stat6 pathway  (MedChemExpress)

Journal: Breast Cancer Research : BCR

Article Title: Mechanism of IL-4 mediated RPL19 promoting malignant progression in HER2 positive breast cancer

doi: 10.1186/s13058-026-02240-9

Figure Lengend Snippet: IL-4 regulates p-STAT6 nuclear translocation to promote breast cancer cell proliferation, migration, and invasion(A, B) Western blot analysis further demonstrated the activation of STAT6, as indicated by increased p-STAT6/STAT6 ratios in IL-4 overexpressing cells (*p < 0.05). (C, D) Western blot analysis further demonstrated the activation of STAT6, as indicated by increased p-STAT6/STAT6 ratios in RPL19 overexpressing cells (*p < 0.05, **p < 0.01). (E, F, G) Immunofluorescence showed altered localization of p-STAT6 (red) in IL-4 overexpressing cells, with scale bar set at 20μm.(H, I) Western blot analysis assessed p-STAT6/STAT6 expression levels in PLKO control and ShIL4#66, ShIL4#150 IL-4 knockdown cell models, with PLKO as the control of UACC812. Quantitative analysis revealed a significant reduction in p-STAT6/STAT6 levels in the IL-4 knockdown groups, * p < 0.05.(J, K) Western blot analysis assessed p-STAT6/STAT6 expression levels in PLKO control and ShRPL19#530, ShRPL19#328 RPL19 knockdown cell models, with PLKO as the control of UACC812. Quantitative analysis revealed a significant reduction in p-STAT6/STAT6 levels in the IL-4 knockdown groups, * p < 0.05.

Article Snippet: Our results demonstrated that IL-4 knockdown reduced p-STAT6 levels and attenuated RPL19-induced cell proliferation, migration, and invasion while also inhibiting M2 macrophage differentiation (Fig. ).Additionally, supplementation with the IL-4 receptor antagonist [ ] (αIL4R,5ug/ml,R&D Systems, Cat# MAB230-100) or STAT6 pathway inhibitor [ ] (AS1517499,5uM,Medchemexpress, HY-100614) in RPL19-overexpressing groups attenuated the RPL19-mediated promotion of breast cancer progression (Figs. , ).

Techniques: Translocation Assay, Migration, Western Blot, Activation Assay, Immunofluorescence, Expressing, Control, Knockdown

Journal: Breast Cancer Research : BCR

Article Title: Mechanism of IL-4 mediated RPL19 promoting malignant progression in HER2 positive breast cancer

doi: 10.1186/s13058-026-02240-9

Figure Lengend Snippet: Downregulation of IL-4 restores the effects of RPL19 overexpression in Her2-amplified breast cancer. (A, C) Western blot analysis was conducted to assess RPL19, IL-4, and p-STAT6/STAT6 expression in PLVX, RPL19, Sh IL4#66, and RPL19 + Sh IL4#66 cell models of UACC812. Statistical analysis of Western blot band intensities revealed no significant difference (NS > 0.05) in RPL19 expression, while significant changes in IL-4 and p-STAT6 expression were observed (*p < 0.05, **p < 0.01). (B, C) Western blot analysis was performed to evaluate IL-1β, TNF-α, IL-10, and ARG1 expression in macrophages co-cultured with PLVX, RPL19, Sh IL4#66, and RPL19 + Sh IL4#66 UACC812 cells. Statistical analysis of band intensities showed significant differences (NS > 0.05, *p < 0.05, **p < 0.01). (D) The MTT assay evaluated the rescue effect of IL-4 on RPL19 overexpression-induced UACC812 cell proliferation. Data were collected at specified time points, with statistical analysis indicating significant differences (NS > 0.05, *p < 0.05, **p < 0.01, ***p < 0.001). (E, F) Transwell migration and invasion assays were performed to assess the effect of IL-4 on cell migration and invasion in RPL19 overexpression models of UACC812. Statistical analysis revealed significant differences between groups (NS > 0.05, *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001). (G, H) Scratch assays demonstrated increased cell migration after RPL19 overexpression and IL-4 treatment of UACC812, with statistical analysis showing significant migration differences at different time points (NS＞0.05,*p < 0.05, **p < 0.01, ***p < 0.001).

Article Snippet: Our results demonstrated that IL-4 knockdown reduced p-STAT6 levels and attenuated RPL19-induced cell proliferation, migration, and invasion while also inhibiting M2 macrophage differentiation (Fig. ).Additionally, supplementation with the IL-4 receptor antagonist [ ] (αIL4R,5ug/ml,R&D Systems, Cat# MAB230-100) or STAT6 pathway inhibitor [ ] (AS1517499,5uM,Medchemexpress, HY-100614) in RPL19-overexpressing groups attenuated the RPL19-mediated promotion of breast cancer progression (Figs. , ).

Techniques: Over Expression, Amplification, Western Blot, Expressing, Cell Culture, MTT Assay, Migration

Journal: Scientific Reports

Article Title: Biocompatible ionized air alleviates rat osteoarthritis by modulating polarization from M1 to M2 macrophages

doi: 10.1038/s41598-024-83198-6

Figure Lengend Snippet: BIA regulates M1 macrophage polarization to M2 macrophages through the ROS-mediated STAT6 pathway. ( A ) Western blot analysis of p-STAT6, iNOS, and CD206 expression levels in macrophages from different groups after BIA intervention. ( B ) Quantitative analysis of p-STAT6, iNOS, and CD206 expression levels in macrophages. ( C ) Immunofluorescence assay to visualize representative fluorescence images of p-STAT6 and corresponding macrophage polarization markers iNOS and CD206 in M1 macrophages after different intervention conditions, with DAPI staining cell nuclei. Scale bar = 20 μm. N = 3. *Significant difference compared to the M1 group: *p < 0.05, **p < 0.01, ***p < 0.001. # Significant difference compared to the M1 BIA180 group: ## p < 0.01, ### p < 0.001. & Significant difference compared to the M1 BIA180 group: && p < 0.01, &&& p < 0.001. Abbreviations: BIA: Biocompatible ionized air; ROS: reactive oxygen species; STAT6: Signal transducer and activator of transcription 6; qRT-PCR: quantitative reverse transcription polymerase chain reaction; iNOS: inducible nitric oxide synthase; CD206: Cluster of Differentiation 206; DAPI: 4',6-diamidino-2-phenylindole; NAC: N-Acetyl-L-cysteine; LEF: Leflunomide.

Article Snippet: To investigate whether BIA regulates M1 macrophage polarization to M2 through the ROS-mediated STAT6 pathway, this study used Leflunomide (LEF; HY-B0083, MCE, USA) and N-acetyl-L-cysteine (NAC; HY-B0215, MCE, USA) to pretreat M1 macrophages.

Techniques: Western Blot, Expressing, Immunofluorescence, Fluorescence, Staining, Quantitative RT-PCR, Reverse Transcription, Polymerase Chain Reaction