Bay11-7082

This mechanism can be effectively inhibited by silencing CXCR2 or by employing the NF-κB inhibitor BAY 11-7082...Additionally, in EC tissue samples, CXCL1 and CXCR2 expression, as well as the extent of macrophage infiltration, exhibited a significant positive relationship with disease progression, suggesting an unfavorable prognosis. In conclusion, targeting the CXCL1/CXCR2 axis is a potential therapeutic approach for EC treatment.

GSDME functions as a tumor suppressor by enhancing radiosensitivity and inhibiting proliferation and migration in ESCC, through the suppression of the NF-κB signaling pathway. These findings nominate GSDME as a promising biomarker and the NF-κB signaling pathway as a therapeutic target for overcoming radioresistance in ESCC.

Differentiated adipocytes were used for (1) treatment with 0, 5, 10, or 15 ng/mL of GH for 8 h, or 15 ng/mL of GH for 0, 4, 8 or 12 h; (2) co-treatment with 15 ng/mL GH and 0.1 ng/mL tumor necrosis factor α (TNF-α); (3) pretreatment with 10 μM BAY 11-7082, a nuclear factor kappa B (NF-κB) inhibitor, and then treatment with 15 ng/mL GH...Furthermore, TNF-α exacerbated GH-induced lipolysis and inflammation, whereas inhibition of NF-κB signaling pathway partially reverses these metabolic alterations of GH-treated adipocytes. These findings suggested that GH promote lipolysis in bovine adipocytes by activating inflammatory pathways.

A nuclear factor-kappa B (NF-κB) inhibitor, BAY11-7082, and a cyclooxygenase 2 (COX2) inhibitor, celecoxib, significantly inhibited PGE2 secretion, indicating that NF-κB and COX2 played a crucial role in reovirus-induced PGE2 production. These results indicate that reovirus replication in tumor cells is important for reovirus-induced PGE2 production. Attention should be paid to possible PGE2 production in tumors following reovirus treatment.

Mechanistically, SUN5 activates the NF-κB signaling pathway, which can be inhibited by the IKK inhibitor BAY11-7082...Moreover, xenograft transplantation experiments reveal that the knockdown of SUN5 inhibits glycolysis and tumorigenesis in vivo. Taken together, these findings indicate that SUN5 enhances the glycolysis and tumorigenesis of CRC cells via interaction with TRIM28, which provides a potential target for the diagnosis and treatment of CRC.

These findings underscore the critical role of peripheral nerve injury in reshaping the interplay between TAMs and antitumor immunity, via NFL-driven NF-κB activation and T cell dysfunction. Suggesting that neuroprotection could serve as a promising strategy to restore anticancer immunosurveillance.

However, NF-κ B signaling pathway inhibitor BAY11-7082 improved the above indicators. Animal studies revealed that TMAO induced intracranial inflammation, affected the expression of functional proteins in the cerebral lymphatic system, and intensified SNCA aggregation in the mouse brain. TMAO can activate the NF-κB signaling pathway and damage the cellular function of brain glymphatic system and meningeal lymphatic vessels, and promote intracranial inflammation and SNCA deposition in mice, which may be a potential mechanism for TMAO involvement in neurodegenerative diseases.

Notably, when NF-κB was inhibited (BAY11-7082) alongside MALAT1 overexpression, the reversal effect was abolished. Taken together, our findings suggest that decreased DNA hypomethylation mediated by DNMT1 leads to increased MALAT1 expression, subsequently activating the NF-κB pathway in ASCVD.

ALOX5 overexpression promoted the release of LDH, PI-positive cells, pyroptosis related protein expression, oxidative stress and inflammatory cytokine release induced by Ang II in MA-VSMCs, while they were reversed by BAY11-7082 (BAY, NF-κB inhibitors)...The addition of NF-κB pathway inhibitor BAY inhibited the increase of inflammatory factors and pyroptosis caused by ALOX5 overexpression. These results indicated that ALOX5 promoted pyroptosis through NF-κB pathway, and then promoted AAA development.

We further demonstrate that the NF-κB inhibitor BAY11-7082 directly interacts with RNF25, reversing its pro-survival effects and restoring apoptosis sensitivity. Our findings establish RNF25 as a druggable orchestrator of therapy resistance through NF-κB pathway modulation and propose pharmacological targeting of RNF25 by BAY11-7082 as a strategy to overcome apoptosis resistance in renal malignancies.

While NF-κB signaling was activated in treated cells, indium-dependent changes of CDH1 and SNAI1 mRNA expression were not affected by BAY 11-7082, an NF-κB inhibitor, suggesting that NF-κB activation may be dispensable for indium-induced EMT...Overall, our study is the first to demonstrate that EMT is caused by indium compounds. This will contribute biologically to understanding the mechanism of EMT induction and clinically to unveiling the pathophysiology of indium lung disease.

Furthermore, BAY 11-7082, an inhibitor of the NF-κB signalling pathway, reversed the promotion of PTC proliferation and metastasis by P4HA2 both in vivo and in vitro. In conclusion, P4HA2 activates the NF-κB signaling pathway by promoting proteasome-dependent degradation of IκBα, which in turn contributes to the proliferation and migration of PTC. Therefore, P4HA2 could be used as a potential therapeutic target for the treatment of PTC patients.