Journal: Advanced Science

Article Title: Cryoablation Activates the cGAS–STING‐CXCL10 Axis in Macrophages to Enhance Anti‐Tumor Immunity in NSCLC

doi: 10.1002/advs.202521931

Figure Lengend Snippet: Cryoablation activates the cGAS–STING signaling in macrophages. (A) Bubble plots of enriched pathways in PBMC macrophages from patients treated with cryoablation versus thermal ablation. (B) Pathway enrichment bubble plots comparing tumor macrophages from CA + anti‐PD‐1 versus MWA + anti‐PD‐1 treated mice. (C) Pathway enrichment analysis for CA + anti‐PD‐1 compared to anti‐PD‐1 alone. (D) Immunofluorescence staining (left) and quantitative analysis of fluorescence colocalization (right) of distal tumors from the anti‐PD‐1 and CA + anti‐PD‐1 groups after ablation. (E) Serum dsDNA quantification in mice from Ctrl, CA+PBS, and MWA+PBS groups at 7 days post‐ablation. (F) dsDNA quantification in cell supernatants from KP and PC‐9 cells after cryoablation and microwave ablation, respectively. Liquid nitrogen was used to simulate cryoablation, and a water bath was used to simulate microwave ablation. (G) In vitro stimulation schema: Resuspend PC‐9 cells in PBS, lyse in liquid nitrogen, and centrifuge the supernatant, which was complexed with Lipofectamine 2000 and transfected into THP‐1 cells for culture of 48 h with or without Sting‐IN‐2. H, I) ELISA of secreted CXCL10 in culture supernatants (H) and qPCR for CXCL10 mRNA (I). (J) Flow‐cytometry plots (left) and quantification (right) of CD86 + THP‐1 cells. (K) Western blot of cGAS–STING pathway proteins 48 h post stimulation. (L) Experimental design of STING agonist treatment based on CA + anti‐PD‐1. M–O) Tumor growth curves (M), representative tumors (N), and excised tumor weights (O) under combined treatment; n=5 per group. T, THP‐1 cells; TP, THP‐1 cells incubated with supernatant of PC‐9 tumor cells lysed in liquid nitrogen; TPS, THP‐1 cells incubated with supernatant of PC‐9 tumor cells lysed in liquid nitrogen and STING‐IN‐2. The p‐ values of F, H J, M, and O were calculated using one‐way ANOVA. Data were shown as mean ± SEM. ns, not significant. * p < 0.05, **** p < 0.0001. SEM, standard error of the mean.

Article Snippet: To block the cGAS–STING pathway, 10 n m STING‐IN‐2 (MCE, HY‐138682) was added immediately after transfection.

Techniques: Immunofluorescence, Staining, Fluorescence, In Vitro, Transfection, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Western Blot, Incubation

Journal: Advanced Science

Article Title: Cryoablation Activates the cGAS–STING‐CXCL10 Axis in Macrophages to Enhance Anti‐Tumor Immunity in NSCLC

doi: 10.1002/advs.202521931

Figure Lengend Snippet: Mechanism schematic of cryoablation activating the cGAS–STING signaling pathway in macrophages. In patients with oligo‐residual disease undergoing cryoablation and thermal ablation after immunotherapy, in mouse models comparing CA + anti‐PD‐1 with MWA + anti‐PD‐1 or with anti‐PD‐1 alone, scRNA‐seq consistently showed that cryoablation enhances macrophage activation and anti‐tumor efficacy. Mechanistically, cryoablation‐induced tumor cell lysis releases dsDNA that is engulfed by macrophages, triggering cGAS–STING signaling and secretion of CXCL10. This chemokine recruits CXCR3 + CD8 + and CXCR3 + CD4 + T cells from draining lymph nodes into the tumor microenvironment to mount anti‐tumor immunity. CA, cryoablation; MWA, microwave ablation.

Article Snippet: To block the cGAS–STING pathway, 10 n m STING‐IN‐2 (MCE, HY‐138682) was added immediately after transfection.

Techniques: Activation Assay, Lysis

Journal: Frontiers in Immunology

Article Title: UNC93B1 promotes pancreatic cancer progression through modulation of cGAS–STING signaling

doi: 10.3389/fimmu.2026.1718849

Figure Lengend Snippet: Intercellular communication network analysis in tumor microenvironment. (A) Comprehensive cell-cell interaction networks comparing tumor versus normal microenvironments and UNC93B1-dependent signaling contexts. (B) Differential intensity analysis of outgoing and incoming signaling patterns across UNC93B1-dependent cell clusters. (C) Heatmap visualization of UNC93B1-dependent outgoing and incoming signaling patterns. (D) Comparative visualization of pathway activity differences between tumor and normal microenvironments. (E) Differential pathway activity analysis in UNC93B1-dependent subgroups. (F) cGAS-STING signaling interaction networks in tumor versus normal microenvironments. (G) UNC93B1-dependent cGAS-STING signaling interaction networks.

Article Snippet: To establish a causal link between UNC93B1 knockdown-induced phenotypes and cGAS-STING pathway activation, rescue experiments were performed using the selective STING inhibitor H-151 (MedChemExpress).

Techniques: Activity Assay

Journal: Frontiers in Immunology

Article Title: UNC93B1 promotes pancreatic cancer progression through modulation of cGAS–STING signaling

doi: 10.3389/fimmu.2026.1718849

Figure Lengend Snippet: Molecular profiling of cGAS-STING pathway and associated phenotypes following UNC93B1 manipulation. (A–F) Quantitative PCR analysis of key genes in the cGAS-STING pathway (STING, IFN-β, cGAS), cellular senescence marker (p16INK4A), and epithelial-mesenchymal transition regulators (VIM, CDH1) following UNC93B1 knockdown. (*P < 0.05, **P < 0.01, ***P < 0.001).

Article Snippet: To establish a causal link between UNC93B1 knockdown-induced phenotypes and cGAS-STING pathway activation, rescue experiments were performed using the selective STING inhibitor H-151 (MedChemExpress).

Techniques: Real-time Polymerase Chain Reaction, Marker, Knockdown

Journal: Journal of Innate Immunity

Article Title: Pharmacological Stimulator of Interferon Genes Activation Enhances Autophagy-Mediated Clearance of Mycobacterium tuberculosis in Human Macrophages

doi: 10.1159/000550530

Figure Lengend Snippet: Activation of the cGAS-STING pathway enhances Mtb phagocytosis and intracellular clearance. a Effects of different concentrations of ADU-S100 and HCQ on THP-1 cell viability, assessed by CCK-8 assay after 24 h of treatment. b Quantification of Mtb CFU counts at 2 h post-infection to assess bacterial uptake. Both HCQ and si-cGAS significantly reduced uptake compared to control (* p < 0.05; *** p < 0.001). c Time-course analysis of intracellular Mtb survival at 24 and 48 h post-infection. ADU-S100 treatment significantly reduced intracellular bacterial load over time, while HCQ and si-cGAS treatments favored bacterial survival. Data are presented as mean ± SD from three independent experiments ( n = 3). Statistical analysis was performed using one-way ANOVA with Tukey’s post hoc test. * p < 0.05; ** p < 0.01; *** p < 0.001.

Article Snippet: The cGAS-STING signaling pathway agonists ADU-S100 (HY-12885A) and autophagy inhibitor hydroxychloroquine (HCQ) (HY-B1370) were obtained from MCE (China).

Techniques: Activation Assay, CCK-8 Assay, Infection, Control

Journal: Journal of Innate Immunity

Article Title: Pharmacological Stimulator of Interferon Genes Activation Enhances Autophagy-Mediated Clearance of Mycobacterium tuberculosis in Human Macrophages

doi: 10.1159/000550530

Figure Lengend Snippet: Activation of the STING signaling pathway enhances autophagy in Mtb-infected macrophages. a Western blot analysis of LC3-I to LC3-II conversion in THP-1 cells treated with 4 µ m ADU-S100, 20 µ m HCQ, or si-cGAS for 24 h during Mtb infection. β-actin was used as a loading control. b Densitometric analysis of the LC3-II/β-actin ratio from three independent experiments ( n = 3). ADU-S100 significantly increased LC3-II levels (* p < 0.05). c Representative confocal microscopy images showing the colocalization of Mtb-EGFP (green) and LysoTracker Red-stained lysosomes (red). Nuclei were stained with DAPI (blue). Scale bar = 10 µm. Quantitative analysis is provided in online suppl. Fig. 2. Data in ( b ) are presented as mean ± SD. Statistical analysis was performed using one-way ANOVA with Tukey’s post hoc test. * p < 0.05; *** p < 0.001.

Article Snippet: The cGAS-STING signaling pathway agonists ADU-S100 (HY-12885A) and autophagy inhibitor hydroxychloroquine (HCQ) (HY-B1370) were obtained from MCE (China).

Techniques: Activation Assay, Infection, Western Blot, Control, Confocal Microscopy, Staining