Journal: Journal of Translational Autoimmunity

Article Title: Exploring the immunomodulatory effects of environmental contaminants on autoimmune patients: An in vitro approach

doi: 10.1016/j.jtauto.2025.100341

Figure Lengend Snippet: Modulation of intracellular signaling pathways in HD, RA, and SLE cells exposed to environmental contaminants. Heatmap showing the relative expression and phosphorylation levels of key signaling proteins involved in immune regulation, inflammation, and cell survival (STAT1, STAT3, p38, AKT, and NFκB) and their phosphorylated forms in HD, RA, and SLE after exposure to PM, silica, and TCDD. Data are represented as z-score normalized values. Asterisks indicate statistically significant differences compared with the unstimulated control within each group (p < 0.05). AKT: protein kinase B; HD: healthy donors; NFκB: nuclear factor kappa-light-chain-enhancer of activated B cells; P: phosphorylated form; p38: p38 mitogen-activated protein kinase; PM: particulate matter; RA: rheumatoid arthritis; SLE: systemic lupus erythematosus; STAT: signal transducer and activator of transcription; TCDD: 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Article Snippet: Membranes were blocked with 5 % non-fat milk in TBS-T and incubated overnight at 4 °C with primary antibodies against phospho-AKT (Thr308), phospho-NFκB p65 (Ser536), phospho-p38 MAPK (Thr180/Tyr182), phospho-STAT1 (Tyr701), and phospho-STAT3 (Tyr705) (Cell Signaling Technology, Danvers, MA, USA; Santa Cruz Biotechnology, Dallas, TX, USA).

Techniques: Protein-Protein interactions, Expressing, Phospho-proteomics, Control

Journal: Nature Communications

Article Title: Defective O-fucosylation of EDIL3 attenuates invasion and vascular remodeling of trophoblasts via LIFR signaling pathway in preeclampsia

doi: 10.1038/s41467-026-73139-4

Figure Lengend Snippet: A Representative images of placental villous explants cultured in rEDIL3 WT and rEDIL3 T88A groups. The bar represents 50 μm. B Western blot analysis of STAT3 and p-STAT3 expression, as well as the expression of EMT markers (E-cadherin, N-cadherin, Vimentin and Snail). C Transwell assay analysis of cell invasion and migration ability of HTR8/SVneo cells. D Bright field images of tube formation. E Western blot analysis of angiogenesis-related protein (CD31, CD34, VE-cadherin, VEGFR2 and VEGFA) expression. F CAM assay analysis of vascular formation. Data ( A , C , D , F ) are presented as mean ± SEM (3 independent biological replicates). Two-tailed unpaired Student’s t test. * p < 0.05, ** p < 0.01, *** p < 0.001. Source data are provided as a Source Data file.

Article Snippet: The membranes were incubated with blocking buffer containing 5% BSA (CAS:9048-46-8, Solarbio, China) and probed with the following primary antibodies at 4 °C overnight: poFUT1 (Cat No.14929-1-AP, Proteintech, 1:1000), EDIL3 (Cat No.12580-1-AP, Proteintech, 1:1000), His (Cat No.66005-1-Ig, Proteintech, 1:1000), CD31 (Cat No.11265-1-AP, Proteintech, 1:1000), CD34 (Cat No.BS45128, Bioworld, 1:1000), E-cadherin (Cat No.20874-1-AP, Proteintech, 1:1000), N-cadherin (Cat No.22018-1-AP, Proteintech, 1:1000), Vimentin (Cat No.10366-1-AP, Proteintech, 1:2000), Snail (Cat No.13099-1-AP, Proteintech, 1:1000), VE-cadherin (Cat No.sc-515467, SantaCruz, 1:500), VEGFR2(Cat No. 26415-1-AP, Proteintech, 1:1000), VEGFA (Cat No.sc-7269, SantaCruz, 1:500), PCNA (Cat No.AF0261, Beyotime, 1:1000), Cyclin D1 (Cat No.AF0126, Beyotime, 1:1000), Cyclin E1 (Cat No.AF6384, Beyotime, 1:1000), SQSTM1 (Cat No.18420-1-AP, Proteintech, 1:1000), LAMP2A (Cat No.66301-1-Ig, Proteintech, 1:1000), HSPA8 (Cat No.66442-1-Ig, Proteintech, 1:1000), ACTB (Cat No.20536-1-AP, Proteintech, 1:3000), p-STAT3 Tyr705 (Cat No.AP0705, Abclonal, 1:1000), STAT3 (Cat No.A19566, Abclonal, 1:1000), LIFR (Cat No.22779-1-AP, Proteintech, 1:1000) and GAPDH (Cat No.10494-1-AP, Proteintech, 1:1000).

Techniques: Cell Culture, Western Blot, Expressing, Transwell Assay, Migration, Chick Chorioallantoic Membrane Assay, Two Tailed Test

Journal: Oncology Reports

Article Title: Knockdown of CCT2 inhibits the malignant progression of hepatocellular carcinoma cells by impairing STAT3 activation

doi: 10.3892/or.2026.9086

Figure Lengend Snippet: Knockdown of CCT2 inhibits STAT3 signaling activation in hepatocellular carcinoma cells. The protein levels of STAT3, p-STAT3, MCL1, MMP2 and SOX2 in (A) Huh-7 and (B) HCCLM3 cells were measured by western blotting. The protein levels of (C) p-STAT3, (D) MCL1, (E) MMP2 and (F) SOX2 in subcutaneous tumor tissue were detected by immunohistochemical staining. *P<0.05, **P<0.01 vs. sh-NC. CCT2, chaperonin containing TCP1 subunit 2; sh, short hairpin; NC, negative control; p, phosphorylated; MCL1, myeloid cell leukemia sequence 1; SOX2, SRY-box transcription factor 2.

Article Snippet: The primary antibodies were as follows: CCT2 (cat. no. 24896-1-AP), β-actin (cat. no. 66009-1-Ig), MMP2 (cat. no. 10373-2-AP), myeloid cell leukemia sequence 1 (MCL1; cat. no. 16225-1-AP) and SRY-box transcription factor 2 (SOX2; cat. no. 11064-1-AP; all Proteintech Group, Inc.) and STAT3 (cat. no. 4904) and phosphorylated (p-)STAT3 (Tyr705; cat. no. 4113; both Cell Signaling Technology, Inc.) The membranes were washed three times in TBST (0.1% Tween-20) for 5 min each at room temperature.

Techniques: Knockdown, Activation Assay, Western Blot, Immunohistochemical staining, Staining, Negative Control, Sequencing

Journal: Oncology Reports

Article Title: Knockdown of CCT2 inhibits the malignant progression of hepatocellular carcinoma cells by impairing STAT3 activation

doi: 10.3892/or.2026.9086

Figure Lengend Snippet: IL-6 abolishes the effects of CCT2 knockdown on the proliferation and invasion of hepatocellular carcinoma cells. The protein levels of STAT3 and p-STAT3 in (A) Huh-7 and (B) HCCLM3 cells were measured by western blotting. The proliferation of (C) Huh-7 and (D) HCCLM3 cells following CCT2 knockdown and IL-6 treatment was detected using EdU incorporation assay. The invasion of (E) Huh-7 and (F) HCCLM3 cells was assessed using Transwell assay. *P<0.05, **P<0.01 vs. PBS. CCT2, chaperonin containing TCP1 subunit 2; sh, short hairpin; p-, phosphorylated.

Article Snippet: The primary antibodies were as follows: CCT2 (cat. no. 24896-1-AP), β-actin (cat. no. 66009-1-Ig), MMP2 (cat. no. 10373-2-AP), myeloid cell leukemia sequence 1 (MCL1; cat. no. 16225-1-AP) and SRY-box transcription factor 2 (SOX2; cat. no. 11064-1-AP; all Proteintech Group, Inc.) and STAT3 (cat. no. 4904) and phosphorylated (p-)STAT3 (Tyr705; cat. no. 4113; both Cell Signaling Technology, Inc.) The membranes were washed three times in TBST (0.1% Tween-20) for 5 min each at room temperature.

Techniques: Knockdown, Western Blot, Transwell Assay

Journal: Advances in Radiation Oncology

Article Title: Kupffer Cell-Derived Interleukin-6 Aggravates Radiation-Induced Liver Disease by Activating Hepatocyte STAT3 to Promote Ccng1 Transcription

doi: 10.1016/j.adro.2026.102003

Figure Lengend Snippet: Role of the JAK–STAT signaling pathway in hepatocytes during radiation-induced liver disease (RILD). (A) Volcano plot of differential gene expression analysis in hepatocytes after irradiation (IR). Red and blue indicate upregulated and downregulated genes, respectively. The dotted horizontal line represents a P value of 0.05. The dotted vertical lines represent a log2-fold change of 1.5 or −1.5. (Right) Bubble chart depicting the top 5 Kyoto Encyclopedia of Genes and Genomes (KEGG)-enriched pathways corresponding to down/upregulated genes in hepatocytes after IR (screening the pathways and sorting them from large to small according to the −log 10 P value). (B) Western blot analysis showing p-STAT3 and GAPDH expression in primary hepatocytes isolated from Ctrl rats or IR rats treated with placebo, anti-interleukin (IL)-6, or sgp130Fc (n = 5). (C) Western blot analysis showing p-STAT3 and GAPDH expression in primary hepatocytes isolated from IR rats treated with placebo, ruxolitinib (RUX), or tofacitinib (TOF) (n = 5). (D) Quantitative enzyme-linked immunosorbent assay (ELISA) analysis of serum liver enzymes in IR rats treated with placebo, RUX, or TOF (n = 5). (E) Hematoxylin–eosin (H&E) staining of the livers of IR rats treated with placebo, RUX, or TOF (n = 5). (F) Costaining of HNF4α (red) and TUNEL (green) in the livers of IR rats treated with placebo, RUX, or TOF (n = 5). (G) Overlap of p-STAT3-binding genes identified using ChIP-Seq with upregulated genes ( P < .05 and log2-fold change > 2) in hepatocytes identified using scRNA-seq. (H) Violin plots showing the expression levels of overlapping genes identified using scRNA-seq. (I) qRT‒PCR analysis of overlapping genes in isolated primary hepatocytes from IR rats treated with placebo, RUX, or TOF (n = 5). Analysis of variance (ANOVA); *, P < .05; ⁎⁎ , P < .01; ⁎⁎⁎ , P < .001; ns, nonsignificant.

Article Snippet: After sonication, immunoprecipitation was performed with a p-STAT3 (Tyr705) antibody (Cell Signaling Technology, #9145).

Techniques: Gene Expression, Irradiation, Western Blot, Expressing, Isolation, Enzyme-linked Immunosorbent Assay, Staining, TUNEL Assay, Binding Assay, ChIP-sequencing

Journal: Advances in Radiation Oncology

Article Title: Kupffer Cell-Derived Interleukin-6 Aggravates Radiation-Induced Liver Disease by Activating Hepatocyte STAT3 to Promote Ccng1 Transcription

doi: 10.1016/j.adro.2026.102003

Figure Lengend Snippet: Schematic of the Kuppfer cell (KC)-hepatocyte crosstalk mechanism in RILD. Irradiation (IR) stimulates KCs to secrete IL-6, which binds to the IL-6R/gp130 complex on hepatocytes to activate JAK; phosphorylated JAK induces STAT3 phosphorylation, and nuclear-translocated p-STAT3 binds to the Ccng1 promoter to promote its transcription; CCNG1 then regulates MDM2 to mediate ubiquitination-dependent TP53 proteolysis, ultimately enhancing hepatocyte apoptosis and driving radiation-induced liver disease (RILD) progression.

Article Snippet: After sonication, immunoprecipitation was performed with a p-STAT3 (Tyr705) antibody (Cell Signaling Technology, #9145).

Techniques: Irradiation, Phospho-proteomics, Ubiquitin Proteomics