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nf κb inhibitor jsh 23  (MedChemExpress)


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    MedChemExpress nf κb inhibitor jsh 23
    a , SM metabolic pathway and inhibitors targeting enzymes. b – d , Spheroid invasion of oSCC with control media (grey), 5 µM SM (blue) or 5 µM SM and 20 µM imipramine (yellow) ( b ), oral FB secretomes (grey), with 20 µM imipramine (blue) or 20 µM imipramine and 2 µM S1P (yellow) ( c ) and oral FB secretomes (grey), with 2 µM PF543 (blue) or 2 µM PF543 and 2 µM S1P ( d ) (two-sided Mann–Whitney U- test, n = 6 replicates, two cell lines, two independent experiments). e , S1P immunofluorescence quantification of FADU control (grey), dermal (yellow) and oral (blue) FB secretomes (two-sided Mann–Whitney U- test, n = 6 replicates, three independent FB secretomes). f , Immunofluorescence images of FADU + dermal (left) or oral (right) FB secretomes; blue, Hoechst; orange, phalloidin; green, S1P; scale bar, 20 µm (representative images from n = 6 biologically independent wells). g , Spheroid invasion of oSCC cells treated with oral FB secretomes (grey) with 5 µM S1PR1 inhibitor (S1PR1i, ponesimod, blue) or 10 µM S1PR3 inhibitor (S1PR3i, TY-52156, yellow; Kruskal–Wallis, Dunn’s multiple comparisons, n = 5 replicates). h , Spheroid invasion of oSCC treated with oral FB secretomes (grey) with 20 µM STAT3 inhibitor (STAT3i, STX-0119, blue), 10 µM NF-κB inhibitor (NF-κBi; <t>JSH-23,</t> yellow) or 2 µM AKT inhibitor (AKTi; MK-2206, red; Kruskal–Wallis, Dunn’s multiple comparisons, n = 5 replicates). i , Western blot of STAT3, phospho-STAT3 Tyr705 , B-actin in oSCC (FADU) + dermal or oral FB secretomes, ±PF543, S1P rescue, S1PR1 inhibitor (ponesimod) or STAT3 inhibitor (STX-0119); numbers represent normalized pSTAT3 to total STAT3 fold change relative to oral FB secretomes, run on separate blots with independent loading controls under identical conditions (western blots representative of two independent experiments). j , oSCC basal respiration in oSCC cells treated with oral FB secretomes ± lipid stripping (Cleanascite, blue, 24 h; OCR, oxygen consumption rate; n = 24 replicates in two cell lines treated with three FB secretomes, two independent experiments, two-sided Mann–Whitney U- test). k , Mitochondrial activity in oSCC cell lines treated with oral FB secretomes (blue) measured by membrane potential-dependent immunofluorescence (two-sided Mann–Whitney U- test, n = 8 replicates, two independent cell lines). l , Mitochondrial abundance in oSCC cell lines treated with oral FB secretomes (blue) measured by immunofluorescence (two-sided Mann–Whitney U- test, n = 8 replicates, two independent cell lines). m , Basal respiration in oSCC cells treated with combinations of oral FB secretomes, 20 µM imipramine, 2 µM S1P or 20 µM STAT3i (STX-0119; n = 5 independent replicates, two-sided Mann–Whitney U- test). n , Subcutaneous tumour growth rate in NSG mice injected with oSCC UMSCC01 (grey), UMSCC01 + dermal FBs (oSCC + dermal FB, yellow) or UMSCC01 + oral FBs (oSCC + oral FB, blue; two-sided Mann–Whitney U- test, n = 7 per group). o , Ki67 proliferation quantification in oSCC (grey), oSCC + dermal FB (yellow) and oSCC + oral FBs (blue) tumours (two-sided Mann–Whitney U- test, n = 14, two measurements per tumour). p , Kaplan–Meier survival curve of oSCC (black) and oSCC + oral FBs (blue; n = 7 per group, two-sided Mantel–Cox test). Box plots show minimum to maximum values (error bars), the box indicates 25th and 75th percentiles, and the line denotes the median.
    Nf κb Inhibitor Jsh 23, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 224 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/nf+%CE%BAb+inhibitor+jsh+23/JSH-23/pmc13218938-345-11-14
    Average 97 stars, based on 224 article reviews
    nf κb inhibitor jsh 23 - by Bioz Stars, 2026-09
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    Images

    1) Product Images from "Tissue-specific fibroblast lipid cues impose the rate of epithelial cancer invasion"

    Article Title: Tissue-specific fibroblast lipid cues impose the rate of epithelial cancer invasion

    Journal: Nature Metabolism

    doi: 10.1038/s42255-026-01514-y

    a , SM metabolic pathway and inhibitors targeting enzymes. b – d , Spheroid invasion of oSCC with control media (grey), 5 µM SM (blue) or 5 µM SM and 20 µM imipramine (yellow) ( b ), oral FB secretomes (grey), with 20 µM imipramine (blue) or 20 µM imipramine and 2 µM S1P (yellow) ( c ) and oral FB secretomes (grey), with 2 µM PF543 (blue) or 2 µM PF543 and 2 µM S1P ( d ) (two-sided Mann–Whitney U- test, n = 6 replicates, two cell lines, two independent experiments). e , S1P immunofluorescence quantification of FADU control (grey), dermal (yellow) and oral (blue) FB secretomes (two-sided Mann–Whitney U- test, n = 6 replicates, three independent FB secretomes). f , Immunofluorescence images of FADU + dermal (left) or oral (right) FB secretomes; blue, Hoechst; orange, phalloidin; green, S1P; scale bar, 20 µm (representative images from n = 6 biologically independent wells). g , Spheroid invasion of oSCC cells treated with oral FB secretomes (grey) with 5 µM S1PR1 inhibitor (S1PR1i, ponesimod, blue) or 10 µM S1PR3 inhibitor (S1PR3i, TY-52156, yellow; Kruskal–Wallis, Dunn’s multiple comparisons, n = 5 replicates). h , Spheroid invasion of oSCC treated with oral FB secretomes (grey) with 20 µM STAT3 inhibitor (STAT3i, STX-0119, blue), 10 µM NF-κB inhibitor (NF-κBi; JSH-23, yellow) or 2 µM AKT inhibitor (AKTi; MK-2206, red; Kruskal–Wallis, Dunn’s multiple comparisons, n = 5 replicates). i , Western blot of STAT3, phospho-STAT3 Tyr705 , B-actin in oSCC (FADU) + dermal or oral FB secretomes, ±PF543, S1P rescue, S1PR1 inhibitor (ponesimod) or STAT3 inhibitor (STX-0119); numbers represent normalized pSTAT3 to total STAT3 fold change relative to oral FB secretomes, run on separate blots with independent loading controls under identical conditions (western blots representative of two independent experiments). j , oSCC basal respiration in oSCC cells treated with oral FB secretomes ± lipid stripping (Cleanascite, blue, 24 h; OCR, oxygen consumption rate; n = 24 replicates in two cell lines treated with three FB secretomes, two independent experiments, two-sided Mann–Whitney U- test). k , Mitochondrial activity in oSCC cell lines treated with oral FB secretomes (blue) measured by membrane potential-dependent immunofluorescence (two-sided Mann–Whitney U- test, n = 8 replicates, two independent cell lines). l , Mitochondrial abundance in oSCC cell lines treated with oral FB secretomes (blue) measured by immunofluorescence (two-sided Mann–Whitney U- test, n = 8 replicates, two independent cell lines). m , Basal respiration in oSCC cells treated with combinations of oral FB secretomes, 20 µM imipramine, 2 µM S1P or 20 µM STAT3i (STX-0119; n = 5 independent replicates, two-sided Mann–Whitney U- test). n , Subcutaneous tumour growth rate in NSG mice injected with oSCC UMSCC01 (grey), UMSCC01 + dermal FBs (oSCC + dermal FB, yellow) or UMSCC01 + oral FBs (oSCC + oral FB, blue; two-sided Mann–Whitney U- test, n = 7 per group). o , Ki67 proliferation quantification in oSCC (grey), oSCC + dermal FB (yellow) and oSCC + oral FBs (blue) tumours (two-sided Mann–Whitney U- test, n = 14, two measurements per tumour). p , Kaplan–Meier survival curve of oSCC (black) and oSCC + oral FBs (blue; n = 7 per group, two-sided Mantel–Cox test). Box plots show minimum to maximum values (error bars), the box indicates 25th and 75th percentiles, and the line denotes the median.
    Figure Legend Snippet: a , SM metabolic pathway and inhibitors targeting enzymes. b – d , Spheroid invasion of oSCC with control media (grey), 5 µM SM (blue) or 5 µM SM and 20 µM imipramine (yellow) ( b ), oral FB secretomes (grey), with 20 µM imipramine (blue) or 20 µM imipramine and 2 µM S1P (yellow) ( c ) and oral FB secretomes (grey), with 2 µM PF543 (blue) or 2 µM PF543 and 2 µM S1P ( d ) (two-sided Mann–Whitney U- test, n = 6 replicates, two cell lines, two independent experiments). e , S1P immunofluorescence quantification of FADU control (grey), dermal (yellow) and oral (blue) FB secretomes (two-sided Mann–Whitney U- test, n = 6 replicates, three independent FB secretomes). f , Immunofluorescence images of FADU + dermal (left) or oral (right) FB secretomes; blue, Hoechst; orange, phalloidin; green, S1P; scale bar, 20 µm (representative images from n = 6 biologically independent wells). g , Spheroid invasion of oSCC cells treated with oral FB secretomes (grey) with 5 µM S1PR1 inhibitor (S1PR1i, ponesimod, blue) or 10 µM S1PR3 inhibitor (S1PR3i, TY-52156, yellow; Kruskal–Wallis, Dunn’s multiple comparisons, n = 5 replicates). h , Spheroid invasion of oSCC treated with oral FB secretomes (grey) with 20 µM STAT3 inhibitor (STAT3i, STX-0119, blue), 10 µM NF-κB inhibitor (NF-κBi; JSH-23, yellow) or 2 µM AKT inhibitor (AKTi; MK-2206, red; Kruskal–Wallis, Dunn’s multiple comparisons, n = 5 replicates). i , Western blot of STAT3, phospho-STAT3 Tyr705 , B-actin in oSCC (FADU) + dermal or oral FB secretomes, ±PF543, S1P rescue, S1PR1 inhibitor (ponesimod) or STAT3 inhibitor (STX-0119); numbers represent normalized pSTAT3 to total STAT3 fold change relative to oral FB secretomes, run on separate blots with independent loading controls under identical conditions (western blots representative of two independent experiments). j , oSCC basal respiration in oSCC cells treated with oral FB secretomes ± lipid stripping (Cleanascite, blue, 24 h; OCR, oxygen consumption rate; n = 24 replicates in two cell lines treated with three FB secretomes, two independent experiments, two-sided Mann–Whitney U- test). k , Mitochondrial activity in oSCC cell lines treated with oral FB secretomes (blue) measured by membrane potential-dependent immunofluorescence (two-sided Mann–Whitney U- test, n = 8 replicates, two independent cell lines). l , Mitochondrial abundance in oSCC cell lines treated with oral FB secretomes (blue) measured by immunofluorescence (two-sided Mann–Whitney U- test, n = 8 replicates, two independent cell lines). m , Basal respiration in oSCC cells treated with combinations of oral FB secretomes, 20 µM imipramine, 2 µM S1P or 20 µM STAT3i (STX-0119; n = 5 independent replicates, two-sided Mann–Whitney U- test). n , Subcutaneous tumour growth rate in NSG mice injected with oSCC UMSCC01 (grey), UMSCC01 + dermal FBs (oSCC + dermal FB, yellow) or UMSCC01 + oral FBs (oSCC + oral FB, blue; two-sided Mann–Whitney U- test, n = 7 per group). o , Ki67 proliferation quantification in oSCC (grey), oSCC + dermal FB (yellow) and oSCC + oral FBs (blue) tumours (two-sided Mann–Whitney U- test, n = 14, two measurements per tumour). p , Kaplan–Meier survival curve of oSCC (black) and oSCC + oral FBs (blue; n = 7 per group, two-sided Mantel–Cox test). Box plots show minimum to maximum values (error bars), the box indicates 25th and 75th percentiles, and the line denotes the median.

    Techniques Used: Control, MANN-WHITNEY, Immunofluorescence, Western Blot, Stripping Membranes, Activity Assay, Membrane, Injection

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    Incubation:

    Article Title: Allograft inflammatory Factor-1 induces the dedifferentiation of Vascular Smooth Muscle cells into a macrophage-like phenotype both in vivo and in vitro.
    Article Snippet: .. For the rescue experiment, 10 μM of the NF-κB inhibitor JSH-23 (HY-13982, MedChemExpress) was added to the AIF1-overexpressing cells and incubated at 37 ◦C for 24 h. Subsequently, the cells were collected for further experiments. ..

    Phospho-proteomics:

    Article Title: Activation of the TLR2/NF-κB signaling axis by capsid proteinVP1 of feline calicivirus promotes IL-1β expression in vitro.
    Article Snippet: Feline calicivirus (FCV) induces systemic inflammation in felines, posing a serious threat to feline health worldwide.. Severe cases may lead to chronic stomatitis and other inflammatory conditions.. However, the precise mechanisms underlying FCV-induced inflammation remain unclear.

    Activation Assay:

    Article Title: ROS-Responsive Wedelolactone Hydrogel Promotes Intervertebral Disc Repair by Disrupting the NF-κB-LCN2 Inflammatory Feedback Loop.
    Article Snippet: To verify the role of LCN2, recombinant LCN2 (rLCN2, 200 ng mL− 1 ) or an LCN2 inhibitor (LCN2i, 10 μm , MedChemExpress, Cat# HY-Q45780) was added to AFC or RAW264.7 cultures with or without WDL treatment for 24 h. LCN2 and P-p65 localization were analyzed by immunofluorescence. .. To confirm the involvement of the NF- κB pathway, cells were pretreated with the NF- κB inhibitor JSH-23 (10 μm , MedChemExpress, Cat# HY-13982) for 1 h before LPS stimulation, followed by WDL (6.25 μg mL− 1 ) treatment for 24 h. NFκB activation was assessed by P-p65 nuclear translocation, and downstream targets LCN2 and MMP9 were evaluated by immunofluorescence. ..

    Article Title: ROS‐Responsive Wedelolactone Hydrogel Promotes Intervertebral Disc Repair by Disrupting the NF‐κB–LCN2 Inflammatory Feedback Loop
    Article Snippet: To verify the role of LCN2, recombinant LCN2 (rLCN2, 200 ng mL −1 ) or an LCN2 inhibitor (LCN2i, 10 μ m , MedChemExpress, Cat# HY‐ Q45780 ) was added to AFC or RAW264.7 cultures with or without WDL treatment for 24 h. LCN2 and P‐p65 localization were analyzed by immunofluorescence. .. To confirm the involvement of the NF‐κB pathway, cells were pretreated with the NF‐κB inhibitor JSH‐23 (10 μ m , MedChemExpress, Cat# HY‐13982) for 1 h before LPS stimulation, followed by WDL (6.25 μg mL −1 ) treatment for 24 h. NF‐κB activation was assessed by P‐p65 nuclear translocation, and downstream targets LCN2 and MMP9 were evaluated by immunofluorescence. ..

    Translocation Assay:

    Article Title: ROS-Responsive Wedelolactone Hydrogel Promotes Intervertebral Disc Repair by Disrupting the NF-κB-LCN2 Inflammatory Feedback Loop.
    Article Snippet: To verify the role of LCN2, recombinant LCN2 (rLCN2, 200 ng mL− 1 ) or an LCN2 inhibitor (LCN2i, 10 μm , MedChemExpress, Cat# HY-Q45780) was added to AFC or RAW264.7 cultures with or without WDL treatment for 24 h. LCN2 and P-p65 localization were analyzed by immunofluorescence. .. To confirm the involvement of the NF- κB pathway, cells were pretreated with the NF- κB inhibitor JSH-23 (10 μm , MedChemExpress, Cat# HY-13982) for 1 h before LPS stimulation, followed by WDL (6.25 μg mL− 1 ) treatment for 24 h. NFκB activation was assessed by P-p65 nuclear translocation, and downstream targets LCN2 and MMP9 were evaluated by immunofluorescence. ..

    Article Title: ROS‐Responsive Wedelolactone Hydrogel Promotes Intervertebral Disc Repair by Disrupting the NF‐κB–LCN2 Inflammatory Feedback Loop
    Article Snippet: To verify the role of LCN2, recombinant LCN2 (rLCN2, 200 ng mL −1 ) or an LCN2 inhibitor (LCN2i, 10 μ m , MedChemExpress, Cat# HY‐ Q45780 ) was added to AFC or RAW264.7 cultures with or without WDL treatment for 24 h. LCN2 and P‐p65 localization were analyzed by immunofluorescence. .. To confirm the involvement of the NF‐κB pathway, cells were pretreated with the NF‐κB inhibitor JSH‐23 (10 μ m , MedChemExpress, Cat# HY‐13982) for 1 h before LPS stimulation, followed by WDL (6.25 μg mL −1 ) treatment for 24 h. NF‐κB activation was assessed by P‐p65 nuclear translocation, and downstream targets LCN2 and MMP9 were evaluated by immunofluorescence. ..

    Immunofluorescence:

    Article Title: ROS-Responsive Wedelolactone Hydrogel Promotes Intervertebral Disc Repair by Disrupting the NF-κB-LCN2 Inflammatory Feedback Loop.
    Article Snippet: To verify the role of LCN2, recombinant LCN2 (rLCN2, 200 ng mL− 1 ) or an LCN2 inhibitor (LCN2i, 10 μm , MedChemExpress, Cat# HY-Q45780) was added to AFC or RAW264.7 cultures with or without WDL treatment for 24 h. LCN2 and P-p65 localization were analyzed by immunofluorescence. .. To confirm the involvement of the NF- κB pathway, cells were pretreated with the NF- κB inhibitor JSH-23 (10 μm , MedChemExpress, Cat# HY-13982) for 1 h before LPS stimulation, followed by WDL (6.25 μg mL− 1 ) treatment for 24 h. NFκB activation was assessed by P-p65 nuclear translocation, and downstream targets LCN2 and MMP9 were evaluated by immunofluorescence. ..

    Article Title: ROS‐Responsive Wedelolactone Hydrogel Promotes Intervertebral Disc Repair by Disrupting the NF‐κB–LCN2 Inflammatory Feedback Loop
    Article Snippet: To verify the role of LCN2, recombinant LCN2 (rLCN2, 200 ng mL −1 ) or an LCN2 inhibitor (LCN2i, 10 μ m , MedChemExpress, Cat# HY‐ Q45780 ) was added to AFC or RAW264.7 cultures with or without WDL treatment for 24 h. LCN2 and P‐p65 localization were analyzed by immunofluorescence. .. To confirm the involvement of the NF‐κB pathway, cells were pretreated with the NF‐κB inhibitor JSH‐23 (10 μ m , MedChemExpress, Cat# HY‐13982) for 1 h before LPS stimulation, followed by WDL (6.25 μg mL −1 ) treatment for 24 h. NF‐κB activation was assessed by P‐p65 nuclear translocation, and downstream targets LCN2 and MMP9 were evaluated by immunofluorescence. ..



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    a , SM metabolic pathway and inhibitors targeting enzymes. b – d , Spheroid invasion of oSCC with control media (grey), 5 µM SM (blue) or 5 µM SM and 20 µM imipramine (yellow) ( b ), oral FB secretomes (grey), with 20 µM imipramine (blue) or 20 µM imipramine and 2 µM S1P (yellow) ( c ) and oral FB secretomes (grey), with 2 µM PF543 (blue) or 2 µM PF543 and 2 µM S1P ( d ) (two-sided Mann–Whitney U- test, n = 6 replicates, two cell lines, two independent experiments). e , S1P immunofluorescence quantification of FADU control (grey), dermal (yellow) and oral (blue) FB secretomes (two-sided Mann–Whitney U- test, n = 6 replicates, three independent FB secretomes). f , Immunofluorescence images of FADU + dermal (left) or oral (right) FB secretomes; blue, Hoechst; orange, phalloidin; green, S1P; scale bar, 20 µm (representative images from n = 6 biologically independent wells). g , Spheroid invasion of oSCC cells treated with oral FB secretomes (grey) with 5 µM S1PR1 inhibitor (S1PR1i, ponesimod, blue) or 10 µM S1PR3 inhibitor (S1PR3i, TY-52156, yellow; Kruskal–Wallis, Dunn’s multiple comparisons, n = 5 replicates). h , Spheroid invasion of oSCC treated with oral FB secretomes (grey) with 20 µM STAT3 inhibitor (STAT3i, STX-0119, blue), 10 µM NF-κB inhibitor (NF-κBi; JSH-23, yellow) or 2 µM AKT inhibitor (AKTi; MK-2206, red; Kruskal–Wallis, Dunn’s multiple comparisons, n = 5 replicates). i , Western blot of STAT3, phospho-STAT3 Tyr705 , B-actin in oSCC (FADU) + dermal or oral FB secretomes, ±PF543, S1P rescue, S1PR1 inhibitor (ponesimod) or STAT3 inhibitor (STX-0119); numbers represent normalized pSTAT3 to total STAT3 fold change relative to oral FB secretomes, run on separate blots with independent loading controls under identical conditions (western blots representative of two independent experiments). j , oSCC basal respiration in oSCC cells treated with oral FB secretomes ± lipid stripping (Cleanascite, blue, 24 h; OCR, oxygen consumption rate; n = 24 replicates in two cell lines treated with three FB secretomes, two independent experiments, two-sided Mann–Whitney U- test). k , Mitochondrial activity in oSCC cell lines treated with oral FB secretomes (blue) measured by membrane potential-dependent immunofluorescence (two-sided Mann–Whitney U- test, n = 8 replicates, two independent cell lines). l , Mitochondrial abundance in oSCC cell lines treated with oral FB secretomes (blue) measured by immunofluorescence (two-sided Mann–Whitney U- test, n = 8 replicates, two independent cell lines). m , Basal respiration in oSCC cells treated with combinations of oral FB secretomes, 20 µM imipramine, 2 µM S1P or 20 µM STAT3i (STX-0119; n = 5 independent replicates, two-sided Mann–Whitney U- test). n , Subcutaneous tumour growth rate in NSG mice injected with oSCC UMSCC01 (grey), UMSCC01 + dermal FBs (oSCC + dermal FB, yellow) or UMSCC01 + oral FBs (oSCC + oral FB, blue; two-sided Mann–Whitney U- test, n = 7 per group). o , Ki67 proliferation quantification in oSCC (grey), oSCC + dermal FB (yellow) and oSCC + oral FBs (blue) tumours (two-sided Mann–Whitney U- test, n = 14, two measurements per tumour). p , Kaplan–Meier survival curve of oSCC (black) and oSCC + oral FBs (blue; n = 7 per group, two-sided Mantel–Cox test). Box plots show minimum to maximum values (error bars), the box indicates 25th and 75th percentiles, and the line denotes the median.

    Journal: Nature Metabolism

    Article Title: Tissue-specific fibroblast lipid cues impose the rate of epithelial cancer invasion

    doi: 10.1038/s42255-026-01514-y

    Figure Lengend Snippet: a , SM metabolic pathway and inhibitors targeting enzymes. b – d , Spheroid invasion of oSCC with control media (grey), 5 µM SM (blue) or 5 µM SM and 20 µM imipramine (yellow) ( b ), oral FB secretomes (grey), with 20 µM imipramine (blue) or 20 µM imipramine and 2 µM S1P (yellow) ( c ) and oral FB secretomes (grey), with 2 µM PF543 (blue) or 2 µM PF543 and 2 µM S1P ( d ) (two-sided Mann–Whitney U- test, n = 6 replicates, two cell lines, two independent experiments). e , S1P immunofluorescence quantification of FADU control (grey), dermal (yellow) and oral (blue) FB secretomes (two-sided Mann–Whitney U- test, n = 6 replicates, three independent FB secretomes). f , Immunofluorescence images of FADU + dermal (left) or oral (right) FB secretomes; blue, Hoechst; orange, phalloidin; green, S1P; scale bar, 20 µm (representative images from n = 6 biologically independent wells). g , Spheroid invasion of oSCC cells treated with oral FB secretomes (grey) with 5 µM S1PR1 inhibitor (S1PR1i, ponesimod, blue) or 10 µM S1PR3 inhibitor (S1PR3i, TY-52156, yellow; Kruskal–Wallis, Dunn’s multiple comparisons, n = 5 replicates). h , Spheroid invasion of oSCC treated with oral FB secretomes (grey) with 20 µM STAT3 inhibitor (STAT3i, STX-0119, blue), 10 µM NF-κB inhibitor (NF-κBi; JSH-23, yellow) or 2 µM AKT inhibitor (AKTi; MK-2206, red; Kruskal–Wallis, Dunn’s multiple comparisons, n = 5 replicates). i , Western blot of STAT3, phospho-STAT3 Tyr705 , B-actin in oSCC (FADU) + dermal or oral FB secretomes, ±PF543, S1P rescue, S1PR1 inhibitor (ponesimod) or STAT3 inhibitor (STX-0119); numbers represent normalized pSTAT3 to total STAT3 fold change relative to oral FB secretomes, run on separate blots with independent loading controls under identical conditions (western blots representative of two independent experiments). j , oSCC basal respiration in oSCC cells treated with oral FB secretomes ± lipid stripping (Cleanascite, blue, 24 h; OCR, oxygen consumption rate; n = 24 replicates in two cell lines treated with three FB secretomes, two independent experiments, two-sided Mann–Whitney U- test). k , Mitochondrial activity in oSCC cell lines treated with oral FB secretomes (blue) measured by membrane potential-dependent immunofluorescence (two-sided Mann–Whitney U- test, n = 8 replicates, two independent cell lines). l , Mitochondrial abundance in oSCC cell lines treated with oral FB secretomes (blue) measured by immunofluorescence (two-sided Mann–Whitney U- test, n = 8 replicates, two independent cell lines). m , Basal respiration in oSCC cells treated with combinations of oral FB secretomes, 20 µM imipramine, 2 µM S1P or 20 µM STAT3i (STX-0119; n = 5 independent replicates, two-sided Mann–Whitney U- test). n , Subcutaneous tumour growth rate in NSG mice injected with oSCC UMSCC01 (grey), UMSCC01 + dermal FBs (oSCC + dermal FB, yellow) or UMSCC01 + oral FBs (oSCC + oral FB, blue; two-sided Mann–Whitney U- test, n = 7 per group). o , Ki67 proliferation quantification in oSCC (grey), oSCC + dermal FB (yellow) and oSCC + oral FBs (blue) tumours (two-sided Mann–Whitney U- test, n = 14, two measurements per tumour). p , Kaplan–Meier survival curve of oSCC (black) and oSCC + oral FBs (blue; n = 7 per group, two-sided Mantel–Cox test). Box plots show minimum to maximum values (error bars), the box indicates 25th and 75th percentiles, and the line denotes the median.

    Article Snippet: STAT3 inhibitor STX-0119 (MedChemExpress, HY-103692-1ml), AKT inhibitor MK-2206 (MedChemExpress, HY-10358-1ml) and NF-κB inhibitor JSH-23 (MedChemExpress, HY-13982-1ml) were supplied at 10 mM in DMSO and diluted to 20 μM, 2 μM and 10 μM, respectively, in secretomes.

    Techniques: Control, MANN-WHITNEY, Immunofluorescence, Western Blot, Stripping Membranes, Activity Assay, Membrane, Injection

    TNFAIP3 modulates M2 polarization of macrophages via NF-κB/Spi1/C/EBPβ signaling pathway. ( A ) Venn diagram of overlapping regulators between p65 ChIP-seq data and database-predicted transcription factors for C/EBPβ. ( B , F – I ) RT-qPCR and western blot analyses of mRNA and proteins of Spi1 among M0 macrophages (NC), M2 macrophages (stimulated by IL-4 and IL-13 for 48 hours), scrambled (Scr) control, siTnfaip3+M2 macrophage (knockdown Tnfaip3 before stimulation with IL-4 and IL-13 for 48 hours), empty vector (vec) control, and Tnfaip3+M2 macrophage (overexpressed Tnfaip3 before stimulation with IL-4 and IL-13 for 48 hours) groups. Results are expressed as mean ± SD ( n = 3). * P < 0.05, ** P < 0.01, **** P < 0.0001. ( C – E ) ChIP-qPCR assays were performed with IgG or Spi1 antibodies to confirm the binding of Spi1 to C/ebpβ promoter. This binding was significantly enriched in M2 macrophages compared to M0 macrophages, which was attenuated by Tnfaip3 overexpression. Results are expressed as mean ± SD ( n = 3). *** P < 0.001, **** P < 0.0001, #### P < 0.0001; ns, not significant. ( J , L ) NF-κB inhibitor (JSH-23) suppressed the upregulation of C/EBPβ in siTnfaip3+M2 macrophage (knockdown Tnfaip3 before being stimulated by IL-4 and IL-13 for 48 hours). Results are expressed as mean ± SD ( n = 3). * P < 0.05, ** P < 0.01. ( K , M ) Spi1 inhibitor (HY) suppressed the upregulation of C/EBPβ in siTnfaip3+M2 macrophage (knockdown Tnfaip3 before being stimulated by IL-4 and IL-13 for 48 hours). Results are expressed as mean ± SD ( n = 3). * P < 0.05, ** P < 0.01.

    Journal: Investigative Ophthalmology & Visual Science

    Article Title: TNFAIP3 in M2 Macrophage Attenuates Subretinal Fibrosis in Laser-Induced Murine Model

    doi: 10.1167/iovs.67.5.25

    Figure Lengend Snippet: TNFAIP3 modulates M2 polarization of macrophages via NF-κB/Spi1/C/EBPβ signaling pathway. ( A ) Venn diagram of overlapping regulators between p65 ChIP-seq data and database-predicted transcription factors for C/EBPβ. ( B , F – I ) RT-qPCR and western blot analyses of mRNA and proteins of Spi1 among M0 macrophages (NC), M2 macrophages (stimulated by IL-4 and IL-13 for 48 hours), scrambled (Scr) control, siTnfaip3+M2 macrophage (knockdown Tnfaip3 before stimulation with IL-4 and IL-13 for 48 hours), empty vector (vec) control, and Tnfaip3+M2 macrophage (overexpressed Tnfaip3 before stimulation with IL-4 and IL-13 for 48 hours) groups. Results are expressed as mean ± SD ( n = 3). * P < 0.05, ** P < 0.01, **** P < 0.0001. ( C – E ) ChIP-qPCR assays were performed with IgG or Spi1 antibodies to confirm the binding of Spi1 to C/ebpβ promoter. This binding was significantly enriched in M2 macrophages compared to M0 macrophages, which was attenuated by Tnfaip3 overexpression. Results are expressed as mean ± SD ( n = 3). *** P < 0.001, **** P < 0.0001, #### P < 0.0001; ns, not significant. ( J , L ) NF-κB inhibitor (JSH-23) suppressed the upregulation of C/EBPβ in siTnfaip3+M2 macrophage (knockdown Tnfaip3 before being stimulated by IL-4 and IL-13 for 48 hours). Results are expressed as mean ± SD ( n = 3). * P < 0.05, ** P < 0.01. ( K , M ) Spi1 inhibitor (HY) suppressed the upregulation of C/EBPβ in siTnfaip3+M2 macrophage (knockdown Tnfaip3 before being stimulated by IL-4 and IL-13 for 48 hours). Results are expressed as mean ± SD ( n = 3). * P < 0.05, ** P < 0.01.

    Article Snippet: Following Tnfaip3 knockdown, macrophages were stimulated with IL-4 and IL-13 in the presence of the NF-κB inhibitor (JSH-23; MedChemExpress, Monmouth Junction, NJ, USA), which suppressed the upregulation of C/EBPβ ( J, L), suggesting that the NF-κB signaling pathway is involved in the regulation of C/EBPβ.

    Techniques: ChIP-sequencing, Quantitative RT-PCR, Western Blot, Control, Knockdown, Plasmid Preparation, ChIP-qPCR, Binding Assay, Over Expression

    A schematic diagram illustrating the mechanism by which TNFAIP3 in macrophages modulates M2 polarization via the NF-κB/Spi1/C/EBPβ signaling pathway, thereby suppressing TGF-β1 expression and attenuating subretinal fibrosis of CNV lesions.

    Journal: Investigative Ophthalmology & Visual Science

    Article Title: TNFAIP3 in M2 Macrophage Attenuates Subretinal Fibrosis in Laser-Induced Murine Model

    doi: 10.1167/iovs.67.5.25

    Figure Lengend Snippet: A schematic diagram illustrating the mechanism by which TNFAIP3 in macrophages modulates M2 polarization via the NF-κB/Spi1/C/EBPβ signaling pathway, thereby suppressing TGF-β1 expression and attenuating subretinal fibrosis of CNV lesions.

    Article Snippet: Following Tnfaip3 knockdown, macrophages were stimulated with IL-4 and IL-13 in the presence of the NF-κB inhibitor (JSH-23; MedChemExpress, Monmouth Junction, NJ, USA), which suppressed the upregulation of C/EBPβ ( J, L), suggesting that the NF-κB signaling pathway is involved in the regulation of C/EBPβ.

    Techniques: Expressing

    The activation of NF-κB serves as a survival mechanism to rescue 64 -induced inhibition of NSCLC cell growth and apoptosis. NCI-H1975 and NCI-H1650 cells were treated with 64 alone or in combination with JSH-23. a . Western blotting of P65 in the cytoplasm and nuclear was conducted under treatment with 64 and JSH-23 for 24 h. b . MTT assay was conducted to determine cell viability under treatment with 64 and JSH-23 for 24 h. c . The cell viability inhibition by 64 (0.5µM, 1µM, 2µM, 3µM, 4µM, 8µM) and JSH-23(2.5µM, 5µM, 10µM, 15µM, 20μΜ, 40μΜ) was also evaluated, as was the combined effect of the two compounds. d . The CI (Combination Index) values were calculated using the software Biosoft CalcuSyn to determine the impact of individual combined concentrations of 64 and JSH-23 (fraction affected (Fa)) accordance with cell viability. e . JC-1 assay to assess MMP under treatment with 64 and JSH-23 for 4 h. f . Annexin V-PI double staining assay to evaluate cell apoptosis under treatment with 64 and JSH-23 for 4 h. The data were obtained from three independent experiments with n = 3 and were presented as mean ± SD. Statistical significance between compared groups was indicated by * P < 0.05, ** P < 0.01, *** P < 0.001.

    Journal: Translational Oncology

    Article Title: NF-κB activation as a pro-survival signal from pharmacological inhibition of pyruvate dehydrogenase kinase 1 in non-small-cell lung carcinoma cell models

    doi: 10.1016/j.tranon.2026.102681

    Figure Lengend Snippet: The activation of NF-κB serves as a survival mechanism to rescue 64 -induced inhibition of NSCLC cell growth and apoptosis. NCI-H1975 and NCI-H1650 cells were treated with 64 alone or in combination with JSH-23. a . Western blotting of P65 in the cytoplasm and nuclear was conducted under treatment with 64 and JSH-23 for 24 h. b . MTT assay was conducted to determine cell viability under treatment with 64 and JSH-23 for 24 h. c . The cell viability inhibition by 64 (0.5µM, 1µM, 2µM, 3µM, 4µM, 8µM) and JSH-23(2.5µM, 5µM, 10µM, 15µM, 20μΜ, 40μΜ) was also evaluated, as was the combined effect of the two compounds. d . The CI (Combination Index) values were calculated using the software Biosoft CalcuSyn to determine the impact of individual combined concentrations of 64 and JSH-23 (fraction affected (Fa)) accordance with cell viability. e . JC-1 assay to assess MMP under treatment with 64 and JSH-23 for 4 h. f . Annexin V-PI double staining assay to evaluate cell apoptosis under treatment with 64 and JSH-23 for 4 h. The data were obtained from three independent experiments with n = 3 and were presented as mean ± SD. Statistical significance between compared groups was indicated by * P < 0.05, ** P < 0.01, *** P < 0.001.

    Article Snippet: P38 MAPK inhibitor SB203580 (S1076) and NF-κB inhibitor JSH-23 (S7351) were purchased from SelleckChem (Houston, TX, USA).

    Techniques: Activation Assay, Inhibition, Western Blot, MTT Assay, Software, Double Staining

    The activation of NF-κB pathway caused by 64 affecting the expressions levels key apoptotic proteins in NSCLC cells. The NSCLC cell lines NCI-H1975 and NCI-H1650 were treated with 64 alone or in combination with JSH-23 for 24 h. a . The expression levels of CytC in the mitochondria and cytoplasm were detected by western blotting. b . The histograms showing the ratios between cytoplasmic CytC to mitochondrial CytC. c . The expressions of apoptotic-related proteins were detected by western blotting. d . The histogram analysis for the expression of Bax and Bcl-2, as well as the ratios between the cleaved form (c-cas3 and c-PARP) and the total form (cas3 and PARP). e . The expression of proteins in the JNK pathway were detected by western blotting. f . The histogram analysis for the ratios of phosphorylated form (p-JNK and p-c-Jun) to total form (JNK and c-Jun). The data were obtained from three independent experiments with n = 3 and were presented as mean ± SD. The statistical significance between the compared groups was indicated by * P < 0.05, ** P < 0.01, *** P <0.001.

    Journal: Translational Oncology

    Article Title: NF-κB activation as a pro-survival signal from pharmacological inhibition of pyruvate dehydrogenase kinase 1 in non-small-cell lung carcinoma cell models

    doi: 10.1016/j.tranon.2026.102681

    Figure Lengend Snippet: The activation of NF-κB pathway caused by 64 affecting the expressions levels key apoptotic proteins in NSCLC cells. The NSCLC cell lines NCI-H1975 and NCI-H1650 were treated with 64 alone or in combination with JSH-23 for 24 h. a . The expression levels of CytC in the mitochondria and cytoplasm were detected by western blotting. b . The histograms showing the ratios between cytoplasmic CytC to mitochondrial CytC. c . The expressions of apoptotic-related proteins were detected by western blotting. d . The histogram analysis for the expression of Bax and Bcl-2, as well as the ratios between the cleaved form (c-cas3 and c-PARP) and the total form (cas3 and PARP). e . The expression of proteins in the JNK pathway were detected by western blotting. f . The histogram analysis for the ratios of phosphorylated form (p-JNK and p-c-Jun) to total form (JNK and c-Jun). The data were obtained from three independent experiments with n = 3 and were presented as mean ± SD. The statistical significance between the compared groups was indicated by * P < 0.05, ** P < 0.01, *** P <0.001.

    Article Snippet: P38 MAPK inhibitor SB203580 (S1076) and NF-κB inhibitor JSH-23 (S7351) were purchased from SelleckChem (Houston, TX, USA).

    Techniques: Activation Assay, Expressing, Western Blot