Journal: EMBO Reports

Article Title: Human ZBP1 is a potent inducer of cell death through mechanisms divergent from mouse ZBP1

doi: 10.1038/s44319-026-00866-6

Figure Lengend Snippet: Reagents and tools table

Article Snippet: Recombinant Human IFN-γ , ABclonal , Cat#RP01038.

Techniques: Recombinant, Sequencing, Magnetic Beads, Protease Inhibitor, Software, Microscopy, Bicinchoninic Acid Protein Assay

Journal: Molecular Medicine Reports

Article Title: Elevated IgG levels induce an M2-to-M1 phenotypic shift in mucosal macrophages and restrict the growth of invasive sphenoid sinus pituitary adenomas

doi: 10.3892/mmr.2026.13878

Figure Lengend Snippet: IFN-γ suppresses tumor growth and invasion. (A) Cytokine profiling of co-culture supernatants via ELISAs: IFN-γ, IL-1β, IL-6, IL-10, TGF-β and TNF-α. (B-D) Spatial expression patterns of IFN-γ. (B) Immunofluorescence imaging of the invasive front in SSIT, showing DAPI (blue), IBA-1 + macrophages (red) and IFN-γ + signals (green), and grayscale intensity distribution. (C) Immunofluorescence imaging of TIM and NIM, showing DAPI (blue), IBA-1 + macrophages (red) and IFN-γ + signals (green). (D) Quantification of relative IFN-γ expression in TIM and NIM. (E) Representative Ki-67 immunohistochemistry images of SSIT cases stratified into IFN-γ-high and IFN-γ-low groups (n=5 each; median split). (F) Quantification of Ki-67 index comparing the two groups. (G) EdU staining demonstrating dose-dependent suppression of TtT/GF pituitary adenoma cell proliferation by IFN-γ (0–100 ng/ml; 48 h). (H) Representative flow cytometry histograms for cell cycle analysis of cells treated with IFN-γ (0–100 ng/ml) in the absence (0 µM) or presence (5 µM) of ruxolitinib. (I) Stacked bar plot showing the percentages of cells in the G 1 , S and G 2 /M phases under the same treatment conditions. (A) One-way ANOVA with Tukey's post hoc multiple comparisons test. (D and F) Unpaired two-tailed Student's t-test. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. CTRL, control; DMC, digested mucosal culture; EdU, 5-ethynyl-2′-deoxyuridine; IBA-1, ionised calcium binding adaptor molecule 1; MTC, mucosal tissue culture; NIM, non-invaded mucosa; ns, not significant; PE-A, phycoerythrin-area; SSIT, sphenoid sinus-invasive tumor; TIM, tumor-invaded mucosa.

Article Snippet: Cells were maintained in serum-free DMEM and treated with IFN-γ (0–100 ng/ml; cat. no. RP01038; ABclonal Biotech Co., Ltd.), IL-6 (100 ng/ml; cat. no. RP00201; ABclonal Biotech Co., Ltd.) or a combination of IFN-γ and IL-6 (50 ng/ml each) at 37°C for 72 h, as indicated.

Techniques: Co-Culture Assay, Expressing, Immunofluorescence, Imaging, Immunohistochemistry, Staining, Flow Cytometry, Cell Cycle Assay, Two Tailed Test, Control, Binding Assay

Journal: Molecular Medicine Reports

Article Title: Elevated IgG levels induce an M2-to-M1 phenotypic shift in mucosal macrophages and restrict the growth of invasive sphenoid sinus pituitary adenomas

doi: 10.3892/mmr.2026.13878

Figure Lengend Snippet: Elevated IgG levels drive macrophage M2-to-M1 reprogramming. (A) Sphenoid sinus-invasive tumor cases stratified into CD19-high (n=5) and CD19-low (n=5) groups based on the cohort median of CD19 + B cell density, with (B) quantitative analyses of macrophage polarization (M1-like versus M2-like). (C) Dural-invasive tumor and non-invasive tumor cases stratified into IgG-high (n=27) and IgG-low (n=26) groups based on the cohort median of relative IgG immunohistochemistry staining intensity, with (D) quantitative analyses of M1-like/M2-like macrophage proportions. (E and F) RAW264.7 macrophages were pre-polarized with IL-4 (20 ng/ml) or with lipopolysaccharide (100 ng/ml) plus IFN-γ (20 ng/ml) for 24 h, followed by IgG (10 µg/ml) exposure. Relative (E) IL-6 and (F) TNF-α mRNA expression in RAW264.7 macrophages pre-polarized to M0, M1 or M2 states. (G) Representative flow cytometric cell-cycle profiles of TtT/GF cells following the indicated treatments. (H) Stacked bar plot summarizing the percentages of cells from (G) in G 1 , S and G 2 /M phases. (I) Representative images from the scratch wound assay at 0, 24, 48 and 72 h under the indicated treatments. (J) Quantification of scratch wound closure. (K) Representative western blot images showing total STAT1, p-STAT1, total STAT3, p-STAT3 and β-actin levels in cells treated with IFN-γ (100 ng/ml), IL-6 (100 ng/ml), IFN-γ + IL-6 (50 ng/ml each), ruxolitinib (5 µM) or IFN-γ + IL-6 (50 ng/ml each) plus ruxolitinib (5 µM), as indicated. (L) Densitometric semi-quantification of p-STAT1/STAT1 (ratio). (B and D) Unpaired two-tailed Student's t-test. (E, F, J and L) One-way ANOVA with Tukey's post hoc multiple comparisons test. *P<0.05, ***P<0.001, ****P<0.0001. CTRL, control; IBA-1, ionised calcium binding adaptor molecule 1; ns, not significant; p-, phosphorylated; PE-A, phycoerythrin-area.

Article Snippet: Cells were maintained in serum-free DMEM and treated with IFN-γ (0–100 ng/ml; cat. no. RP01038; ABclonal Biotech Co., Ltd.), IL-6 (100 ng/ml; cat. no. RP00201; ABclonal Biotech Co., Ltd.) or a combination of IFN-γ and IL-6 (50 ng/ml each) at 37°C for 72 h, as indicated.

Techniques: Immunohistochemistry, Staining, Expressing, Scratch Wound Assay Assay, Western Blot, Two Tailed Test, Control, Binding Assay

Journal: Molecular Medicine Reports

Article Title: Elevated IgG levels induce an M2-to-M1 phenotypic shift in mucosal macrophages and restrict the growth of invasive sphenoid sinus pituitary adenomas

doi: 10.3892/mmr.2026.13878

Figure Lengend Snippet: Anti-CD47 mAb enhances ADCP to suppress tumor cell proliferation. (A) Immunofluorescence staining of CD47 (red) and DAPI (blue) in a representative subset of non-invasive tumor, dural-invasive tumor and sphenoid sinus-invasive tumor cases (n=10 per group). (B) Paired comparison of CD47 fluorescence intensity at the IF versus the TC. (C) RAW264.7 macrophages were pre-polarized with IL-4 (20 ng/ml) or with lipopolysaccharide (100 ng/ml) plus IFN-γ (20 ng/ml) for 24 h, followed by anti-CD47 mAb (10 µg/ml) treatment for 12 h. Quantitative PCR was used to analyze polarization/activation markers. (D) Schematic illustrating anti-CD47 mAb-mediated blockade of the CD47-SIRPα axis and enhancement of ADCP. (E) EdU assay of TtT/GF cell proliferation in a Transwell co-culture with anti-CD47 mAb-treated polarized macrophages. (F) Quantification of EdU-positive cells. (G) Representative microscopy images and flow cytometry plots showing macrophage phagocytosis of pHrodo™ Red-labeled GFP-TtT/GF cells. (H) Quantification of phagocytosis (%). (B) Paired two-tailed Student's t-test. (C, F and H) One-way ANOVA with Tukey's post hoc multiple comparisons test. **P<0.01, ***P<0.001, ****P<0.0001. ADCP, antibody-dependent cellular phagocytosis; Arg-1, arginase 1; EdU, 5-ethynyl-2′-deoxyuridine; FcγR, Fcγ receptor; GFP, green fluorescent protein; IF, invasive front; mAb, monoclonal antibody; NOS2, nitric oxide synthase 2; ns, not significant; PE, phycoerythrin; SIRPα, signal regulatory protein-α; SSCA, side scatter area; TC, tumor core.

Article Snippet: Cells were maintained in serum-free DMEM and treated with IFN-γ (0–100 ng/ml; cat. no. RP01038; ABclonal Biotech Co., Ltd.), IL-6 (100 ng/ml; cat. no. RP00201; ABclonal Biotech Co., Ltd.) or a combination of IFN-γ and IL-6 (50 ng/ml each) at 37°C for 72 h, as indicated.

Techniques: Immunofluorescence, Staining, Comparison, Fluorescence, Real-time Polymerase Chain Reaction, Activation Assay, EdU Assay, Co-Culture Assay, Microscopy, Flow Cytometry, Labeling, Two Tailed Test

Journal: Molecular Medicine Reports

Article Title: Elevated IgG levels induce an M2-to-M1 phenotypic shift in mucosal macrophages and restrict the growth of invasive sphenoid sinus pituitary adenomas

doi: 10.3892/mmr.2026.13878

Figure Lengend Snippet: Summary graphic illustration. This illustration summarizes the proposed model during pituitary adenoma invasion. The tumor invasive front abuts an intact sphenoid sinus mucosa, forming a distinct boundary. The mucosal compartment is enriched for ionised calcium binding adaptor molecule 1-positive macrophages with an M1-like predominance and IgG-high B cells. B cell-derived IgG promotes M2-to-M1 macrophage reprogramming, while coordinated IFN-γ and IL-6 production establishes a tumor-suppressive cytokine gradient that decreases from mucosa toward the tumor core, constraining proliferation and migration via JAK-STAT1 activation. Therapeutically, anti-CD47 monoclonal antibody blocks the CD47-SIRPα ‘don't-eat-me’ axis and augments antibody-dependent cellular phagocytosis, highlighting a strategy for immune checkpoint-targeted therapy that may complement surgical management. FcR, Fc receptor; JAK, Janus kinase; mAb, monoclonal antibody; p-, phosphorylated; SIRPα, signal regulatory protein-α.

Article Snippet: Cells were maintained in serum-free DMEM and treated with IFN-γ (0–100 ng/ml; cat. no. RP01038; ABclonal Biotech Co., Ltd.), IL-6 (100 ng/ml; cat. no. RP00201; ABclonal Biotech Co., Ltd.) or a combination of IFN-γ and IL-6 (50 ng/ml each) at 37°C for 72 h, as indicated.

Techniques: Binding Assay, Derivative Assay, Migration, Activation Assay

Journal: bioRxiv

Article Title: MYC Overexpression Confers Sensitivity to TACC3 Inhibition for Triple-Negative Breast Cancer

doi: 10.64898/2026.04.28.721171

Figure Lengend Snippet: a , Representative cell cycle profiles of RPE MYC and BT549 cells after treatment with BO-264 for 72 h. The percentage of cells in G1, S, and G2-M phases of the cell cycle, as determined by DNA content based on propidium iodide staining, is indicated. b , Flow cytometry gating strategy to identify GFP-positive cells (ISRE-active cells). Representative experimental control sample, untransduced BT549 cells. Side scatter and forward scatter were used to exclude debris. Forward scatter was used to distinguish single cells. Live cells were identified as negative for live/dead staining. GFP-positive live cells were identified by setting the fluorescence threshold based on untransduced BT549 controls. For reference, GFP signal intensity from live BT549 ISRE-GFP cells treated with IFNγ is shown to the left.

Article Snippet: Recombinant human IFNγ (11500-1) was obtained from PBL Assay Biosciences while recombinant mouse IFNγ (PMC4031) was purchased from Gibco.

Techniques: Staining, Flow Cytometry, Control, Fluorescence

Journal: bioRxiv

Article Title: MYC Overexpression Confers Sensitivity to TACC3 Inhibition for Triple-Negative Breast Cancer

doi: 10.64898/2026.04.28.721171

Figure Lengend Snippet: a , Diagram of IFN induction assay: BT549 cells contain an IFN reporter expressing destabilized GFP (dscGFP). ISRE: IFN-stimulated response elements. GFP median fluorescence intensity (MFI) was assessed 72 h after treatment by flow cytometry. Created with BioRender.com. b , Representative flow cytometry plot depicting GFP MFI of BT549 ISRE-GFP cells treated with vehicle, BO-264, or IFNγ for 72 h. Untransduced BT549 cells were used to establish GFP-positivity. c , Quantification of GFP positivity in BT549 ISRE-GFP cells after 72 h treatment. d , Flow cytometry analysis of MHC MFI in RPE (left) and 4T1 (right) cells treated with BO-264 for 72 h. Representative experiment with three samples per condition shown. Error bars are mean ± s.d., and p values calculated using a two-sided t -test. Trends repeated across three independent cell passages. ( e - f ), ELISA analysis of secreted CCL2 ( e ) and CXCL10 ( f ) levels in the indicated cell lines following treatment with vehicle or BO-264 for 72 h. g , ELISA analysis of intracellular cGAMP levels in the indicated cell lines upon treatment with vehicle or BO-264 for 72 h. h , Immunoblot analysis of cGAS-STING pathway activity in MTB/TOM MYC ON , 4T1, BT549, and RPE MYC cells treated with BO-264 for 72 h. β-actin is shown as a loading control. Representative image from n = 3 independent experiments. Data representative of n = 3 independent experiments. Error bars are mean ± s.e.m., and P values calculated using a two-sided t -test.

Article Snippet: Recombinant human IFNγ (11500-1) was obtained from PBL Assay Biosciences while recombinant mouse IFNγ (PMC4031) was purchased from Gibco.

Techniques: Expressing, Fluorescence, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Western Blot, Activity Assay, Control