NKIRAS2 (NFKB Inhibitor Interacting Ras Like 2)

Mechanistically, decreased oar-miR-125b expression relieves its repression of TNFSF4, leading to NF-κB pathway activation and blood-brain barrier disruption. Collectively, our results demonstrate that oar-miR-125b serves as a key anti-inflammatory regulator in bacterial meningitis by targeting TNFSF4 and constraining NF-κB signaling, highlighting its potential as a therapeutic target for attenuating neuroinflammation in meningitis.

Our findings demonstrate the feasibility of combining spatial transcriptomics with AI-driven histopathological analysis for biomarker validation. This integrative framework provides a foundation for future population-scale studies leveraging spatial omics to evaluate arsenic-associated gene signatures and assess their relevance in bladder cancer risk stratification and disease progression.

In summary, our findings indicate that artificially synthesized MIR4726EccDNA is functional in cells and that MIR4726EccDNA enhances tumor progression and partially mediates drug resistance by enhancing MIR4726-5p/NXF1/NKIRAS2 axis dependent autophagy.

GFOD1 may promote the proliferation, migration, and invasion of KIRC. Our findings may provide new prognostic biomarkers and potential therapeutic targets for KIRC patients.

Putting it all together, identifying the precise mechanisms of miR-4492 in the pathogenesis of cancer, could pave the way to find better diagnostic and therapeutic strategies for cancer sufferers. For this reason, it might be a novel potential diagnostic biomarker and therapeutic target for neoplasms.

Reduced expression of human NKIRAS1 alone is associated with worse prognosis in at least four cancer types and linked to a network of genes implicated in tumorigenesis. Our findings provide direct evidence that loss of NKIRAS1 in human tumors that do not carry oncogenic RAS mutations is associated with worse clinical outcomes.

Upregulation of NKIRAS2 led to the deceased level of IκBβ but increased levels of nuclear p65, thus activating the NF-κB signaling pathway. In conclusion, Circ_0001955 activates the NF-κB pathway to promote NSCLC cell proliferation and invasion by regulating miR-29a-3p/NKIRAS2 axis.

Selinexor (an inhibitor of XPO1) could effectively inhibit the proliferation of bladder cancer in the cell proliferation experiments by CCK-8 assays and it could suppress the growth of bladder cancer in mouse bladder cancer model. In this study, a prognostic model with seven hub genes has provided great help for the prognosis prediction of bladder cancer patients. And XPO1 is an important target affecting the prognosis of bladder cancer, and inhibition of XPO1 can effectively inhibit bladder cancer proliferation and growth.

On the other hand, several studies showed that arsenic trioxide (ATO) is useful for anticancer therapy although the mechanisms underlying its paradoxical effects are still not well understood...The study identified a unique set of 147 genes associated with arsenic exposure and linked to molecular mechanisms of cancer. The risk prediction model shows the highest prediction ability for recurrent bladder tumors based on a very small subset (NKIRAS2, AKTIP, and HLA-DQA1) of the 147 genes resulting in AUC of 0.94 (95% CI: 0.744-0.995) and 0.75 (95% CI: 0.343-0.933) on training and validation data, respectively.