Journal: Bioactive Materials

Article Title: Countering postoperative immune suppression with a self-assembling dendritic cell nanovaccine

doi: 10.1016/j.bioactmat.2026.05.005

Figure Lengend Snippet: In vivo therapeutic efficacy of advanced BAITs in a postoperative tumor model. (A) Schematic of in vivo experimental design. LLC tumors were surgically resected, and mice were re-challenged with LLC cells. Mice then received BAIT treatments. (B) Photographs of tumors and tumor weights at day 16 for each group (n = 5; ∗ is P < 0.05, ∗∗ is P < 0.01, ∗∗∗ is P < 0.001 by one-way ANOVA with Bonferroni post-hoc test). (C) Individual tumor growth curves over time (n = 5; ∗∗ is P < 0.01, ∗∗∗∗ is P < 0.0001 by two-way ANOVA with Bonferroni post-hoc test). (D) H&E-stained tumor sections. (E) TUNEL staining of tumor sections (brown, apoptotic cells). Black arrowheads mark TUNEL + areas. (F) Quantification of TUNEL + apoptotic cells (n = 5; ∗∗∗∗ is P < 0.0001 by one-way ANOVA with Bonferroni post-hoc test). (G) Representative immunofluorescence for Ki67 (green) in tumor tissues (nuclei in blue). The Apo-BAIT group shows greatly reduced Ki67 + proliferating cells. (H) Quantification of Ki67 + cell density (n = 5; ∗ is P < 0.05, ∗∗ is P < 0.01, ∗∗∗∗ is P < 0.0001 by one-way ANOVA with Bonferroni post-hoc test). Data are presented as mean ± SD.

Article Snippet: Anti-Ki67 mouse mAb (Cat# GB121141-100), anti-CD3 mouse mAb (Cat# GB15014-100), FITC-conjugated goat anti-mouse IgG (H + L) (Cat# GB22301), and Cy5-conjugated goat anti-mouse IgG (H + L) (Cat# GB27301) for immunofluorescence assays, and DAB (SA-HRP) TUNEL apoptosis detection kit were supplied by Servicebio (Wuhan, China).

Techniques: In Vivo, Drug discovery, Staining, TUNEL Assay, Immunofluorescence

Journal: Journal of Advanced Research

Article Title: Discovery of FBP1 as novel therapeutic target and asiatic acid-hydrogen sulfide donors accelerate diabetic wound healing

doi: 10.1016/j.jare.2025.12.003

Figure Lengend Snippet: Screening-identified asiatic acid inhibits FBP1 and promotes wound healing. (A) The relative FBP1 activity after the candidate compounds (50 μM) treatment using the FBP1 activity assay kit. (B) The chemical structure of AA. (C) Molecular docking structural model depicting asiatic acid-FBP1 binding interactions at the catalytic pocket (D) The effect of AA and AMP (0.01–100 μM) on FBP1 activity was detected by FBP1 activity assay kit. (E) CETSA analysis demonstrated enhanced FBP1 thermostability in asiatic acid-treated HaCaT cells. (F) Scratch wound healing assay demonstrated the migration changes after AA administration in HaCaT cells stimulated with MGO and overexpressing FBP1. (G) HaCaT cells exposed to asiatic acid (0.2–200 μM) for 24 h underwent MTT assay to quantify dose-dependent viability effects. (H) Clonal numbers after AA administration in HaCaT cells stimulated with MGO and overexpressing FBP1. (I) Transwell assay assessing invasion of HaCaT cells stimulated with MGO and overexpressing FBP1 after the introduction of AA. (J, K) Observation of HaCaT cells proliferation following AA administration using Ki67 staining (Scale bar = 100 μm). (L) Phalloidin staining after AA introduction in HaCaT cells stimulated with MGO and overexpressing FBP1. Data represent mean ± SEM from three independent replicates. * P < 0.05, ** P < 0.01, *** P < 0.001 vs Ctrl group. ^ P < 0.05, ^^ P < 0.01 vs OE group. & P < 0.05, && P < 0.01 vs NC group. # P < 0.05, ## P < 0.01 vs MGO group.

Article Snippet: For immunostaining, primary antibody targeting Ki67 (ABclonal, Wuhan, China) was applied and incubated overnight at 4 °C.

Techniques: Activity Assay, Binding Assay, Wound Healing Assay, Migration, MTT Assay, Transwell Assay, Staining

Journal: iScience

Article Title: m6A-dependent regulation of DGUOK-AS1 by RBM15 and HNRNPH1 in lung adenocarcinoma

doi: 10.1016/j.isci.2026.117078

Figure Lengend Snippet: DGUOK-AS1 promotes the growth of lung adenocarcinoma cells (A) Colony formation assay was performed to measure the cell proliferation of A549 and H1975 cells transfected with DGUOK-AS1 siRNA or scrambled controls ( n = 3, ∗∗ p < 0.01). (B) Cell proliferation analysis of A549 and H1975 cells transfected with DGUOK-AS1 201 and DGUOK-AS1 202 overexpression vectors or control vector ( n = 3, ∗∗ p < 0.01; ns, not significant). (C) The migration ability of A549 and H1975 cells transfected with DGUOK-AS1 siRNA or scrambled controls was detected by Transwell assay (scale bars, 100 μm; n = 4, ∗∗∗ p < 0.001). (D) Transwell migration assays of A549 and H1975 cells transfected with DGUOK-AS1 201 and DGUOK-AS1 202 overexpression vectors or control vector (scale bars, 100 μm; n = 4, ∗∗ p < 0.01, ∗∗∗ p < 0.001; ns, not significant). (E) Representative images of the xenograft tumors by subcutaneous injection of A549 cells stably transfected with sh-DGUOK-AS1 or sh-control ( n = 5 mice per group). (H) Images of the tumors formed by stable A549 cells infected with lentivirus expressing DGUOK-AS1 201, DGUOK-AS1 202, or control lentivirus ( n = 5 mice per group). (F, G, I, and J) Growth curves and weight of tumors in subcutaneous xenografts from knockdown or overexpression groups ( n = 5, ∗ p < 0.05, ∗∗ p < 0.01; ns, not significant). (K and L) The Ki67 expression was determined by immunohistochemical assay in the subcutaneous xenograft models (scale bars, 100 μm; n = 3). Data in all graphs are shown as mean ± SEM based on three independent trials. For (A–L), n represents the number of independent biological replicates, unless otherwise specified (mice: n = number of animals). Statistical analysis was performed using a paired t test (A, C, G, and J) or one-way ANOVA (B and D), followed by Tukey’s multiple comparison test.

Article Snippet: [KO Validated] Ki67 Rabbit mAb , ABclonal , Cat# A20018; RRID: AB_3065688.

Techniques: Colony Assay, Transfection, Over Expression, Control, Plasmid Preparation, Migration, Transwell Assay, Injection, Stable Transfection, Infection, Expressing, Knockdown, Immunohistochemical staining, Comparison

Journal: iScience

Article Title: m6A-dependent regulation of DGUOK-AS1 by RBM15 and HNRNPH1 in lung adenocarcinoma

doi: 10.1016/j.isci.2026.117078

Figure Lengend Snippet: RBM15 upregulates the expression of DGUOK-AS1 201 and promotes the proliferation and migration of LUAD cells (A–C) Tumor volume and weight in nude mice injected with A549 cells stably transfected with sh-RBM15 or sh-control ( n = 5 mice per group; ∗∗∗ p < 0.001). (D) Immunohistochemistry (IHC) staining of Ki67 in subcutaneous xenograft tumors (scale bars, 100 μm). (E and F) RT-qPCR analysis of DGUOK-AS1 expression in A549 and H1975 cells upon RBM15 knockdown or overexpression ( n = 3, ∗ p < 0.05, ∗∗∗ p < 0.001; ns, not significant). (G) Relative DGUOK-AS1 RNA levels measured by RT-qPCR following actinomycin D treatment ( n = 3, ∗ p < 0.05, ∗∗∗ p < 0.001). (H) Colony formation assay of proliferation in A549 cells co-transfected with RBM15 knockdown lentivirus and DGUOK-AS1 201 overexpression vector ( n = 3, ∗∗∗ p < 0.001). (I) Transwell migration assay in RBM15-silenced A549 cells overexpressing DGUOK-AS1 201 (scale bars, 100 μm; n = 5, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001). (J) RT-qPCR analysis of miR-2467-5p expression in A549 and H1975 cells upon RBM15 overexpression or knockdown ( n = 3, ∗ p < 0.05, ∗∗∗ p < 0.001). (K) Protein levels of RBM15 and PRMT5 in A549 cells with RBM15 overexpression or knockdown. Data are presented as mean ± SEM from three independent experiments. For (A–K), n represents the number of independent biological replicates, unless otherwise specified (mice: n = number of animals). Statistical analysis was performed using a paired t test (C and J), a one-way ANOVA (H and I), or a two-way ANOVA (E, F, and G) followed by Tukey’s multiple comparison test.

Article Snippet: [KO Validated] Ki67 Rabbit mAb , ABclonal , Cat# A20018; RRID: AB_3065688.

Techniques: Expressing, Migration, Injection, Stable Transfection, Transfection, Control, Immunohistochemistry, Quantitative RT-PCR, Knockdown, Over Expression, Colony Assay, Plasmid Preparation, Transwell Migration Assay, Comparison

Journal: iScience

Article Title: m6A-dependent regulation of DGUOK-AS1 by RBM15 and HNRNPH1 in lung adenocarcinoma

doi: 10.1016/j.isci.2026.117078

Figure Lengend Snippet:

Article Snippet: [KO Validated] Ki67 Rabbit mAb , ABclonal , Cat# A20018; RRID: AB_3065688.

Techniques: Virus, Recombinant, Transfection, RNA Extraction, Transwell Assay, Magnetic Beads, Lysis, Cell Counting, RNA Immunoprecipitation, Labeling, Silver Staining, Methylation, Immunoprecipitation, Immunohistochemistry, Luciferase, Reporter Assay, Mass Spectrometry, Software, RNA sequencing

Journal: iScience

Article Title: Uhrf1 in PDGFRα-lineage cells regulates osteophyte formation in osteoarthritis

doi: 10.1016/j.isci.2026.116927

Figure Lengend Snippet: Uhrf1-positive cells are localized within the synovial thickening, and both Uhrf1 and PDGFRα double-positive cells are present within the mouse knee synovium (A) Uhrf1-positive cell localization within the osteophyte 4 days, 1 week, and 2 weeks after DMM in wild-type (WT) mice. The images show Safranin O/fast green and immunohistochemical staining against DAPI (blue), Uhrf1 (green), and KI67 (red). The borders between the bone and osteophyte (white solid line), between the chondrogenic area and synovial hypertrophic area (white dotted line), the hypertrophic synovial (HS) area (red arrow), and the chondrogenic area (CA) (blue arrow) are shown. Scale bars: 100 μm. (B) The images show Safranin O/fast green and immunohistochemistry for DAPI (blue), Uhrf1 (green), and PDGFRα (magenta) on knee synovium of WT mice 2 weeks after DMM. Uhrf1 and PDGFRα double-positive cells are designated with white arrows. Scale bars: 200 μm.

Article Snippet: Immunofluorescence staining was performed on tissue specimens by autoclaving with 0.5% ImmunoSaver (Wako, Osaka, Japan) for 45 min at 85°C and blocking by treatment with a solution of 1% BSA and 0.02% Triton in PBS for 1 h. Primary antibodies were mouse anti-Uhrf1 monoclonal antibody (Santa Cruz Biotechnology, TX, USA; 1:400), rat anti-KI67 monoclonal antibody (Synaptic systems, Goettingen, Germany; 1:400), goat anti-PDGFRα monoclonal antibody (R&D Systems, MSP, USA; 1:400), rat anti-GFP monoclonal antibody (R&D Systems, MSP, USA; 1:400).

Techniques: Immunohistochemical staining, Staining, Immunohistochemistry

Journal: iScience

Article Title: Uhrf1 in PDGFRα-lineage cells regulates osteophyte formation in osteoarthritis

doi: 10.1016/j.isci.2026.116927

Figure Lengend Snippet: PDGFRα-lineage cell-specific Uhrf1-knockout mice showed reduced osteophyte formation 2 weeks after DMM (A) Uhrf1 mRNA expression levels in PDGFRα-positive cells obtained from lower limb muscles of Ctrl and cKO mice at 12 weeks of age, using FACS. Biological replicates, n = 4. The dots show individual data points. All data are mean ± SD. ∗ p < 0.05 (unpaired two-tailed Student’s t test). (B) Immunocytochemistry for DAPI (blue), Uhrf1 (red), and KI67 (green) on PDGFRα-positive cells from lower limb muscles of Ctrl and cKO mice at 12 weeks of age, using FACS. Scale bars: 20 μm. (C) Uhrf1-positive proportion of PDGFRα-positive cells. Biological replicates, n = 3. The dots show individual data points. All data are mean ± SD. ∗∗∗ p < 0.001 (Mann-Whitney U test). (D) Osteophytes at the medial tibial articular surface with lower (left) and higher (right) magnifications of Ctrl and cKO mice 2 weeks after DMM, stained with Safranin O and fast green. Scale bars: 200 μm. (E–G) The upper line graphs show (E) osteophyte width, (F) osteophyte area, and (G) modified maturity score at each evaluation site for Ctrl and cKO mice 2 weeks after DMM. The dots show the mean values. The lower graphs show area under the curve (AUC) for the osteophyte width, osteophyte area, and modified maturity score. Biological replicates, n = 9. The dots show individual data points. All data are mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01 (Mann-Whitney U test). DMM, destabilization of the medial meniscus.

Article Snippet: Immunofluorescence staining was performed on tissue specimens by autoclaving with 0.5% ImmunoSaver (Wako, Osaka, Japan) for 45 min at 85°C and blocking by treatment with a solution of 1% BSA and 0.02% Triton in PBS for 1 h. Primary antibodies were mouse anti-Uhrf1 monoclonal antibody (Santa Cruz Biotechnology, TX, USA; 1:400), rat anti-KI67 monoclonal antibody (Synaptic systems, Goettingen, Germany; 1:400), goat anti-PDGFRα monoclonal antibody (R&D Systems, MSP, USA; 1:400), rat anti-GFP monoclonal antibody (R&D Systems, MSP, USA; 1:400).

Techniques: Knock-Out, Expressing, Muscles, Two Tailed Test, Immunocytochemistry, MANN-WHITNEY, Staining, Modification