NOX5 (NADPH Oxidase 5)

Furthermore, the phyllanhtin was semi-synthetically modified to give phyllanthin oxadiazole derivatives and was evaluated for neuroprotective activity in scopolamine-injured neuroblastoma-2a (N2A) cells...Furthermore, in silico docking studies predicted phyllanthin derivatives 21 and 31 exhibit neuroprotective activity by binding to the human NADPH-oxidase 5 enzyme. Thus, compounds 21 and 31 can be considered potential neuroprotective leads.

Enrichment analysis indicated that the DEMs (e.g., indole compounds, organic acids, aldosterone, L-kynurenine) and DEGs (pgd, mthfr, nsdhl, nox5, prdx2, mpx, itih2, itih3, eprs1) that were highly and significantly expressed in the 25(OH)D3 group were primarily associated with antioxidant defense and inflammatory responses. Dietary 25(OH)D3 was more effective than VD3 in promoting antioxidant capacity and modulating inflammation in yellow catfish.

Knockdown of NOX5 abolished the effects of Dexmedetomidine in telomerase activity, gene expression of hTERT and TERF2, the p53/p16 signaling, as well as cellular senescence, suggesting that the effects of Dexmedetomidine are mediated by NOX5. In summary, these findings show that Dexmedetomidine blunts the growth of lung cancer cells by inducing premature senescence via ROS-mediated DNA damage.

Finally, using the Genomics of Drug Sensitivity in Cancer and Cancer Therapeutics Response Portal databases, potential drugs [(5Z)-7-oxozeaenol, selumetinib, RDEA119, AZ628, dabrafenib and trametinib] were identified based on the aforementioned seven key carcinogenic genes, focusing on those that targeted multiple genes. In conclusion, the present study identified 14 key ferroptosis-related genes, and seven key carcinogenic genes, which represent promising novel molecular targets for the prognosis and treatment of GC.

The potential TGFβ1 increase and the persistence of NADPH oxidases induction represents long term cellular damage, affecting tissue protection and tumor sensitization. The bystander effect on cell migration demonstrate the importance of the impact of radiotherapy out of the field of irradiation.

We found that 9a, bearing a pargyline moiety, is also able to selectively inhibit MAOB over MAOA (465-fold) with an IC50 of 0.182 μM, being the first-in-class dual NOX2/MAOB covalent inhibitor. Tested in the BV2 microglia neuroinflammation model, 9a decreased ROS production and downregulated proinflammatory cytokines as iNOS, IL-1β, and IL-6 expression more efficiently than the single target inhibitors (rasagiline for MAOB and VAS2870 for NOXs) but also, more importantly, than their combination.

In addition, combination of PD and OXA synergistically exerted anti-CRC activities by promoting DNA damage and activating ER stress signaling pathway. The combination of PD and OXA could be an effective treatment strategy for certain patients with CRC.

BAY11-7082, which is an inhibitor of the inhibitor of nuclear factor κB protein α(IκBα), was used to explore the effect of the expression of phosphorylated nuclear factor κB(p-NF-κB) in the nucleus after the Fur treatment on the NOX4 protein level...In the stably transfected cell strain with PRDX1 gene knockout, the apoptosis rate is considerably higher than that of the negative control group after Fur treatment. The above results indicate that Fur can induce the apoptosis of colorectal cancer cells by promoting the signal transduction of NF-κB in the nucleus and increasing the generation of mitochondrial ROS derived from NOX4 to inhibit the PRDX1 protein expression.

Soluble molecules such as TGF-β and EGF modulate NOX protein activation, enhancing cell invasion through localized ROS production. This review focuses on elucidating the specific role of NOX proteins in regulating signaling pathways promoting cancer cell spread, particularly EMT, invadopodia formation and invasive capacity.

Furthermore, the present study indicated that TPA‑induced MMP‑9 expression and cellular invasion were mediated through PKC, thus linking the NOX1 and 5/ROS signaling pathways. These findings offer novel insights into the potential mechanisms underlying their anti‑invasive effects in breast cancer.

Mice xenograft model further confirmed the synergistic antitumor efficacy of combined therapy with PD and cisplatin. The present study exhibited a superior therapeutic strategy for some patients with NSCLC by combining PD and cisplatin.

We find that calcium binding to the EF-hand domain increases NADPH dynamics, permitting electron transfer between NADPH and FAD and superoxide production. Our structural findings also uncover a zinc-binding motif that is important for NOX5 stability and enzymatic activity, revealing modulation mechanisms of reactive oxygen species (ROS) production.