lrrk2 inhibitor ikk16  (MedChemExpress)

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: SNRPC promotes chemoresistance in Wilms tumor via the NF-κB-CXCL17 axis regulating M2-Type TAMs infiltration and targeted nanotherapy research

doi: 10.1186/s13046-026-03680-z

Figure Lengend Snippet: Tumor SNRPC Gene Positively Regulates CXCL17 via NF-κB Signaling Pathway to Drive M2-type TAM Infiltration in WT and Induce Chemoresistance in vitro. A RNA sequencing analysis of differentially expressed genes in WiT49 cells with stable SNRPC silencing vs. control cells. B Venn diagram showing the overlap among downregulated genes, secreted proteins, and chemokines. C ELISA analysis of CXCL17 concentration secreted by WT cells with SNRPC silencing (sh_SNRPC) or overexpression (oe_SNRPC). D , E Transwell migration assays of macrophages and Flow cytometry analysis of CD68⁺CD206⁺ macrophage proportionin the co-culture system, with SNRPC-silenced WiT49/WT-CLS1 cells and different doses of recombinant human CXCL17 in the lower chamber. F KEGG pathway enrichment analysis of differentially expressed genes. G GSEA analysis of the NF-κB signaling pathway. H Schematic Diagram: SNRPC Gene in Tumor Cells Regulates CXCL17 Secretion via the NF-κB Signaling Pathway to Affect TAMs Recruitment and Polarization. I SNRPC regulates CXCL17 via NF‑κB pathway. (6I‑a) SNRPC expression. GAPDH as control; overexpression verified in Figs. A, C. (6I‑b) Secreted CXCL17 in concentrated supernatants.(6I‑c) NF‑κB pathway proteins. GAPDH as control. J Immunofluorescence analyses of p-P65 nuclear translocation after treatment with TNF-ɑ (NF-κB agonist) or IKK-16 (IκB inhibitor) in SNRPC-silenced WiT49/WT-CLS1 cells

Article Snippet: Reagents and antibodies utilized in this study included: Phorbol 12-myristate 13-acetate (PMA; HY-18739, MCE, USA); Recombinant Human IL-4 (#200-04, PeproTech, USA); Recombinant Human IL-13 (#200 − 13, PeproTech, USA); D-Luciferin potassium salt (HY-12591B, MCE, USA); Tumor necrosis factor-α (TNF-α; HY-P1875, MCE, USA); IKK 16 (HY-13687, MCE, USA); CXCL17 (HY- P71878 , MCE, USA); Rhodamine-WGA (MP6326-1MG, MKbio, China); Anti-CD163 (6646-1-AP, Proteintech, China); Anti-SNRPC (ab192028, Abcam, UK); Anti-PSMA4 ( R25489 , Zen BioScience, China); Anti-PPIH (11651-1-AP, Proteintech, China); Anti-PFDN4 (16045-1-AP, Proteintech, China); Anti-CKS1B (10610-1-AP, Proteintech, China); Anti-GAPDH (81640-5-RR, Proteintech, China); Anti-phospho-IKKα/β (#2697, CST, USA); Anti-IκBα ( R23322 , Zen BioScience, China); Anti-phospho-IκBα (#2859, CST, USA); Anti-NF-κB p65 (310099, Zen BioScience, China); Anti-phospho-NF-κB p65 (#3033, CST, USA); Anti-CXCL17 (18108-1-AP, Proteintech, China); Anti-CD9 (20597-1-AP, Proteintech, China); Anti-TSG101 (28283-1-AP, Proteintech, China); Anti-CD63 (25682-1-AP, Proteintech, China); Anti-calnexin (10427-2-AP, Proteintech, China).

Techniques: In Vitro, RNA Sequencing, Control, Enzyme-linked Immunosorbent Assay, Concentration Assay, Over Expression, Migration, Flow Cytometry, Co-Culture Assay, Recombinant, Expressing, Immunofluorescence, Translocation Assay

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: SNRPC promotes chemoresistance in Wilms tumor via the NF-κB-CXCL17 axis regulating M2-Type TAMs infiltration and targeted nanotherapy research

doi: 10.1186/s13046-026-03680-z

Figure Lengend Snippet: Tumor SNRPC Gene Positively Regulates CXCL17 via NF-κB Signaling Pathway to Drive M2-type TAM Infiltration in WT and Induce Chemoresistance in vivo. A Schematic diagram of the in vivo experiment. B - E WB analysis of protein expression changes in the SNRPC-NF-κB-CXCL17 regulatory axis in tumor tissues. F - G Representative images and relative volume statistics of orthotopic tumors formed by SNRPC-silenced WiT49 cells after different interventions. H Kaplan-Meier survival curves of mice in different treatment groups. I Immunofluorescence analysis of CD68⁺CD206⁺/CD68⁺CD86⁺ macrophage proportions in tumor tissues from different treatment groups. J Predicted binding sites of p-P65 to the CXCL17 promoter using the JASPER database. K Dual-luciferase reporter gene assay was applied to evaluate p-P65-mediated modulation of wild-type CXCL17 promoter transcriptional activity. L Chromatin immunoprecipitation quantitative polymerase chain reaction (ChIP-qPCR) assay was employed to determine the binding affinity of p-P65 to the CXCL17 promoter region

Article Snippet: Reagents and antibodies utilized in this study included: Phorbol 12-myristate 13-acetate (PMA; HY-18739, MCE, USA); Recombinant Human IL-4 (#200-04, PeproTech, USA); Recombinant Human IL-13 (#200 − 13, PeproTech, USA); D-Luciferin potassium salt (HY-12591B, MCE, USA); Tumor necrosis factor-α (TNF-α; HY-P1875, MCE, USA); IKK 16 (HY-13687, MCE, USA); CXCL17 (HY- P71878 , MCE, USA); Rhodamine-WGA (MP6326-1MG, MKbio, China); Anti-CD163 (6646-1-AP, Proteintech, China); Anti-SNRPC (ab192028, Abcam, UK); Anti-PSMA4 ( R25489 , Zen BioScience, China); Anti-PPIH (11651-1-AP, Proteintech, China); Anti-PFDN4 (16045-1-AP, Proteintech, China); Anti-CKS1B (10610-1-AP, Proteintech, China); Anti-GAPDH (81640-5-RR, Proteintech, China); Anti-phospho-IKKα/β (#2697, CST, USA); Anti-IκBα ( R23322 , Zen BioScience, China); Anti-phospho-IκBα (#2859, CST, USA); Anti-NF-κB p65 (310099, Zen BioScience, China); Anti-phospho-NF-κB p65 (#3033, CST, USA); Anti-CXCL17 (18108-1-AP, Proteintech, China); Anti-CD9 (20597-1-AP, Proteintech, China); Anti-TSG101 (28283-1-AP, Proteintech, China); Anti-CD63 (25682-1-AP, Proteintech, China); Anti-calnexin (10427-2-AP, Proteintech, China).

Techniques: In Vivo, Expressing, Immunofluorescence, Binding Assay, Luciferase, Reporter Gene Assay, Activity Assay, Chromatin Immunoprecipitation, Real-time Polymerase Chain Reaction, ChIP-qPCR

Journal: bioRxiv

Article Title: An APP-centered molecular gateway integrates innate immunity and retinoic acid signaling to drive irreversible metamorphic commitment

doi: 10.64898/2026.01.22.700939

Figure Lengend Snippet: (A) Settlement rate of inhibitor-treated larvae. The box plots with superimposed jitter plots display the larval settlement rate under various inhibitor treatments. The biofilm stimulus condition is used as the positive control. The concentration of each inhibitor is indicated on the horizontal axis. The data represent the settlement rate of larvae remaining attached out of 10 larvae across six independent biological replicates (total n = 60). Statistical significance among treatment groups was assessed using one-way ANOVA followed by Tukey’s HSD post hoc test, with grouping letters indicating significant differences ( p < 0.05); treatments sharing a letter are not significantly different. (B) Quantitative assessment of the functional hierarchy. The box plots with superimposed jitter plots show the Metamorphic Progression Scores (MPS) for larvae treated with various pharmacological inhibitors with or without all-trans retinoic acid (RA). The MPS was calculated based on the metamorphic stage reached by the larvae in the identical assays used for the settlement rate analysis in (A). The concentration of each inhibitor is indicated on the horizontal axis. The MPS represents the average metamorphic stage reached (0 = brachiolaria; 1 = early; 2 = middle; 3 = late; 4 = pre-juvenile; 5 = juvenile). Statistical significance among the treatment groups was assessed using one-way ANOVA followed by Tukey’s HSD post hoc test ( *p < 0.05; n.s., not significant). A significant RA-dependent rescue condition (a statistically significant increase in MPS compared with the inhibitor-alone condition) is highlighted in grey, establishing the functional hierarchy of the pathways relative to the RA commitment signal. (C) Representative image illustrating pathway functional hierarchy. Images show representative larval morphology under the control, inhibitor-only, and inhibitor + RA conditions. These images specifically represent the high-concentration inhibitor treatments (MyD88 inhibitor: 50 µM; MAPK inhibitors: 10 µM; IKKβ and HSP90AA1 inhibitors: 1 µM). MyD88 inhibition completely blocks the behavioral decision of settlement. JNK and p38 inhibition caused a distinct early-stage arrest (low MPS), and the effects of their inhibition were significantly rescued by RA co-treatment. In contrast, ERK inhibition arrested metamorphosis at the middle stage, and this block was not rescued by exogenous RA. Similarly, IKKβ and HSP90AA1 inhibition arrested metamorphosis at later stages, and this block was not rescued by exogenous RA, functionally placing all three pathways (ERK, IKKβ, and HSP90AA1) downstream of the RA commitment signal. Scale bar: 200 µm. Inhibitors used: T6167923 (MyD88 inhibitor), IKK-16 (IKKβ inhibitor), U0126 (ERK inhibitor), SP600125 (JNK inhibitor), SB202190 (p38 inhibitor), and Luminespib (HSP90AA1 inhibitor).

Article Snippet: The inhibitors were dissolved in DMSO and applied at the indicated concentrations: the MyD88 inhibitor T6167923 (5 or 50 μM; MedChemExpress), the IKKβ inhibitor IKK-16 (0.1 or 1 μM; MedChemExpress), and MAPK inhibitors SP600125 (JNK), SB202190 (p38), and U0126 (ERK) (1 or 10 μM; MedChemExpress or FUJIFILM Wako Pure Chemical Corporation), and the HSP90AA1 inhibitors luminespib (0.1 or 1 μM; Chemscene).

Techniques: Positive Control, Concentration Assay, Functional Assay, Control, Inhibition, Blocking Assay

Journal: Cancers

Article Title: L1CAM Promotes Human Endometrial Cancer Via NF-κB Activation

doi: 10.3390/cancers18020198

Figure Lengend Snippet: The combination of NF-κB inhibition and cisplatin more effectively inhibits proliferation of human endometrial cancer cells. ( A ) Western blotting of L1CAM, pNF-κB (p65), NF-κB (p65), and GAPDH in HHUA with drug addition. GAPDH was used as a loading control. ( B ) MTT assay of HHUA and SPAC-1-L cells were performed 48 h after treatment with cisplatin(CDDP), an IKK inhibitor, or their combination. ( C ) MTT assay of SPAC-1-L with control or L1CAM knockdown evaluated 48 h after cisplatin (CDDP) addition. ( D ) MTT assay of Ishikawa cells with control or L1CAM overexpression, evaluated 48 h after the addition of cisplatin (CDDP) or an IKK inhibitor. ( p < 0.05 *, p < 0.01 **, p < 0.001 ***, n.s.: not significant). The uncropped blots are shown in .

Article Snippet: IKK inhibitor (Selleck, S2882, Tokyo, Japan) and cisplatin (CDDP) (Selleck, S1166, Tokyo, Japan) were used to investigate their effects on cell viability.

Techniques: Inhibition, Western Blot, Control, MTT Assay, Knockdown, Over Expression