EIF6 (Eukaryotic Translation Initiation Factor 6)

3-ICA, a metabolite of D. newyorkensis, also suppressed CRC progression. eIF6 deficiency exerts protective effects against CRC through the enrichment of D. newyorkensis and its metabolite 3-ICA, revealing a novel mechanism and potential therapeutic strategy for CRC.

Moreover, inhibition of INCENP and CDCA8 enhances NACT sensitivity by promoting multipolar spindle formation. Collectively, our findings establish that INCENP and CDCA8 serve as crucial biomarkers for predicting NACT responsiveness and as potential therapeutic targets for combination therapy with NACT to improve patient survival.

Drug screening identified 22 potential therapeutic compounds, with trichostatin A showing optimal binding affinity. These findings establish TMOD2 and DOCK4 as novel biomarkers linking GM dysbiosis to CRA development, opening new avenues for microbiome-targeted early intervention strategies.

Silencing circEIF6 suppressed glycolysis, angiogenesis, and proliferation (P<0.05) by sponging miR-296-3p to downregulate MT2A. We conclude that circEIF6 promotes aerobic glycolysis and angiogenesis in TNBC via the miR-296-3p to target MT2A.

Additionally, we identified four potential drug targets, including PFAS, EIF2S3, EIF6, and NFKB2. Molecular docking analysis suggested that neratinib, a clinically approved drug, could serve as a promising therapeutic agent for GSRCC, offering new avenues for clinical intervention.

C5ORF13 drives the malignant progression of HCC by increasing eIF6 levels, including proliferation, invasion, migration, and the EMT process. VPA, as an eIF6 inhibitor, shows potential application value in the treatment of HCC.

Our results show that DIALRP is utilized as a robust and cost-effective approach for investigating redox-regulated cellular processes. Moreover, these findings provide significant insights into translation regulation under oxidative stress and provide a valuable framework for future studies on redox-mediated cellular processes.

Both models exhibited satisfactory calibration after updating in external validation. The models' web calculator is provided at https://lhj0520.shinyapps.io/M7G-LGG_model/ .

This study reveals the new role of CSDE1 in enhancing resistance to genotoxic drugs, and the detailed zipper-like cross ternary structural of CSDE1. It provides a new strategy for enhancing genotoxic drugs sensitivity.

Knockdown of eIF3a inhibited EndMT in PAECs regulating TGFβ1/SMAD signaling pathway, significantly alleviated the changes of RVSP, RVH and vascular remodeling in MCT-induced PAH rats, eIF3a may be a promising and novel therapeutic target for the treatment of PAH.

Besides, ROBO1-mediated eIF3A degradation interrupted P53 translation process which in turn provoked downstream mTOR signaling and increased DNA repair associated genes expressions, resulting in radio-resistance enhancement in cancer cells. In conclusion, our findings revealed a novel role of eIF3A in modulating P53/mTOR signaling activity and provided a drug candidate (ROBO1) for overcoming radio-resistance in esophageal cancer.

This facilitates delivery of eukaryotic initiation factor 6 (eIF6), a key 60S biogenesis factor, which binds to CRNDEUCE through a sequence element adjacent to the UCE. These findings highlight the functional versatility of snoRNA sequences and expand the known mechanisms through which noncoding RNAs orchestrate ribosome biogenesis.