Journal: Oncology Letters

Article Title: Methylglyoxal-derived glycated albumin enhances the stemness potential of invasive ductal carcinoma-derived breast cancer stem-like cell line KAIMRC1

doi: 10.3892/ol.2026.15541

Figure Lengend Snippet: GA effects on ERK1/2 phosphorylation in invasive ductal carcinoma-derived KAIMRC1 stem-like cells. Representative western blot analyses showed p-ERK1/2 in KAIMRC1 stem-like cells treated with 100 µg/ml GA for (A) 30 to 120 min and with (B) 50–100 µg/ml GA or unglycated BSA for 90 min of incubation. Bar graphs show the relative expression level of p-ERK1/2 normalized to total ERK1/2. GAPDH served as the loading control. Data are presented as the mean ± SD from three independent experiments. Statistical significance relative to the untreated control is indicated as *P < 0.05 and **P < 0.01. C, control; GA, glycated albumin; p-ERK1/2, phosphorylated-ERK1/2; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.

Article Snippet: Mouse primary monoclonal antibodies directed against extracellular signal-regulated kinase (ERK)1 (clone G-8; cat. no. sc-271269), phosphorylated-ERK1/2 (p-ERK1/2; clone E-4; Tyr204 of ERK1; cat. no. sc-7383), OCT3/4 (clone A-9; cat. no. sc-365509) and RAGE (clone E-1; cat. no. sc-74473) were obtained from Santa Cruz Biotechnology, Inc.

Techniques: Phospho-proteomics, Derivative Assay, Western Blot, Incubation, Expressing, Control

Journal: ImmunoTargets and Therapy

Article Title: Kasugamycin Inhibits Melanoma Lung Metastasis and CHI3L1-Driven M2-Like Tumor-Associated Macrophage Differentiation

doi: 10.2147/ITT.S563951

Figure Lengend Snippet: KSM inhibits CHI3L1-stimulated Erk and Akt activation and the antiapoptotic effect of CHI3L1 in macrophages. ( A ) AMJ-C11 mouse lung macrophages were stimulated with recombinant (r) CHI3L1 overnight, and the activation of Erk and Akt was detected by Western blot evaluations. pErk, phosphorylated Erk; T-Erk, total Erk; pAkt, phosphorylated Akt, T-Akt, total Akt. Right panel, densitometric quantitation on the blots of pErk and pAkt. ( B ) After exposure of AMJ-C11 cells with H 2 O 2 (1 mM, 24 hours) with and without rCHI3L1 and KSM treatment, cellular apoptosis (% of Annexin V+ cells) was measured by FACS evaluations. ( A and B ) are representatives of 3 independent experiments. Right panel, the values of Annexin 5 (+) cells (%) are the mean ± SEM. * P <0.05, ** P <0.01, *** P <0.001 (One-Way ANOVA, multiple comparisons).

Article Snippet: Protein lysates (25 μg) from lung tissues or cells were subjected to SDS-PAGE, transferred to membranes, and immunoblotted with primary antibodies against CD163 (#PA5-109327, Thermo Fisher Scientific), CD206 (E6T5J, #24595S, Cell Signaling Technology), phosphorylated AKT (p-Akt) (193H12, #4058S, Cell Signaling Technology), and total Akt (11E7, #4685S, Cell Signaling Technology), phosphorylated EGFR (Tyr1068) (p-EGFR) (#44-788G, Thermo Fisher Scientific), EGFR (D38B1, #4267S, Cell Signaling Technology), phosphorylated Erk (p-Erk) (#9101S, Cell Signaling Technology), total Erk (#9102S, Cell Signaling Technology), phosphorylated STAT3 (Tyr705) (p-STAT3) (D3A7, #9145, Cell Signaling Technology), total STAT3 (79D7, #4904, Cell Signaling Technology) and b-actin (C4, #sc-47778 HRP, Santa Cruz Biotechnology).

Techniques: Activation Assay, Recombinant, Western Blot, Quantitation Assay

Journal: Theranostics

Article Title: Panax notoginseng -Derived Carbon Dots Herbzymes Ameliorate Renal Ischemia-Reperfusion Injury via Anti-Inflammation, Antioxidation and Gut-Kidney Axis Regulation

doi: 10.7150/thno.126643

Figure Lengend Snippet: Multi-omics investigation into the mechanism by which PN-CDs alleviate renal injury. (A) Volcano plot of fecal metabolites comparing PN-CDs vs. RIRI groups; red/blue dots indicate significantly upregulated (167) or downregulated (62) metabolites (P < 0.05, VIP > 1, |log2FC| > 0.58). (B) Hierarchical clustering of differential metabolites, demonstrating distinct metabolic profiles across Sham, RIRI, and PN-CDs groups. (C) GSEA enrichment plot. (D-E) Quantification of uremic toxins p-cresyl sulfate (D) and indoxyl sulfate (E) in feces. (F) PCA of targeted tryptophan metabolites. (G) KEGG enrichment of targeted metabolites. (H-K) Quantification of key tryptophan-indole metabolites: indoxyl sulfate (H), β-indole-3-acetic acid (I), indolylpropionic acid (J), and indole-3-lactic acid (K). (L) Venn diagram of differential genes between RIRI vs. Sham and PN-CDs vs. RIRI. (M) Bubble plot of KEGG enrichment for overlapping genes, highlighting tryptophan metabolism and inflammatory pathways. (N-O) qPCR analysis of AHR (N) and CYP1A1 (O) mRNA levels in kidneys. (P) Western blot of AHR, p-ERK, ERK, and Actin in renal tissues. Data are mean ± SEM (ns, not significant, ** P < 0.01, *** P < 0.001).

Article Snippet: The membranes were treated with a 5% non-fat milk solution to block non-specific binding, targeting AHR (Abways, CY3431), ERK (Servicebio, GB11560), and phosphorylated ERK (P-ERK) (Servicebio, GB11004).

Techniques: Biomarker Discovery, Western Blot