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: 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

Journal: mBio

Article Title: Potential mechanisms underlying Enterococcus faecalis -driven pancreatic cancer cell proliferation

doi: 10.1128/mbio.03963-25

Figure Lengend Snippet: E. faecalis promoted the proliferation of pancreatic cancer cells. ( A ) An in vitro co-culture system was established to explore the influence of E. faecalis on pancreatic cancer cells. PANC1 and PANC02 cells were briefly co-cultured with V583 or EF at various MOIs, followed by removal of extracellular bacteria via washing and further culture for 48 h with a triple-antibiotic cocktail. ( B ) Cell survival was assessed by Calcein-AM/PI staining after 4 h of co-culture. Scale bar = 100 µm. ( C ) The impact of E. faecalis on the viability of pancreatic cancer cells was assessed using MTT assay at 48 h. ( D and E ) PANC1 or PANC02 cell numbers were quantified using a cell counter after 48 h with or without V583 stimulation. ( F ) The proliferation of PANC1 cells was assessed by EdU assay at multiple time points post-V583 infection. ( G and H ) Ki67 immunofluorescence staining and quantitative analysis were performed 48 h after infection with V583 ( G ) or EF ( H ) to assess PANC1 proliferation. * P < 0.05, ** P < 0.01 ( N = 6).

Article Snippet: Endogenous peroxidase activity was blocked with serum, and the cells were incubated overnight at 4°C with anti-Ki67 primary antibody (Abclonal, 1:1000).

Techniques: In Vitro, Co-Culture Assay, Cell Culture, Bacteria, Staining, MTT Assay, EdU Assay, Infection, Immunofluorescence

Journal: mBio

Article Title: Potential mechanisms underlying Enterococcus faecalis -driven pancreatic cancer cell proliferation

doi: 10.1128/mbio.03963-25

Figure Lengend Snippet: E. faecalis enhanced the migration and invasion of pancreatic cancer cells. ( A ) Wound healing assay showing PANC1 cell migration after V583 infection (scale bar = 200 µm). ( B ) Wound healing assay assessing the effect of EF infection on PANC1 cell migration (scale bar = 200 µm). ( C, D ) Quantification of wound closure in panels A and B . ( E ) Transwell assay evaluating the invasive potential of PANC1 cells after V583 infection (scale bar = 100 µm). ( F ) Statistical analysis of panel E . ( G ) Transwell assay assessing invasion of EF-infected PANC1 cells (scale bar = 100 µm). ( H ) Statistical analysis of panel G . ( I ) Western blot analysis of proliferation markers (PCNA, cyclin D1) and apoptosis markers (caspase-9, cleaved caspase-3) in PANC1 cells following V583 stimulation. ( J ) Quantitative analysis of panel I . ( K ) RNA-seq data showing upregulation of proliferation-related genes (CCNB2, CCND1, PCNA, MKI67) in PANC1 cells 48 h post-V583 treatment. ( L ) Western blot analysis of E-cadherin and N-cadherin expression in V583-treated PANC1 cells. ( M ) Quantitation of panel L . ( N ) RNA-seq results showing altered expression of E-cadherin and N-cadherin genes in PANC1 cells after V583 stimulation. * P < 0.05, ** P < 0.01 ( N = 4).

Article Snippet: Endogenous peroxidase activity was blocked with serum, and the cells were incubated overnight at 4°C with anti-Ki67 primary antibody (Abclonal, 1:1000).

Techniques: Migration, Wound Healing Assay, Infection, Transwell Assay, Western Blot, RNA Sequencing, Expressing, Quantitation Assay

Journal: mBio

Article Title: Potential mechanisms underlying Enterococcus faecalis -driven pancreatic cancer cell proliferation

doi: 10.1128/mbio.03963-25

Figure Lengend Snippet: The impact of E. faecalis on pancreatic tumor growth in vivo . ( A ) Schematic of the in vivo experimental model for V583 infection in pancreatic cancer. ( B ) Representative ex vivo tumor images at day 60, showing visible differences between V583 and control groups. ( C ) Comparison of tumor weights between the V583-inoculated and control groups at day 60. * P < 0.05 ( N = 6). ( D ) H&E staining and immunohistochemical analysis of EGFR and Ki67 expression in tumor tissues.

Article Snippet: Endogenous peroxidase activity was blocked with serum, and the cells were incubated overnight at 4°C with anti-Ki67 primary antibody (Abclonal, 1:1000).

Techniques: In Vivo, Infection, Ex Vivo, Control, Comparison, Staining, Immunohistochemical staining, Expressing