Journal: Advanced Science

Article Title: Aged ZnO Nanoparticles Promote Breast Cancer Lung Metastasis by Remodeling the Pulmonary Microenvironment Through the CXCL10/Wnt/β‐Catenin Axis

doi: 10.1002/advs.78249

Figure Lengend Snippet: CXCL10 is upregulated in both macrophages and fibroblasts responding to aged ZnO NPs exposure. (A) Heatmaps exhibited multiplex cytokine profiling of serum and BALF from IT (PBS/fresh NPs/aged NPs intratracheal instillation) and IT + IV (IT exposure followed by intravenous injection of 4T1 cells) models ( n = 3). (B–E) Concentrations of significantly dyregulated cytokines in serum and BALF from mice exposed to ZnO NPs (fresh or aged), with or without subsequent 4T1 cell injection ( n = 3). (F) Venn plot showed the overlapping cytokines in serum and BALF between IT and IT + IV models. (G) ELISA detection of CXCL10 concentrations in serum and BALF of IT and IT + IV groups ( n = 3). (H) qPCR analysis of CXCL10 mRNA in lung tissue, primary fibroblasts, and alveolar macrophages post‐IT, normalized to GAPDH ( n = 3). (I, J) UMAP visualization (I) and dot plot (J) displaying CXCL10 expression across annotated cell types. (K, L) UMAP visualization (K) and dot plot (L) displaying CXCL10 expression across myeloid cell types. (M) Representative images of invasion and migration assays of 4T1 cells stimulated with 50 or 100 ng/mL murine recombinant CXCL10 (rCXCL10) for 72 h ( n = 3). (N) Quantification of invasion and migration assays ( n = 3). All data were represented as the mean ± SD. P values were calculated by one‐way ANOVA followed by Tukey's test. * p < 0.05, ** p < 0.01 vs control group; # p < 0.05, ## p < 0.01 vs fresh NPs group.

Article Snippet: CXCL10 (IP‐10) levels were measured using a mouse ELISA kit (Elabscience, E‐EL‐M0021) following the manufacturer's instructions.

Techniques: Multiplex Assay, Profiling, Injection, Enzyme-linked Immunosorbent Assay, Analysis, Tissue, Expressing, Migration, Recombinant, Control

Journal: Cells

Article Title: Liraglutide Potently Protects Against Streptozotocin-Induced Islet Injury Associated with Inhibition of HMGB1 Release

doi: 10.3390/cells15131203

Figure Lengend Snippet: Liraglutide reduces STZ-induced TLR4 expression in mouse pancreas and inflammatory factor levels in vivo. ( A ) Immunohistochemistry detection of the expression of HMGB1 receptor AGER, TLR4, and TLR2 in pancreatic tissues. ( B ) ELISA detection of IL-1β expression, by group ( n = 3). ( C ) ELISA detection of IFN-γ expression, by group ( n = 3). ( D ) ELISA detection of CXCL10 expression, by group ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: ELISA kits were used to detect HMGB1 ( F10620 , Xitang, Changsha, China), insulin (CSB-E05071m, CUSABIO, Wuhan, China), IL-1β (RK00006, ABclonal, Wuhan, China), IFN-γ (RK00019, ABclonal, China), and CXCL10 (RK00056, ABclonal, Wuhan, China).

Techniques: Expressing, In Vivo, Immunohistochemistry, Enzyme-linked Immunosorbent Assay

Journal: Cancer Research

Article Title: METTL3 Methylation Induces Decay of Endogenous Retroelement Transcripts to Promote Tumor Immune Evasion

doi: 10.1158/0008-5472.CAN-25-2893

Figure Lengend Snippet: METTL3 K513 dimethylation suppresses type I IFN response and antitumor immune responses. A, GSEA of differentially expressed genes between METTL3 WT and METTL3 K513R cells based on prior sequencing data. NES, normalized enrichment score. B, IF staining using the J2 antibody to detect dsRNA levels in METTL3 WT and METTL3 K513R LoVo cells. C, IB analysis of DNA and RNA sensors, along with signaling proteins involved in the type I IFN pathway. D, Heatmap showing differential expression of ISGs in METTL3 WT and METTL3 K513R LoVo cells. E, ELISA analysis of IFNβ and CXCL10 secretion in METTL3 KO, METTL3 WT, and METTL3 K513R CT26 cells. F, Flow cytometry analysis of MHC-I expression in METTL3 KO, METTL3 WT, and METTL3 K513R CT26 cells. MFI, mean fluorescence intensity. G, Subcutaneous implantation of METTL3 KO, METTL3 WT, and METTL3 K513R CT26 cells into BALB/c mice ( n = 5). Representative bioluminescent images and tumor bioluminescence intensity. H, Flow cytometric analysis of the proportions of CD8 + T cells, NK cells, and M1 and M2 macrophages in tumor-infiltrating lymphocytes (TIL) from subcutaneous tumors ( G ). I, Subcutaneous implantation of METTL3 WT and METTL3 K513R CT26 cells into NOD/SCID/IL2Rγ null (NCG) mice ( n = 5). Tumor volumes were monitored. Data information: All immunoblots were performed independently three times with similar results. Data are presented as mean ± SD. In E , F , and G , statistical analysis was performed using one-way ANOVA with the Tukey test. In H , statistical analysis was performed using two-way ANOVA with Tukey test. In I , statistical analysis was performed using the Student two-tailed t test. ns, not significant; *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Article Snippet: IFNβ and CXCL10 levels in conditioned media were quantified using the Mouse IFNβ Enzyme-Linked Immunosorbent Assay (ELISA) Kit (RK00420, ABclonal) and the Mouse CXCL10 ELISA Kit (RK00056, ABclonal) according to the manufacturer’s protocol.

Techniques: Sequencing, Staining, Quantitative Proteomics, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Expressing, Fluorescence, Western Blot, Two Tailed Test

Journal: Cancer Research

Article Title: METTL3 Methylation Induces Decay of Endogenous Retroelement Transcripts to Promote Tumor Immune Evasion

doi: 10.1158/0008-5472.CAN-25-2893

Figure Lengend Snippet: SETD1A mediates colorectal cancer immune evasion via METTL3 K513 dimethylation. A, IF staining using J2 antibody to detect dsRNA levels in control and SETD1A knockdown LoVo cells. B, IB analysis of DNA and RNA sensors, along with signaling proteins involved in the type I IFN pathway. C, qRT-PCR analysis of ISGs in control and SETD1A knockdown LoVo cells. D, ELISA analysis of IFNβ and CXCL10 secretion in control and SETD1A knockdown CT26 cells. E, Flow cytometry analysis of MHC-I expression in control and SETD1A knockdown CT26 cells. F, Subcutaneous implantation of control and SETD1A knockdown CT26 cells into BALB/c mice ( n = 5). Tumor volumes were monitored. G, Flow cytometric analysis of the proportions of CD8 + T cells, NK cells, and M1 and M2 macrophages in tumor-infiltrating lymphocytes (TIL) from subcutaneous tumors ( F ). H, IB analysis of DNA and RNA sensors, along with signaling proteins involved in the type I IFN pathway. I, qRT-PCR analysis of ISGs in METTL3 WT and METTL3 K513R LoVo cells with or without SETD1A knockdown. J, Subcutaneous implantation of METTL3 WT and METTL3 K513R CT26 cells with or without SETD1A knockdown into BALB/c mice ( n = 5). Tumor volumes were monitored. K, Flow cytometric analysis of the proportions of CD8 + T cells, NK cells, and M1 and M2 macrophages in TILs from subcutaneous tumors ( J ). Data information: All immunoblots were performed independently three times with similar results. Data are presented as mean ± SD. In C–E , G , I , and K , statistical analysis was performed using one-way ANOVA with the Tukey test. In F and J , statistical analysis was performed using two-way ANOVA with Tukey test. ns, not significant; *, P < 0.05; **, P < 0.01; ***, P < 0.001. NC, negative control.

Article Snippet: IFNβ and CXCL10 levels in conditioned media were quantified using the Mouse IFNβ Enzyme-Linked Immunosorbent Assay (ELISA) Kit (RK00420, ABclonal) and the Mouse CXCL10 ELISA Kit (RK00056, ABclonal) according to the manufacturer’s protocol.

Techniques: Staining, Control, Knockdown, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Expressing, Western Blot, Negative Control