^
27d
The mechanism of NF-κB-TERT feedback regulation of granulosa cell apoptosis in PCOS rats. (PubMed, PLoS One)
Using letrozole and a high-fat diet, a PCOS rat model was established, along with a Lipopolysaccharide (LPS) -treated KGN cell inflammation model was established. NF-κB and TERT inhibitors (BAY 11-7082 and BIBR1532) were then administered to LPS-induced KGN cells...LPS-treated KGN cells demonstrated increased expression of inflammatory and pro-apoptotic factors, later restored post-treatment with NF-κB and TERT inhibitors (P are all less than 0.05). In conclusion, TERT may induce granulosa cell apoptosis by participating in the regulation of the NF-κB signaling pathway, thereby mediating the chronic inflammatory response of PCOS through downstream inflammatory factors IL-6 and TNF-α.
Preclinical • Journal • IO biomarker
|
BCL2 (B-cell CLL/lymphoma 2) • TERT (Telomerase Reverse Transcriptase) • IL6 (Interleukin 6) • TNFA (Tumor Necrosis Factor-Alpha) • CASP3 (Caspase 3)
|
letrozole • BIBR1532 • Bay11-7082
27d
Molecular Mechanisms of Skatole-Induced Inflammatory Responses in Intestinal Epithelial Caco-2 Cells: Implications for Colorectal Cancer and Inflammatory Bowel Disease. (PubMed, Cells)
In addition to activating NF-κB, the NF-κB inhibitor BAY 11-7082 reduced skatole-induced cell survival and the mRNA expression of IL-6 and TNF-α. NF-κB activation was attenuated by the extracellular signal-regulated kinase (ERK) pathway inhibitor U0126 and the p38 inhibitor SB203580, but not by the c-Jun N-terminal kinase (JNK) inhibitor SP600125...Moreover, the balance between NF-κB and AhR activation appears to govern the skatole-induced increases in IL-6 and TNF-α expression. Therefore, the present findings provide new insights into the mechanisms linking tryptophan-derived gut microbiota metabolites with colorectal disease.
Journal
|
IL6 (Interleukin 6) • TNFA (Tumor Necrosis Factor-Alpha) • MAPK8 (Mitogen-activated protein kinase 8)
|
IL6 expression
|
Bay11-7082 • SP600125
1m
Early divergent modulation of NLRP2's and NLRP3's inflammasome sensors vs. AIM2's one by signals from Aβ•Calcium-sensing receptor complexes in human astrocytes. (PubMed, Brain Res)
These effects were specific, being significantly hindered by NPS2143 and inhibitors of PI3K (LY294002), AMPKα (Dorsomorphin), mTOR (Torin1), and JAK/TYK (Brepoticinib). The neatly divergent modulation of NLRP3's vs. AIM2's PRR proteins by Aβ•CaSR cues and by Bay11-7082 suggests that, when bacterial or viral DNA fragments are absent, AIM2 might play "anti-inflammasomal" or other roles in HCAs. However, Bay11-7082's no effect on NLRP2 PRR overexpression also reveals that CaSR's downstream mechanisms controlling inflammasomes' sensors are quite complex in HCAs, and hence, given AD's impact on human health, well worth further studies.
Journal
|
IL6 (Interleukin 6) • IL18 (Interleukin 18) • AIM2 (Absent In Melanoma 2) • IL1B (Interleukin 1, beta) • NLRP3 (NLR Family Pyrin Domain Containing 3) • NLRP2 (NLR Family Pyrin Domain Containing 2)
|
LY294002 • Torin1 • dorsomorphin (Compound C) • Bay11-7082
2ms
HSP70 promotes pancreatic cancer cell epithelial-mesenchymal transformation and growth via the NF-κB signaling pathway. (PubMed, Pancreas)
HSP70 promotes the EMT and enhances pancreatic cancer cell proliferation, migration, and invasion by activating the NF-κB pathway.
Journal
|
CDH1 (Cadherin 1) • VIM (Vimentin) • CDH2 (Cadherin 2) • NFKBIA (NFKB Inhibitor Alpha 2) • RELA (RELA Proto-Oncogene)
|
VIM expression
|
Bay11-7082
3ms
Berberine suppressed the epithelial-mesenchymal transition (EMT) of colon epithelial cells through the TGF-β1/Smad and NF-κB pathways associated with miRNA-1269a. (PubMed, Heliyon)
SMAD2 and NF-κB p65 were overexpressed and transfected into cells, and the inhibitors SB431542 and BAY 11-7082 were added to block the TGF-β1/Smad and NF-κB pathways, respectively...BBR can significantly inhibit TGF-β1-induced EMT in normal and cancerous colon epithelial cells through the inhibition of the TGF-β1/Smad and NF-κB p65 pathways. TGF-β1/Smads can promote the NF-κB p65 pathway, which is a common target of miR-1269a, and can partially regulate the expression of miR-1269a.
Journal
|
CDH1 (Cadherin 1) • TGFB1 (Transforming Growth Factor Beta 1) • CDH2 (Cadherin 2) • MIR1269A (MicroRNA 1269a) • NFKBIA (NFKB Inhibitor Alpha 2) • RELA (RELA Proto-Oncogene) • SMAD2 (SMAD Family Member 2)
|
CDH1 expression
|
Bay11-7082
3ms
Eugenol: A Potential Modulator of Human Platelet Activation and Mouse Mesenteric Vascular Thrombosis via an Innovative cPLA2-NF-κB Signaling Axis. (PubMed, Biomedicines)
Our study uncovered a novel pathway in platelet activation involving the cPLA2-NF-κB axis, which plays a key role in the antiplatelet effects of eugenol. These findings suggest that eugenol could serve as a valuable and potent prophylactic or therapeutic option for arterial thrombosis.
Preclinical • Journal
|
PLCG2 (Phospholipase C Gamma 2) • NFKBIA (NFKB Inhibitor Alpha 2)
|
Bay11-7082
3ms
α-amanitin induce inflammatory response by activating ROS/NF-κB-NLRP3 signaling pathway in human hepatoma HepG2 cells. (PubMed, Chemosphere)
The inflammatory responses were reversed by NLRP3 inhibitor MCC950 and NF-κB inhibitor Bay11-7082. Additionally, N-acetylcysteine (NAC) blocked the upregulation of the NF-κB/NLRP3 signaling pathway and remarkably alleviated the inflammatory response. These results demonstrated that AMA could induce inflammation through activating the NLRP3 inflammasome triggered by ROS/NF-κB signaling pathway. Our research provides new insights into the molecular mechanism of AMA-induced inflammation damage and may contribute to establish new prevention strategies for AMA hepatotoxicity.
Journal
|
NLRP3 (NLR Family Pyrin Domain Containing 3)
|
Bay11-7082
4ms
In Vivo Effects of Bay 11-7082 on Fibroid Growth and Gene Expression: A Preclinical Study. (PubMed, Cells)
Ki67, CCND1, and E2F1 expression decreased with Bay treatment. This preclinical study suggests NF-kB inhibition as an effective fibroid treatment, suppressing genes involved in proliferation, inflammation, and ECM remodeling.
Preclinical • Journal
|
PGR (Progesterone receptor) • MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • CCND1 (Cyclin D1) • IL6 (Interleukin 6) • TNFA (Tumor Necrosis Factor-Alpha) • MIR200C (MicroRNA 200c) • VEGFC (Vascular Endothelial Growth Factor C) • TGFB1 (Transforming Growth Factor Beta 1) • PDGFA (Platelet Derived Growth Factor Subunit A) • TLR3 (Toll Like Receptor 3) • COL3A1 (Collagen Type III Alpha 1 Chain) • IL1B (Interleukin 1, beta) • TDO2 (Tryptophan 2,3-Dioxygenase) • TNFRSF11A (TNF Receptor Superfamily Member 11a) • CKS2 (CDC28 Protein Kinase Regulatory Subunit 2) • E2F1 (E2F transcription factor 1)
|
Bay11-7082
4ms
IκBα kinase inhibitor BAY 11-7082 promotes anti-tumor effect in RAS-driven cancers. (PubMed, J Transl Med)
Our study identifies BAY 11-7082 to be an efficacious inhibitor for treating RAS oncogene (HRAS, KRAS, and NRAS) mutant cancer cells. This finding provides new therapeutic opportunity for effective treatment of RAS-mutant cancers.
Journal
|
KRAS (KRAS proto-oncogene GTPase) • NRAS (Neuroblastoma RAS viral oncogene homolog) • HRAS (Harvey rat sarcoma viral oncogene homolog) • NFKBIA (NFKB Inhibitor Alpha 2)
|
Bay11-7082
5ms
Inhibition of STAT3-NF-κB pathway facilitates SSPH I-induced ferroptosis in HepG2 cells. (PubMed, Med Oncol)
Using HepG2 cells, we employed specific inhibitors (Stattic for STAT3 and Bay11-7082 for Nf-κB) and a ferroptosis inducer, SSPH I, to dissect their collective impact on ferroptosis...This study offers a deeper understanding of the ferroptosis mechanisms in HCC. It highlights the therapeutic potential of targeting STAT3 and Nf-κB pathways to enhance the efficacy of ferroptosis-based treatments.
Journal
|
GPX4 (Glutathione Peroxidase 4)
|
Bay11-7082
5ms
IL-32/NFκB/miR-205 loop sustains the high expression of IL-32 and enhances the motility of cervical cancer cells. (PubMed, Hum Cell)
Treatment with BAY11-7082 (an NFκB inhibitor) notably decreased miR-205 expression but had no effect on IL-32 levels...Knockdown of IL-32 significantly inhibited the migration and invasion of HeLa and SiHa; conversely, treatment with rIL-32α and rIL-32γ notably promoted their migration and invasion. In brief, IL-32 is highly expressed via the formation of a positive regulatory loop with NFκB/miR-205, contributing to the persistence of inflammation and promoting the progression of cervical cancer.
Journal
|
MMP2 (Matrix metallopeptidase 2) • NFKB1 (Nuclear factor of kappa light polypeptide gene enhancer in B-cells 1) • IL32 (Interleukin 32) • MMP9 (Matrix metallopeptidase 9) • MIR205 (MicroRNA 205)
|
Bay11-7082
6ms
Perfluorooctane sulfonate promotes the migration of colorectal cancer cells by inducing epithelial-mesenchymal transition. (PubMed, J Environ Sci (China))
In a mechanistic investigation, the up-stream signal pathway PI3K/Akt-NF-κB was activated by PFOS, and the process was suppressed by LY294002 (PI3K/Akt inhibitor) and BAY11-7082 (NF-κB inhibitor) respectively, leading to less proliferation of HCT116 cells. Taken together, our results indicated that PFOS promotes colorectal cancer cell migration and proliferation by activating the PI3K/Akt-NF-κB signal pathway and epithelial-mesenchymal transition. This could be a potential toxicological mechanism of PFOS-induced malignant development of colorectal cancer.
Journal
|
CXCL8 (Chemokine (C-X-C motif) ligand 8)
|
LY294002 • Bay11-7082
6ms
Se-methylselenocysteine inhibits the progression of non-small cell lung cancer via ROS-mediated NF-κB signaling pathway. (PubMed, Exp Cell Res)
Our investigation extended to the ROS-mediated NF-κB signaling pathway, utilizing western blot analysis, P65 overexpression, and the application of IκB-α inhibitor (BAY11-7082) or N-acetyl-cysteine (NAC) to elucidate MSC's mechanism of action...Moreover, MSC significantly curtailed tumor growth in vivo and disrupted the NF-κB signaling pathway. In conclusion, our research demonstrates that MSC exhibits anticancer effects against NSCLC by modulating the ROS/NF-κB signaling pathway, suggesting its potential as a therapeutic agent in NSCLC treatment.
Journal • PARP Biomarker
|
CDK4 (Cyclin-dependent kinase 4) • CDH1 (Cadherin 1) • CASP3 (Caspase 3) • CDKN1A (Cyclin-dependent kinase inhibitor 1A) • NFKBIA (NFKB Inhibitor Alpha 2) • RELA (RELA Proto-Oncogene) • SOD2 (Superoxide Dismutase 2)
|
Bay11-7082
8ms
Piperine alleviates nonalcoholic steatohepatitis by inhibiting NF-κB-mediated hepatocyte pyroptosis. (PubMed, PLoS One)
Pip ameliorates NASH progression, and the therapeutical effect was associated with inhibition of hepatocyte pyroptosis induced by NF-κB.
Journal
|
COL1A1 (Collagen Type I Alpha 1 Chain) • IL1B (Interleukin 1, beta) • NLRP3 (NLR Family Pyrin Domain Containing 3) • CASP1 (Caspase 1)
|
Bay11-7082
8ms
Saponins from Allium macrostemon Bulbs Attenuate Endothelial Inflammation and Acute Lung Injury via the NF-κB/VCAM-1 Pathway. (PubMed, Molecules)
By employing the NF-κB inhibitor BAY-117082, we demonstrated that the inhibitory effect of SAMB on VCAM-1 expression may be attributed to the NF-κB pathway's inactivation, as characterized by the suppressed IκBα degradation and NF-κB p65 phosphorylation. Subsequently, we employed a murine model of lipopolysaccharide-induced septic acute lung injury to substantiate the potential of SAMB in ameliorating endothelial inflammation and acute lung injury in vivo. These findings provide novel insight into potential preventive and therapeutic strategies for the clinical management of diseases associated with endothelial inflammation.
Journal
|
TNFA (Tumor Necrosis Factor-Alpha) • NFKBIA (NFKB Inhibitor Alpha 2) • VCAM1 (Vascular Cell Adhesion Molecule 1)
|
Bay11-7082
8ms
YY1 Contributes to the Inflammatory Responses of Mycobacterium tuberculosis-Infected Macrophages Through Transcription Activation-Mediated Upregulation TLR4. (PubMed, Mol Biotechnol)
Meanwhile, TLR4 inhibitor BAY11-7082 might overturn the repression effect of TLR4 on M.tb-infected HTP-1 cell damage. YY1-activated TLR4 might aggravate mycobacterial injury in human macrophages after M.tb infection by the NF-kB pathway, providing a promising therapeutic target for TB treatment.
Journal • IO biomarker
|
IL6 (Interleukin 6) • TNFA (Tumor Necrosis Factor-Alpha) • TLR4 (Toll Like Receptor 4) • IL1B (Interleukin 1, beta) • YY1 (YY1 Transcription Factor)
|
Bay11-7082
10ms
Gold Nanoparticles Downregulate IL-6 Expression/Production by Upregulating microRNA-26a-5p and Deactivating the RelA and NF-κBp50 Transcription Pathways in Activated Breast Cancer Cells. (PubMed, Int J Mol Sci)
The activity of RelA and NF-κBp50 was assessed and confirmed using Bay 11-7082...The GNP suppressed IL-6 overexpression and secretion by deactivating NF-κBp65/NF-κBp50 transcription activity and upregulating miR-26a-5p expression in activated BC cells. These findings suggest that GNP have potential as a therapeutic intervention for BC by targeting IL-6 expression and associated pathways.
Journal
|
IL6 (Interleukin 6) • MIR26A1 (MicroRNA 26a-1)
|
IL6 expression
|
Bay11-7082
10ms
Lactate dehydrogenase A promotes nasopharyngeal carcinoma progression through the TAK1/NF-κB Axis. (PubMed, Mol Biol Rep)
Our results suggest that LDHA and its major metabolite lactate drive NPC progression by regulating TAK1 and its downstream NF-κB signaling, which could become a therapeutic target in NPC.
Journal
|
LDHA (Lactate dehydrogenase A) • TGFB1 (Transforming Growth Factor Beta 1)
|
Bay11-7082
12ms
Qing Yan Li Ge Tang Induces Apoptosis in Human OEC-M1 Oral Cancer Cells. (PubMed, Altern Ther Health Med)
Additionally, QYLGT-activated c-Jun N-terminal kinase, extracellular signal-regulated kinase, p38 mitogen-activated protein kinase, and nuclear factor-kappa B (NF-κB), and the related inhibitors, including SP600125, PD184352, SB202190, and Bay11-7082, were used to confirm which signaling was involved in QYLGT-induced apoptosis. Moreover, only Bay11-7082, the NF-κB inhibitor, could suppress QYLGT-induced the release of cytokeratin 18 fragments from OEC-M1 cells. QYLGT induced apoptosis in OEC-M1 cells via the NF-κB pathway.
Journal • PARP Biomarker
|
CASP3 (Caspase 3) • CASP8 (Caspase 8) • CASP9 (Caspase 9) • MAPK8 (Mitogen-activated protein kinase 8)
|
CI-1040 • SB202190 • Bay11-7082 • SP600125
1year
Matrine alleviates hypoxia-induced inflammation and pulmonary vascular remodelling via RPS5/NF-κB signalling pathway. (PubMed, J Biochem Mol Toxicol)
Matrine, sildenafil and NF-κB inhibitor Bay 11-7082 could reverse these changes and impel the cell cycle in phase S retardation, and reduced the expression of p50, p65, proliferating cell nuclear antigen (PCNA), Bcl-2. In addition, matrine could lower right ventricular systolic pressure and mean pulmonary artery pressure of rats, α-smooth muscle actin and PCNA expression in pulmonary artery media, the levels of tumor necrosis factor-α and interleuki-1β, thus improved hypoxia-induced PVR. This study indicated that matrine could alleviate inflammation and improve PVR through reversing the imbalance of proliferation and apoptosis of PASMCs, thus it had a therapeutic effect on HPAH.
Journal • IO biomarker
|
BCL2 (B-cell CLL/lymphoma 2) • TNFA (Tumor Necrosis Factor-Alpha) • PCNA (Proliferating cell nuclear antigen) • RELA (RELA Proto-Oncogene)
|
PCNA expression
|
Bay11-7082
1year
Inhibition of USP21 leads to ovarian carcinoma cell death by suppressing MAPK signaling. (PubMed, Biotechnol Appl Biochem)
Conversely, OE of USP21 promoted the cell proliferation of ovarian cancers and conferred resistance to BAY 11-7082. These findings provide evidences supporting the notion of USP21 as a promising therapeutic target for the treatment of ovarian cancer.
Journal
|
MAP2K2 (Mitogen-activated protein kinase kinase 2)
|
Bay11-7082
1year
Dendritic Cell-Derived Exosomes Stimulated by Treponema pallidum Induce Endothelial Cell Inflammatory Response through the TLR4/MyD88/NF-κB Signaling Pathway. (PubMed, ACS Infect Dis)
Additionally, suppression of the activity of NF-κB with BAY11-7082, an NF-κB inhibitor, also reduced the exosome-treated inflammatory response. Our results suggested that dendritic cell-derived exosomes stimulated by T. pallidum induced endothelial cell inflammation, and the TLR4/MyD88/NF-κB signal axis was activated, significantly increasing IL-1β, IL-6, and TNF-α expression. This may have a significant role in the vascular inflammatory response in syphilis, which would contribute to the understanding of the pathogenesis of syphilis and the host immunological response to T. pallidum.
Journal • IO biomarker
|
MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • IL6 (Interleukin 6) • TNFA (Tumor Necrosis Factor-Alpha) • TLR4 (Toll Like Receptor 4) • IL1B (Interleukin 1, beta)
|
IL6 expression
|
Bay11-7082
1year
Semaphorin4A promotes lung cancer by activation of NF-κB pathway mediated by PlexinB1. (PubMed, PeerJ)
Consistently, Sema4A promoted IL-6 production, which was down-regulated by PlexinB1 blocking antibody and BAY 11-7082. Sema4A may facilitate LC development via the activation of the NF-κB pathway mediated by PlexinB1, suggesting that Sema4A would be a novel therapeutic target for LC treatment.
Journal
|
IL6 (Interleukin 6) • STAT3 (Signal Transducer And Activator Of Transcription 3)
|
Bay11-7082
1year
The Expression and Activation of the NF-κB Pathway Correlate with Methotrexate Resistance and Cell Proliferation in Acute Lymphoblastic Leukemia. (PubMed, Genes (Basel))
Acute lymphoblastic leukemia (ALL) is the most common childhood cancer. At the individual gene level, NFKB1 expression was directly associated with a poorer clinical response to MTX and with both an increased TNF-α-triggered NF-κB activation and MTX resistance in the cell lines. Despite these results, the pharmacological inhibition (using BAY 11-7082 and parthenolide) or stimulation (using exogenous TNF-α supplementation) of the NF-κB pathway did not alter the MTX resistance of the cell lines significantly, evidencing a complex interplay between MTX and NF-κB in ALL.
Journal
|
TNFA (Tumor Necrosis Factor-Alpha)
|
NFKB1 expression
|
methotrexate • Bay11-7082
1year
NOTCH2 gene mutation and gamma-secretase inhibitor in mediating the malignancy of ovarian cancer. (PubMed, Aging (Albany NY))
Furthermore, the NOTCH2-mediated tumorigenesis was mostly reversed after NF-κB inhibitor Bay11-7082 treatment. These findings identified the NOTCH2 P2113S mutation in ovarian carcinogenesis, and NOTCH2 P2113S is a potential target in treating OC.
Journal • IO biomarker
|
BCL2 (B-cell CLL/lymphoma 2) • NOTCH2 (Notch 2) • BAX (BCL2-associated X protein) • HES1 (Hes Family BHLH Transcription Factor 1)
|
NOTCH2 mutation • NOTCH mutation
|
Bay11-7082
1year
GDNF triggers proliferation of rat C6 glioma cells via the NF-κB/CXCL1 signaling pathway. (PubMed, PLoS One)
Additionally, we used BAY 11-7082, a phosphorylation inhibitor of NF-κB, to elucidate NF-κB mediated the effect of GDNF on CXCL1. These results demonstrated that GDNF enhanced the proliferation of rat C6 glioma cells through activating the NF-κB/CXCL1 signaling pathway. In summary, these studies not only revealed the mechanism of action of exogenous GDNF in promoting the proliferation of C6 glioma cells but may also provide a new biological target for the treatment of malignant glioma.
Preclinical • Journal
|
CXCL1 (Chemokine (C-X-C motif) ligand 1)
|
Bay11-7082
over1year
Therapeutic efficacy of the resorcylic acid lactone LL-Z1640-2 for adult T-cell leukaemia/lymphoma. (PubMed, EJHaem)
LL-Z1640-2 as well as the NF-κB inhibitor BAY11-7082 decreased the expression of IRF4 and MYC at the protein and mRNA levels, indicating the suppression of the NF-κB-IRF4-MYC axis...Therefore, LL-Z1640-2 appears to be an effective treatment for ATL. Further studies are needed to develop more potent compounds that retain the active motifs of LL-Z1640-2.
Journal
|
MYC (V-myc avian myelocytomatosis viral oncogene homolog) • STAT3 (Signal Transducer And Activator Of Transcription 3) • IL2 (Interleukin 2) • MAPK1 (Mitogen-activated protein kinase 1) • TGFB1 (Transforming Growth Factor Beta 1)
|
MYC expression • IRF4 expression
|
Bay11-7082
over1year
PHF6 maintains acute myeloid leukemia via regulating NF-κB signaling pathway. (PubMed, Leukemia)
Treating PHF6 over-expressed myeloid leukemia cells with NF-κB inhibitor (BAY11-7082) significantly increased their apoptosis and decreased their proliferation. Taken together, in contrast to PHF6 as a tumor suppressor in T-ALL as reported, we found that PHF6 also plays a pro-oncogenic role in myeloid leukemia, and thus potentially to be a therapeutic target for treating myeloid leukemia patients.
Journal • IO biomarker
|
BCL2 (B-cell CLL/lymphoma 2) • RUNX1 (RUNX Family Transcription Factor 1) • PHF6 (PHD Finger Protein 6)
|
BCL2 expression
|
Bay11-7082
over1year
NF-κB pathway affects silica nanoparticle-induced fibrosis via inhibited inflammatory response and epithelial-mesenchymal transition in 3D co-culture. (PubMed, Toxicol Lett)
Conversely, utilizing the NF-κB-specific inhibitor BAY 11-7082 effectively downregulated the expression of TNF-α, IL-6, interleukin-1β (IL-1β), N-cad, α-SMA, collagen-I (COL I), and fibronectin (FN), the expression of E-cad was upregulated. These findings suggest that NF-κB is involved in regulating SiNPs-induced inflammatory, EMT, and fibrosis in the 3D co-culture state.
Journal
|
IL6 (Interleukin 6) • TNFA (Tumor Necrosis Factor-Alpha) • CDH1 (Cadherin 1) • FN1 (Fibronectin 1) • CDH2 (Cadherin 2) • IL1B (Interleukin 1, beta)
|
IL6 expression
|
Bay11-7082
over1year
Acyclic retinoid peretinoin reduces hemorrhage-associated brain injury in vitro and in vivo. (PubMed, Eur J Pharmacol)
On the other hand, nuclear factor-κB (NF-κB) inhibitors such as pyrrolidine dithiocarbamate (50 μM) and Bay11-7082 (10 μM) prevented thrombin-induced shrinkage of the striatal region...We also found that daily administration of peretinoin reduced histopathological injury and alleviated motor deficits in a mouse model of intracerebral hemorrhage. These results indicate that NR1B agonists including peretinoin may serve as a therapeutic option for hemorrhagic brain injury.
Preclinical • Journal
|
Amnolake (tamibarotene) • Bay11-7082 • peretinoin (K-333)
over1year
Therapeutic Potential of BAY-117082, a Selective NLRP3 Inflammasome Inhibitor, on Metastatic Evolution in Human Oral Squamous Cell Carcinoma (OSCC). (PubMed, Cancers (Basel))
Additionally, BAY-117082 treatment modulated the epithelial-mesenchymal transition (EMT) process in tongue tissue as well as in metastatic organs such as lymph node, lung, and spleen, also reducing the expression of matrix metalloproteinases (MMPs), particularly MMP2 and MMP9, markers of cell invasion and migration. In conclusion, the obtained data demonstrated that BAY-117082 at doses of 2.5 mg/kg and 5 mg/kg were able to reduce the tongue tumor area as well as the degree of metastasis in lymph node, lung, and spleen tissues through the NLRP3 inflammasome pathway inhibition.
Journal • Metastases
|
MMP2 (Matrix metallopeptidase 2) • MMP9 (Matrix metallopeptidase 9) • NLRP3 (NLR Family Pyrin Domain Containing 3)
|
Bay11-7082
over1year
Replication of Porcine Astrovirus Type 1-Infected PK-15 Cells In Vitro Affected by RIG-I and MDA5 Signaling Pathways. (PubMed, Microbiol Spectr)
Treatment of PAstV1-infected cells with the interferon regulatory factor 3 (IRF3) inhibitor BX795 decreased IFN-β expression, whereas the nuclear factor kappa light chain enhancer of activated B cells (NF-κB) inhibitor BAY11-7082 did not...In addition, the knockdown of RIG-I and MDA5 attenuated the production of IFN-β induced by PAstV1 in PK-15 cells and increased efficient viral replication in vitro. We believe that these findings will help us to better understand the mechanism of how AstVs affect the host IFN response.
Preclinical • Journal
|
IFIH1 (Interferon Induced With Helicase C Domain 1) • IFNB1 (Interferon Beta 1)
|
Bay11-7082
over1year
Sodium selenite inhibits proliferation of lung cancer cells by inhibiting NF-κB nuclear translocation and down-regulating PDK1 expression which is a key enzyme in energy metabolism expression. (PubMed, J Trace Elem Med Biol)
In vitro experiment showed that SSe could inhibit the activation of NF-κB signaling pathway, knowing that NF-κB is an important intracellular nuclear transcription factor that regulates the expression of pyruvate dehydrogenase kinase 1 (PDK1), a key energy metabolism switch affecting the survival status of the whole cell.At the same time, Bay11-7082(NF-κB signaling pathway inhibitors) and SSe resulted in phosphorylation of p65 and IκBα, decreased expression of PDK1 and Bcl-2,and increased expression of Bax in lung cancer cells...The in vivo experiment revealed that SSe inhibited the activation of NF-κB signaling pathway, decreased the expression of PDK1, and induced lung cancer cell proliferation and apoptosis. All these findings indicated that SSe promoted lung cancer cell apoptosis by inhibiting the activation of NF-κB signaling pathway, down-regulating PDK1 and activating mitochondrial apoptosis pathway.
Journal • IO biomarker
|
BCL2 (B-cell CLL/lymphoma 2) • BAX (BCL2-associated X protein) • NFKBIA (NFKB Inhibitor Alpha 2) • PDK1 (Pyruvate Dehydrogenase Kinase 1)
|
BCL2 expression • BAX expression
|
Bay11-7082
over1year
Regulation of programmed death ligand 1 expression by interferon-γ and tumour necrosis factor-α in canine tumour cell lines. (PubMed, Vet Comp Oncol)
The expression level of cell surface PD-L1 induced by IFN-γ and TNF-α treatment was reduced by oclacitinib and BAY 11-7082, respectively, indicating that upregulation of PD-L1 expression by IFN-γ and TNF-α stimulation is regulated via the JAK-STAT and NF-κB signalling pathways, respectively. These results provide insights into the role of inflammatory signalling in PD-L1 regulation in canine tumours.
Clinical • Preclinical • Retrospective data • Review • Journal • PD(L)-1 Biomarker • IO biomarker • Tumor cell
|
PD-L1 (Programmed death ligand 1) • IFNG (Interferon, gamma) • STAT3 (Signal Transducer And Activator Of Transcription 3) • STAT1 (Signal Transducer And Activator Of Transcription 1) • RELA (RELA Proto-Oncogene)
|
PD-L1 expression • IFNG expression
|
Bay11-7082
over1year
Simultaneously Targeting Two Coupled Signalling Molecules in the Mesenchymal Stem Cell Support Efficiently Sensitises the Multiple Myeloma Cell Line H929 to Bortezomib. (PubMed, Int J Mol Sci)
PKC-mediated cell survival inhibition and bortezomib susceptibility induction were better performed by the chimeric peptide HKPS than by the classical enzastaurin inhibitor, probably due to its greatest ability to inhibit cell adhesion and its increased capability to counteract the NF-κB-related signalling molecules increased by the co-cultivation of BM-MSC with H929 cells. Considering that H929 cells were also directly susceptible to PKC and NF-κB inhibition, we showed that treatment of co-cultures with the HKPS peptide and BAY11-7082, followed by bortezomib, increased H929 cell death. Therefore, targeting simultaneously connected signalling elements of BM-MSC responsible for MM cells support with compounds that also have anti-MM activity can be an improved treatment strategy.
Preclinical • Journal
|
bortezomib • Kinenza (enzastaurin) • Bay11-7082
over1year
Focused ultrasound restrains the growth of orthotopic colon cancer is via promoting pyroptosis. (PubMed, Folia Histochem Cytobiol)
Our results pointed out that FUS presented anti-tumor activity in experimental CC, and its mechanism was correlated with the promotion of pyroptosis.
Journal
|
IL18 (Interleukin 18) • IL1B (Interleukin 1, beta) • NLRP3 (NLR Family Pyrin Domain Containing 3)
|
Bay11-7082
over1year
Induction of Antimicrobial Protein S100A15 Expression by Oral Microbial Pathogens Is Toll-like Receptors-Dependent Activation of c-Jun-N-Terminal Kinase (JNK), p38, and NF-κB Pathways. (PubMed, Int J Mol Sci)
Pre-treatment of GF and KB cells with JNK (SP600125), p38 (SB-203580), or NF-κB (Bay11-7082) specific inhibitors further demonstrates the importance of JNK, p38 and NF-κB pathways in the regulation of gram/gram bacterial pathogen-induced S100A15 expression. Our data provide evidence that S100A15 is induced in cancer and non-cancer oral mucosa-derived cell lines by gram/gram bacterial pathogens and provide insight into the molecular mechanisms by which gram and gram bacterial pathogens induce S100A15 expression in the oral mucosa.
Journal • IO biomarker
|
TLR4 (Toll Like Receptor 4) • MAPK8 (Mitogen-activated protein kinase 8) • TLR2 (Toll Like Receptor 2)
|
Bay11-7082 • SP600125
almost2years
DNA damage to bone marrow stromal cells by anti-leukemia drugs induces chemo-resistance in acute myeloid leukemia via paracrine FGF10-FGFR2 signaling. (PubMed, J Biol Chem)
Here, we determined anti-leukemia drugs induce DNA damage in bone marrow stromal cells (BMSCs), resulting in resistance of AML cell lines to adriamycin and idarubicin killing. Damaged BMSCs induced an inflammatory microenvironment through NF-κB; suppressing NF-κB with small molecule inhibitor Bay11-7082 attenuated the pro-survival effects of BMSCs on AML cell lines...Finally, release of FGF10 was mediated by β-catenin signaling in damaged BMSCs. Our data indicate FGF10-FGFR2 signaling acts as an effector of damaged BMSC-mediated chemo-resistance in AML cells, and FGFR2 inhibition can reverse stromal protection and AML cell chemo-resistance in the BMM.
Journal
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FGFR2 (Fibroblast growth factor receptor 2) • FGFR1 (Fibroblast growth factor receptor 1) • FGF10 (Fibroblast Growth Factor 10)
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FGFR1 expression
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doxorubicin hydrochloride • idarubicin hydrochloride • Bay11-7082
almost2years
TLR9 Exerts an Oncogenic Role in Promoting Osteosarcoma Progression Depending on the Regulation of NF-κB Signaling Pathway. (PubMed, Biol Pharm Bull)
Moreover, the nuclear factor kappa B (NF-κB) signaling pathway was activated by TLR9, and TLR9-induced malignant phenotype of OS cells was abrogated by the NF-κB antagonist BAY11-7082. Our study indicated that TLR9 might play a critical role in facilitating OS progression by activating the NF-κB signaling pathway, which may provide a valuable therapeutic target for OS.
Journal • IO biomarker
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CCND1 (Cyclin D1) • MMP2 (Matrix metallopeptidase 2) • TLR9 (Toll Like Receptor 9) • CDK2 (Cyclin-dependent kinase 2) • MMP9 (Matrix metallopeptidase 9)
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CCND1 expression • TLR9 expression • CDK2 expression
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Bay11-7082
2years
Tumor-promoting properties of enolase-phosphatase 1 in breast cancer via activating the NF-κB signaling pathway. (PubMed, Mol Biol Rep)
These findings indicated the significance of ENOPH1 in promoting cell proliferation and invasion, mainly through activating the NF-κB pathway, suggesting that ENOPH1 might be an attractive prognostic factor and a potential target for BC therapy.
Journal
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RELA (RELA Proto-Oncogene)
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Bay11-7082