1@nmEVs in Sham and IRI groups. (F-G) Representative H&E-stained lung sections (F) and corresponding lung injury scores (G). (H) Lung wet/dry weight ratio. (I-K) Levels of inflammatory cytokines in lung tissue. (L-N) Pulmonary oxidative stress markers: T-SOD2 activity (L), GSH/GSSG ratio (M), and MDA content (N). (O) Representative fluorescence images of ROS in lung tissue. Scale bar: 50 μm. (P-R) Immunofluorescence staining and co-localization of tight junction proteins Occludin-1 (green) and ZO-1 (red) in lung tissues (DAPI: blue). Scale bar: 50 μm. Quantitative analysis of ZO-1 (Q) and Occludin-1 (R) fluorescence intensity. ∗ vs. Sham; # vs. IRI; & vs. IRI + PD-L1@nmEVs, p < 0.05.

Article Snippet: For assessing PD-L1 overexpression efficiency, the primary antibodies included PD-L1 (ET1701-4, HUABIO, China) and β-actin (66009-1, Proteintech, China).

Techniques: Ex Vivo, Fluorescence, Imaging, Labeling, In Vivo, Marker, Staining, Activity Assay, Immunofluorescence

Journal: Bioactive Materials

Article Title: Inhalable PD-L1-engineered hybrid cellular vesicles suppress excessive neutrophil activation and restore mitochondrial homeostasis to alleviate ischemia–reperfusion lung injury and pneumonia

doi: 10.1016/j.bioactmat.2026.03.024

Figure Lengend Snippet: Res-PD-L1@nmEVs Suppresses Neutrophil Activation and Preserves Mitochondrial Integrity via PD-L1 Delivery (A-B) Rats subjected to lung IRI received nebulized administration of different formulations (Res, nEVs, PD-L1@mEVs, PD-L1@nmEVs, or Res-PD-L1@nmEVs) before ischemia and after reperfusion. Lung tissues were collected 2 h post-reperfusion. (A) Representative immunofluorescence images showing the expression and localization of CD11b (green), MPO (red), and PD-1 (yellow) in lung sections across treatment groups. (B) Enlarged view of the IRI group from (A). (C-D) mRNA levels of CD95 (C) and CD206 (D) in lung tissues. (E-F) Levels of myeloperoxidase (MPO) (E) and matrix metalloproteinase-9 (MMP-9) (F) in bronchoalveolar lavage fluid (BALF). (G-I) (G) Representative transmission electron microscopy (TEM) images of lung tissues (scale bar: 2 μm). (H) Proportion of damaged mitochondria. (I) Average number of mitophagic events per cell. (J) Immunofluorescence co-localization of mitochondrial marker TOMM20 (red) and EpCAM (green) in lung tissues (nuclei stained with DAPI, scale bar: 50 μm). (K-L) Protein expression levels of Beclin-1 (K) and LC3 (L) in lung tissues, with insets showing immunofluorescence co-localization of Beclin-1 (green) and LC3 (red) across treatment groups (nuclei stained with DAPI, scale bar: 50 μm). ∗ vs. Sham; # vs. IRI; & vs. IRI + PD-L1@nmEVs, p < 0.05.

Article Snippet: For assessing PD-L1 overexpression efficiency, the primary antibodies included PD-L1 (ET1701-4, HUABIO, China) and β-actin (66009-1, Proteintech, China).

Techniques: Activation Assay, Immunofluorescence, Expressing, Transmission Assay, Electron Microscopy, Marker, Staining

Journal: Bioactive Materials

Article Title: Inhalable PD-L1-engineered hybrid cellular vesicles suppress excessive neutrophil activation and restore mitochondrial homeostasis to alleviate ischemia–reperfusion lung injury and pneumonia

doi: 10.1016/j.bioactmat.2026.03.024

Figure Lengend Snippet: Transcriptomic Analysis Reveals the Mechanism of Res-PD-L1@nmEVs Against IRI-Induced Lung Injury (A-B) Transcriptome sequencing of lung tissues from the Res-PD-L1@nmEVs-treated IRI group (N = 3) and the IRI-only group (N = 3). (A) Volcano plot and (B) heatmap display differentially expressed genes (DEGs) between the IRI + Res-PD-L1@nmEVs and IRI groups. (C-D) GO term and KEGG pathway enrichment analyses of upregulated DEGs after Res-PD-L1@nmEVs treatment. (E-F) GO term and KEGG pathway enrichment analyses of downregulated DEGs following Res-PD-L1@nmEVs treatment. (G-J) Gene Set Enrichment Analysis (GSEA) revealed enrichment in energy metabolism pathways (G) (TCA cycle and oxidative phosphorylation), biosynthetic pathways (H) (ribosome, amino acid biosynthesis, DNA replication), immune pathways (I) (allograft rejection, PD-L1 expression and PD-1 checkpoint pathway), and inflammatory responses (J) (chemokine signaling pathway, ECM-receptor interaction, cytokine-cytokine receptor interaction).

Article Snippet: For assessing PD-L1 overexpression efficiency, the primary antibodies included PD-L1 (ET1701-4, HUABIO, China) and β-actin (66009-1, Proteintech, China).

Techniques: Sequencing, Phospho-proteomics, Expressing

Journal: Bioactive Materials

Article Title: Inhalable PD-L1-engineered hybrid cellular vesicles suppress excessive neutrophil activation and restore mitochondrial homeostasis to alleviate ischemia–reperfusion lung injury and pneumonia

doi: 10.1016/j.bioactmat.2026.03.024

Figure Lengend Snippet: Res-PD-L1@nmEVs Effectively Attenuates MRSA-Induced Pneumonia (A-B) Rats with MRSA-induced pneumonia received three bronchial nebulization treatments over one week with different formulations (Res, nEVs, PD-L1@mEVs, PD-L1@nmEVs, or Res-PD-L1@nmEVs). (A) Representative H&E-stained lung sections and (B) corresponding lung injury scores are shown (n = 5). (C) TUNEL staining of lung tissues to assess apoptosis. (D) Representative micro-CT images of anesthetized rats. (E-G) Flow cytometric analysis of immune cell proportions in lung single-cell suspensions: CD8 + T cells (E), neutrophils (F), and classical monocytes (G). (H-J) Plasma levels of inflammatory cytokines IL-6 (H), IL-1β (I), and TNF-α (J) (n = 5). (K) Immunofluorescence staining of tight junction proteins Occludin (green) and ZO-1 (red) in lung tissues (nuclei stained with DAPI). Scale bar: 50 μm. (L-N) Pulmonary function parameters: lung compliance (L), airway resistance (M), and oxygenation index (N) (n = 4). ∗ vs. Sham; # vs. MRSA; & vs. MRSA + PD-L1@nmEVs, p < 0.05.

Article Snippet: For assessing PD-L1 overexpression efficiency, the primary antibodies included PD-L1 (ET1701-4, HUABIO, China) and β-actin (66009-1, Proteintech, China).

Techniques: Staining, TUNEL Assay, Micro-CT, Single Cell, Clinical Proteomics, Immunofluorescence

Journal: iScience

Article Title: Hyaluronic acid and folic acid-modified mesoporous silica nanoparticles delivering sulforaphane suppress NSCLC via SPI1/miR-616-5p axis

doi: 10.1016/j.isci.2026.116293

Figure Lengend Snippet: SPI1 regulates NSCLC cell viability and proliferation (A–C) Western blot analysis of transfection efficiency for SPI1 overexpression and knockdown ( n = 3, n represents biological replicates). (D) CCK-8 assay assessing the effects of SPI1 overexpression and knockdown on NSCLC cell viability ( n = 6, n represents biological replicates). (E) Colony formation assay evaluating the impact of SPI1 overexpression and knockdown on NSCLC cell proliferation ( n = 3, n represents biological replicates). Data are represented as mean ± SD. p values are based on a one-way ANOVA test. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Article Snippet: Lentiviral SPI1 overexpression virus , GeneChem , N/A.

Techniques: Western Blot, Transfection, Over Expression, Knockdown, CCK-8 Assay, Colony Assay

Journal: iScience

Article Title: Hyaluronic acid and folic acid-modified mesoporous silica nanoparticles delivering sulforaphane suppress NSCLC via SPI1/miR-616-5p axis

doi: 10.1016/j.isci.2026.116293

Figure Lengend Snippet: SPI1 regulates NSCLC cell migration, invasion, and EMT (A) Transwell assay assessing the effects of SPI1 on cell migration and invasion ( n = 3, n represents biological replicates), scale bars, 200 μm. (B) Western blot analysis of the impact of SPI1 on the expression levels of EMT-related proteins (N-cadherin, E-cadherin, and vimentin, n = 3, n represents biological replicates). Data are represented as mean ± SD. p values are based on a one-way ANOVA test. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Ⅰ, N-cadherin. Ⅱ, E-cadherin. Ⅲ, vimentin. Ⅳ, GAPDH.

Article Snippet: Lentiviral SPI1 overexpression virus , GeneChem , N/A.

Techniques: Migration, Transwell Assay, Western Blot, Expressing

Journal: iScience

Article Title: Hyaluronic acid and folic acid-modified mesoporous silica nanoparticles delivering sulforaphane suppress NSCLC via SPI1/miR-616-5p axis

doi: 10.1016/j.isci.2026.116293

Figure Lengend Snippet: SPI1 promotes NSCLC cell invasion and migration by transcriptionally regulating miR-616-5p (A and B) RT-PCR analysis of miR-616-5p expression following SPI1 overexpression or knockdown ( n = 3, n represents biological replicates). (C–E) Transwell assay evaluating cell migration and invasion ( n = 3, n represents biological replicates), scale bars, 200 μm. Data are represented as mean ± SD. p values are based on a one-way ANOVA test. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Article Snippet: Lentiviral SPI1 overexpression virus , GeneChem , N/A.

Techniques: Migration, Reverse Transcription Polymerase Chain Reaction, Expressing, Over Expression, Knockdown, Transwell Assay

Journal: iScience

Article Title: Hyaluronic acid and folic acid-modified mesoporous silica nanoparticles delivering sulforaphane suppress NSCLC via SPI1/miR-616-5p axis

doi: 10.1016/j.isci.2026.116293

Figure Lengend Snippet: SF downregulates miR-616-5p activity by directly binding to and inhibiting SPI1 (A) Molecular docking analysis of SF with SPI1. (B) SPRi binding curve of SF to SPI1. (C and D) Western blot analysis of SPI1 expression in cells ( n = 3, n represents biological replicates). (E) RT-PCR analysis of miR-616-5p expression in cells ( n = 3, n represents biological replicates). Data are represented as mean ± SD. p values are based on a one-way ANOVA test. ∗ p < 0.05, ∗∗ p < 0.01.

Article Snippet: Lentiviral SPI1 overexpression virus , GeneChem , N/A.

Techniques: Activity Assay, Binding Assay, Western Blot, Expressing, Reverse Transcription Polymerase Chain Reaction

Journal: iScience

Article Title: Hyaluronic acid and folic acid-modified mesoporous silica nanoparticles delivering sulforaphane suppress NSCLC via SPI1/miR-616-5p axis

doi: 10.1016/j.isci.2026.116293

Figure Lengend Snippet: In vivo targeting and anti-NSCLC efficacy of MSNs@SF-HA-FA (A) In vivo fluorescence imaging analysis ( n = 5, n represents the number of mice). (B) Ex vivo fluorescence imaging of major organs ( n = 5, n represents the number of mice). (C) Images of lung tumor tissues from mice ( n = 5, n represents the number of mice). (D) H&E-stained images and immunohistochemical analysis of SPI1 expression in xenograft tumors ( n = 5, n represents the number of mice), scale bars, 100 μm.

Article Snippet: Lentiviral SPI1 overexpression virus , GeneChem , N/A.

Techniques: In Vivo, Fluorescence, Imaging, Ex Vivo, Staining, Immunohistochemical staining, Expressing

Journal: iScience

Article Title: Hyaluronic acid and folic acid-modified mesoporous silica nanoparticles delivering sulforaphane suppress NSCLC via SPI1/miR-616-5p axis

doi: 10.1016/j.isci.2026.116293

Figure Lengend Snippet: SPI1 regulates NSCLC cell viability and proliferation (A–C) Western blot analysis of transfection efficiency for SPI1 overexpression and knockdown ( n = 3, n represents biological replicates). (D) CCK-8 assay assessing the effects of SPI1 overexpression and knockdown on NSCLC cell viability ( n = 6, n represents biological replicates). (E) Colony formation assay evaluating the impact of SPI1 overexpression and knockdown on NSCLC cell proliferation ( n = 3, n represents biological replicates). Data are represented as mean ± SD. p values are based on a one-way ANOVA test. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Article Snippet: Specific short hairpin RNA targeting SPI1 (sh-SPI1) and the SPI1 overexpression construct (OE-SPI1) were purchased from GeneChem (Shanghai, China).

Techniques: Western Blot, Transfection, Over Expression, Knockdown, CCK-8 Assay, Colony Assay

Journal: iScience

Article Title: Hyaluronic acid and folic acid-modified mesoporous silica nanoparticles delivering sulforaphane suppress NSCLC via SPI1/miR-616-5p axis

doi: 10.1016/j.isci.2026.116293

Figure Lengend Snippet: SPI1 regulates NSCLC cell migration, invasion, and EMT (A) Transwell assay assessing the effects of SPI1 on cell migration and invasion ( n = 3, n represents biological replicates), scale bars, 200 μm. (B) Western blot analysis of the impact of SPI1 on the expression levels of EMT-related proteins (N-cadherin, E-cadherin, and vimentin, n = 3, n represents biological replicates). Data are represented as mean ± SD. p values are based on a one-way ANOVA test. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Ⅰ, N-cadherin. Ⅱ, E-cadherin. Ⅲ, vimentin. Ⅳ, GAPDH.

Article Snippet: Specific short hairpin RNA targeting SPI1 (sh-SPI1) and the SPI1 overexpression construct (OE-SPI1) were purchased from GeneChem (Shanghai, China).

Techniques: Migration, Transwell Assay, Western Blot, Expressing

Journal: iScience

Article Title: Hyaluronic acid and folic acid-modified mesoporous silica nanoparticles delivering sulforaphane suppress NSCLC via SPI1/miR-616-5p axis

doi: 10.1016/j.isci.2026.116293

Figure Lengend Snippet: SPI1 promotes NSCLC cell invasion and migration by transcriptionally regulating miR-616-5p (A and B) RT-PCR analysis of miR-616-5p expression following SPI1 overexpression or knockdown ( n = 3, n represents biological replicates). (C–E) Transwell assay evaluating cell migration and invasion ( n = 3, n represents biological replicates), scale bars, 200 μm. Data are represented as mean ± SD. p values are based on a one-way ANOVA test. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Article Snippet: Specific short hairpin RNA targeting SPI1 (sh-SPI1) and the SPI1 overexpression construct (OE-SPI1) were purchased from GeneChem (Shanghai, China).

Techniques: Migration, Reverse Transcription Polymerase Chain Reaction, Expressing, Over Expression, Knockdown, Transwell Assay

Journal: iScience

Article Title: Hyaluronic acid and folic acid-modified mesoporous silica nanoparticles delivering sulforaphane suppress NSCLC via SPI1/miR-616-5p axis

doi: 10.1016/j.isci.2026.116293

Figure Lengend Snippet: SF downregulates miR-616-5p activity by directly binding to and inhibiting SPI1 (A) Molecular docking analysis of SF with SPI1. (B) SPRi binding curve of SF to SPI1. (C and D) Western blot analysis of SPI1 expression in cells ( n = 3, n represents biological replicates). (E) RT-PCR analysis of miR-616-5p expression in cells ( n = 3, n represents biological replicates). Data are represented as mean ± SD. p values are based on a one-way ANOVA test. ∗ p < 0.05, ∗∗ p < 0.01.

Article Snippet: Specific short hairpin RNA targeting SPI1 (sh-SPI1) and the SPI1 overexpression construct (OE-SPI1) were purchased from GeneChem (Shanghai, China).

Techniques: Activity Assay, Binding Assay, Western Blot, Expressing, Reverse Transcription Polymerase Chain Reaction

Journal: iScience

Article Title: Hyaluronic acid and folic acid-modified mesoporous silica nanoparticles delivering sulforaphane suppress NSCLC via SPI1/miR-616-5p axis

doi: 10.1016/j.isci.2026.116293

Figure Lengend Snippet: In vivo targeting and anti-NSCLC efficacy of MSNs@SF-HA-FA (A) In vivo fluorescence imaging analysis ( n = 5, n represents the number of mice). (B) Ex vivo fluorescence imaging of major organs ( n = 5, n represents the number of mice). (C) Images of lung tumor tissues from mice ( n = 5, n represents the number of mice). (D) H&E-stained images and immunohistochemical analysis of SPI1 expression in xenograft tumors ( n = 5, n represents the number of mice), scale bars, 100 μm.

Article Snippet: Specific short hairpin RNA targeting SPI1 (sh-SPI1) and the SPI1 overexpression construct (OE-SPI1) were purchased from GeneChem (Shanghai, China).

Techniques: In Vivo, Fluorescence, Imaging, Ex Vivo, Staining, Immunohistochemical staining, Expressing

Journal: iScience

Article Title: Gastric cancer-secreted galectin-1 promotes peritoneal mesothelial-mesenchymal transition to prime peritoneal metastasis soil

doi: 10.1016/j.isci.2026.115908

Figure Lengend Snippet: Galectin-1 expression in GC is associated with peritoneal MMT and PM (A and B) Representative H&E and IHC staining for E-cadherin and vimentin in peritoneal tissues without or with MMT, at ×100, ×200, and ×400 magnification. (C) Immunofluorescence co-staining of E-cadherin, and vimentin to assess MMT status. (D and E) Quantification of mean fluorescence intensity for E-cadherin and vimentin ( n = 6). (F and G) Representative H&E and IHC staining for galectin-1 in GC tissues without or with MMT, at ×100, ×200, and ×400 magnification. (H) Immunoreactive score (IRS) of galectin-1 expression ( n = 42). (I) Comparison of the PM state in patients without ( n = 24) or with ( n = 18) peritoneal MMT. (J) Volcano plot of differential gene expression from GSE62254 ( n = 300), analyzed by limma; LGALS1 is highlighted as upregulated in PM. (K) Violin plot of LGALS1 expression in the group without PM vs. with PM group. Data are represented as mean ± SD.∗ p < 0.05, ∗∗ p < 0.01.

Article Snippet: Lentiviral vectors for LGALS1 overexpression (OE- LGALS1 ) and negative control (OE-NC), both expressing green fluorescent protein (GFP) and the puromycin resistance gene, were purchased from Genechem Co., Ltd. (Shanghai, China).

Techniques: Expressing, Immunohistochemistry, Immunofluorescence, Staining, Fluorescence, Comparison, Gene Expression

Journal: iScience

Article Title: Gastric cancer-secreted galectin-1 promotes peritoneal mesothelial-mesenchymal transition to prime peritoneal metastasis soil

doi: 10.1016/j.isci.2026.115908

Figure Lengend Snippet: Galectin-1 promotes MMT in HPMCs and upregulates TGF-β1 expression (A and B) Representative bright-field and GFP images of LGALS1 overexpression (OE- LGALS1 ) and negative control (OE-NC) SGC-7901 (A) and HGC-27 (B) cells (Scale bars, 100 μm). (C and D) ELISA analysis of galectin-1 in CM from WT, OE-NC, and OE- LGALS1 SGC-7901 and HGC-27 cell lines ( n = 3). (E and F) RT-qPCR analysis of CDH1 and VIM mRNA in HMrSV5 cells treated with CM from SGC-7901 and HGC-27 cell lines ( n = 3). (G–J) WB confirmed E-cadherin and vimentin expression in HMrSV5 cells treated with CM from SGC-7901 and HGC-27 cell lines ( n = 3). (K–M) ELISA analysis of TGF-β1 (K), WNT5 (L), and WIF1 (M) in CM from SGC-7901 and HGC-27 cell lines ( n = 3). Data are represented as mean ± SD.∗ p < 0.05. ∗∗ p < 0.01, NS, p > 0.05.

Article Snippet: Lentiviral vectors for LGALS1 overexpression (OE- LGALS1 ) and negative control (OE-NC), both expressing green fluorescent protein (GFP) and the puromycin resistance gene, were purchased from Genechem Co., Ltd. (Shanghai, China).

Techniques: Expressing, Over Expression, Negative Control, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR

Journal: iScience

Article Title: Gastric cancer-secreted galectin-1 promotes peritoneal mesothelial-mesenchymal transition to prime peritoneal metastasis soil

doi: 10.1016/j.isci.2026.115908

Figure Lengend Snippet: Galectin-1 promotes MMT in HPMCs through the TGF-β/Smad signaling pathway (A–D) WB analysis of TGF-β1 and p -Smad2/3 in HMrSV5 cells treated with CM from SGC-7901 cells (A and B) and HGC-27 cells (C and D) with different LGALS1 expression levels ( n = 3). (E–H) WB confirmed E-cadherin and vimentin expression in HMrSV5 cells treated with CM from SGC-7901 cells (E and F) and HGC-27 cells (G and H) with different LGALS1 expression levels or CM-OE- LGALS1 supplemented with ITD1. Data are represented as mean ± SD. ∗∗ p < 0.01, NS, p > 0.05.

Article Snippet: Lentiviral vectors for LGALS1 overexpression (OE- LGALS1 ) and negative control (OE-NC), both expressing green fluorescent protein (GFP) and the puromycin resistance gene, were purchased from Genechem Co., Ltd. (Shanghai, China).

Techniques: Expressing

Journal: iScience

Article Title: Gastric cancer-secreted galectin-1 promotes peritoneal mesothelial-mesenchymal transition to prime peritoneal metastasis soil

doi: 10.1016/j.isci.2026.115908

Figure Lengend Snippet: Activation of the TGF-β/Smad signaling pathway promotes MMT in HPMCs (A–D) Representative immunofluorescence images of E-cadherin and vimentin in HMrSV5 cells treated with CM from SGC-7901 cells (A and B) and HGC-27 cells (C and D) with different LGALS1 expression levels or CM-OE- LGALS1 supplemented with ITD1 (Scale bars, 50 μm) ( n = 3). (E–H) Representative immunofluorescence images of TGF-β1 and p -Smad2/3 in HMrSV5 cells treated with CM from SGC-7901 cells (E and F) and HGC-27 cells (G and H) with different LGALS1 expression or CM-OE- LGALS1 supplemented with ITD1 (Scale bars, 50 μm) ( n = 3). Data are represented as mean ± SD.∗ p < 0.05, ∗∗ p < 0.01, NS, p > 0.05.

Article Snippet: Lentiviral vectors for LGALS1 overexpression (OE- LGALS1 ) and negative control (OE-NC), both expressing green fluorescent protein (GFP) and the puromycin resistance gene, were purchased from Genechem Co., Ltd. (Shanghai, China).

Techniques: Activation Assay, Immunofluorescence, Expressing

Journal: iScience

Article Title: Gastric cancer-secreted galectin-1 promotes peritoneal mesothelial-mesenchymal transition to prime peritoneal metastasis soil

doi: 10.1016/j.isci.2026.115908

Figure Lengend Snippet: TGF-β/Smad signaling pathway is activated in peritoneal tissues undergoing MMT, and galectin-1 enhances GC cell adhesion to HPMCs via this pathway (A–C) Representative images of immunofluorescence for TGF-β1 (A) and p -Smad2/3 (B) in peritoneal tissues without or with MMT (×400 magnification). (C) Comparison of the relative fluorescence density of TGF-β1 and p -Smad2/3 in peritoneal tissues without or with MMT ( n = 6). (D and E) GC cells incubated with Calcein-AM were added to HMrSV5 cells treated with CM from SGC-7901 cells (D) or HGC-27 cells (E) or with different LGALS1 expression levels (Scale bars, 100 μm) ( n = 3). (F and G) Mean IODs of SGC-7901 cells (F) and HGC-27 cells (G) adherent to HMrSV5 cells ( n = 3). Data are represented as mean ± SD.∗∗ p < 0.01, NS, p > 0.05.

Article Snippet: Lentiviral vectors for LGALS1 overexpression (OE- LGALS1 ) and negative control (OE-NC), both expressing green fluorescent protein (GFP) and the puromycin resistance gene, were purchased from Genechem Co., Ltd. (Shanghai, China).

Techniques: Immunofluorescence, Comparison, Fluorescence, Incubation, Expressing

Journal: iScience

Article Title: Gastric cancer-secreted galectin-1 promotes peritoneal mesothelial-mesenchymal transition to prime peritoneal metastasis soil

doi: 10.1016/j.isci.2026.115908

Figure Lengend Snippet: Galectin-1 promotes GCPM through the TGF-β/Smad signaling pathway (A) Representative images of the GCPM animal model established in this study. (B) H&E staining confirmed that the peritoneal nodules were metastatic carcinomas (×400 magnification). (C–E) Representative immunofluorescence images of E-cadherin and vimentin (C), TGF-β1 (D) and p -Smad2/3 (E) in the peritoneum of model animals (×400 magnification). (F) The PCI of mice in different groups ( n = 6). (G and H) The mean fluorescence density of vimentin and E-cadherin ( n = 6). (I and J) The relative fluorescence density of TGF-β1 and p -Smad2/3 ( n = 6). Data are represented as mean ± SD. ∗∗ p < 0.01, NS, p > 0.05.

Article Snippet: Lentiviral vectors for LGALS1 overexpression (OE- LGALS1 ) and negative control (OE-NC), both expressing green fluorescent protein (GFP) and the puromycin resistance gene, were purchased from Genechem Co., Ltd. (Shanghai, China).

Techniques: Animal Model, Staining, Immunofluorescence, Fluorescence