mcc950  (TargetMol)

Journal: International Dental Journal

Article Title: Chemerin Promotes Oral Squamous Cell Carcinoma Progression via NLRP3-Mediated Pyroptosis and the GSDMD-N Pathway

doi: 10.1016/j.identj.2026.109541

Figure Lengend Snippet: Expression of chemerin and NLRP3 in OSCC. A, The results indicated that NLRP3 was highly expressed in the high-expression region of chemerin. B, Immunofluorescence double staining showed that chemerin (488 nm) and NLRP3 (650 nm) could be coexpressed and localised in OSCC cells (red for chemerin and green for NLRP3). C, Chemerin overexpression led to the increased expression of pyroptosis-related proteins, and vice versa. When the NLRP3 inhibitor (MCC950) was added to each group, the expression level of pyroptosis-related proteins was decreased. GAPDH was used as a control.

Article Snippet: The NLRP3 inhibitor (MCC950) was purchased from MCE (Item No. CSN18163 ).

Techniques: Expressing, Immunofluorescence, Double Staining, Over Expression, Control

Journal: International Dental Journal

Article Title: Chemerin Promotes Oral Squamous Cell Carcinoma Progression via NLRP3-Mediated Pyroptosis and the GSDMD-N Pathway

doi: 10.1016/j.identj.2026.109541

Figure Lengend Snippet: Chemerin promotes OSCC EMT through pyroptosis. The expression of EMT-related molecules was measured in Cal27 and SCC15 cell lines. After chemerin overexpression, the expression level of N-cadherin and vimentin was increased, and the expression level of E-cadherin was decreased. After MCC950 was added, the expression level of N-cadherin and vimentin was still decreased, whereas the expression level of E-cadherin was increased. Tubulin was used as the control.

Article Snippet: The NLRP3 inhibitor (MCC950) was purchased from MCE (Item No. CSN18163 ).

Techniques: Expressing, Over Expression, Control

Journal: International Dental Journal

Article Title: Chemerin Promotes Oral Squamous Cell Carcinoma Progression via NLRP3-Mediated Pyroptosis and the GSDMD-N Pathway

doi: 10.1016/j.identj.2026.109541

Figure Lengend Snippet: Chemerin promotes cell migration and invasion through pyroptosis. A, Transwell migration and invasion experiments showed that the proliferation and migration of OSCC cells were enhanced after chemerin overexpression. After MCC950 was added, the proliferation and migration abilities of cells were weakened. B, Scratch healing experiments showed that OSCC cell migration was enhanced after chemerin overexpression. After adding MCC950, the cell migration ability was weakened.

Article Snippet: The NLRP3 inhibitor (MCC950) was purchased from MCE (Item No. CSN18163 ).

Techniques: Migration, Over Expression

Journal: International Dental Journal

Article Title: Chemerin Promotes Oral Squamous Cell Carcinoma Progression via NLRP3-Mediated Pyroptosis and the GSDMD-N Pathway

doi: 10.1016/j.identj.2026.109541

Figure Lengend Snippet: Chemerin promotes cell proliferation through pyroptosis. A, The CCK-8 experiment showed that the OD value of OSCC cells increased after the overexpression of chemerin. The OD value decreases after chemerin knockdown. After MCC950 was added, the OD value of the OSCC cells decreased. B, Flow cytometry results indicated that in the GSDMD-N expression group, the proportion of OSCC cells entering the S phase increased, and cell proliferation was promoted. The knockdown group enriched for S-phase cells and inhibited cell proliferation. C, In the group with high GSDMD-N expression level, the expression level of cyclinE1 and cyclinD1 increased, and after adding MCC950, the expression level of cyclinE1 and cyclinD1 decreased. GAPDH was used as the control.

Article Snippet: The NLRP3 inhibitor (MCC950) was purchased from MCE (Item No. CSN18163 ).

Techniques: CCK-8 Assay, Over Expression, Knockdown, Flow Cytometry, Expressing, Control

Journal: International Dental Journal

Article Title: Chemerin Promotes Oral Squamous Cell Carcinoma Progression via NLRP3-Mediated Pyroptosis and the GSDMD-N Pathway

doi: 10.1016/j.identj.2026.109541

Figure Lengend Snippet: Effect of chemerin on the formation of subcutaneous tumours in nude mice. A, The results of tumour transplantation in nude mice indicated that the tumours in the CAL27-Chemerin group were larger and heavier than those in the Cal27 group ( P < .05). The tumours in the SCC15 group were larger and heavier than those in the SCC15-Chemerin-shRNA group ( P < .05). B, The immunohistochemical results indicated that the expression level of pyroptosis-related molecules (GSDMD and IL-1β) and NLRP3 was higher in the chemerin overexpression group and lower in the chemerin knockdown group.

Article Snippet: The NLRP3 inhibitor (MCC950) was purchased from MCE (Item No. CSN18163 ).

Techniques: Transplantation Assay, shRNA, Immunohistochemical staining, Expressing, Over Expression, Knockdown

Journal: European Journal of Immunology

Article Title: SYK Signalling in NLRP3 Inflammasome‐Mediated Response of Murine Microglia Activated by Immune Complexes Formed of Viral Proteins and Specific IgG

doi: 10.1002/eji.70199

Figure Lengend Snippet: The impact of SYK inhibition on NLRP3 activation. Cells were treated with VLPs (20 µg/mL) and mAbs (7.5 µg/mL) for 24 h, and 1 µM of SYK inhibitor R406 or NLRP3 inhibitor MCC950 was added 1 h before treatment. (A) Western blot data show the expression of the indicated protein in microglia lysates, and the images are representative of five to six experiments. (B) Quantification of NLRP3 expression from Western blot data, normalised to a loading control, N = 5–6. (C) Quantification of ASC speck formation in primary microglia, N = 6. (D, E) IL‐1β secretion and (F) TNF‐α secretion were tested by ELISA in microglia supernatants, (D) N = 4, (E) N = 4–6, (F) N = 8–9. (G) Fluorescent microscopy images of the immunostained NLRP3 (cyan) and ASC specks (yellow), NLRP3 was stained with primary Ab anti‐NLRP and secondary Ab—AlexaFluor 488, ASC specks were stained with primary Ab anti‐ASC‐PE. Representative images are shown. The scale bars indicate 50 µm in large images and 20 µm in magnified images. In (B–F), data are represented using a box plot with dots showing the number of individual experiments. Significance was established using one‐way ANOVA followed by Tukey's test * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: SYK kinase inhibitor R406 (#inh‐r406), NLRP3 inhibitor MCC950 (#inh‐mcc), and Zymosan (#tlrl‐zyn) were from Invivogen.

Techniques: Inhibition, Activation Assay, Western Blot, Expressing, Control, Enzyme-linked Immunosorbent Assay, Microscopy, Staining

Journal: Cells

Article Title: Cardiolipin Induces CXCL9/CXCL10 Expression in Tumor-Infiltrating Lymphocytes

doi: 10.3390/cells15090798

Figure Lengend Snippet: Cardiolipin-mediated NLRP3 signaling orchestrates a pro-inflammatory tumor microenvironment and facilitates TIL reactivity. ( A ) RNA sequencing analysis of TIL expanded with 275 nM CL compared to vehicle controls. Differential expression analysis identified upregulation of the CXCR3 ligands CXCL9 and CXCL10, alongside downregulation of KBTBD11. ( B ) To assess the role of the NLRP3 inflammasome in antigen recognition, TIL were expanded in the presence or absence of the specific inhibitor MCC950 (10 µM). Functional reactivity was evaluated against a library of KRAS wild-type (WT) and mutant peptides. A significant reduction in the breadth of KRAS mutation recognition (measured by IFN-γ) was observed in the MCC950-treated group (* p < 0.01). Stimulation with α-CD3 (right panel) confirmed comparable T-cell fitness and viability between both groups (mean 253 pg/mL vs. 211 pg/mL; p > 0.05), ensuring that the observed inhibition was not due to non-specific toxicity. ( C ) To validate the pharmacological findings, TIL were transfected with either a non-targeting (scrambled) siRNA or an NLRP3-specific siRNA for 72 h. Following knockdown, TIL were co-cultured with KRAS mutant peptides for 72 h to assess functional recognition. Reduction in IFN-γ production was noted in the NLRP3-silenced group as compared to both the scrambled control cells and the untreated (nil) cells; red: positive controls (PHA and anti-CD3 crosslinking). ( D ) Tumor microfragments were cultured with or without 275 nM CL, in the presence or absence of the cytokine cocktail (IL-7/IL-15/IL-21). Analysis of the cell culture supernatants showed that CL induces a robust increase in the pro-inflammatory cytokines IL-1β, IL-18, and TNF-α (measured by Legendplex). Notably, this induction occurred independently of exogenous cytokine supplementation. ( E ) Consistent with the transcriptomic data in ( A ), CL-treated microfragments showed an increase in secreted CXCL10, as measured by ELISA. Statistical significance was determined using a two-tailed Student’s t -test for head-to-head comparisons. A p -value < 0.05 was considered statistically significant.

Article Snippet: TIL were expanded from tumor tissue as described above (see TIL expansion), in the presence of CL with or without MCC950 (10 μM/mL) (Invivogen, San Diego, CA, USA), a specific inhibitor of the NLRP3 pathway, starting from culture initiation throughout the entire expansion process.

Techniques: RNA Sequencing, Quantitative Proteomics, Functional Assay, Mutagenesis, Inhibition, Transfection, Knockdown, Cell Culture, Control, Enzyme-linked Immunosorbent Assay, Two Tailed Test