CPLX2 (Complexin 2)

Treatment with sEV-miR-206-3p effectively mitigated these alterations, reducing oxidative stress, suppressing neuroinflammatory responses, restoring mitochondrial function and synaptic protein levels, and attenuating tau and Aβ pathology. These findings demonstrate that miR-206-3p-loaded sEVs protect neuroblastoma cells from Aβ-induced neurodegenerative processes, highlighting their potential as a novel drug delivery system for neuroprotection.

Functionally, IL-27 blockade accelerated tumor growth, whereas recombinant IL-27 restrained tumor progression and enhanced PD-L1/CTLA-4 blockade efficacy by augmenting Th1 and cytotoxic T cell responses. These findings define a TME-based prognostic classifier and position IL-27 as a stage-dependent therapeutic target that restores T cell immunity and boosts checkpoint blockade efficacy.

The results confirmed that CPLX2 and SNAP25 positively regulated the phosphatidylinositol 3 kinase-AKT signaling pathway and promoted the progression of liver metastasis of colorectal cancer. CPLX2 and SNAP25 genes are overexpressed in colorectal cancer liver metastasis and may serve as important molecular targets.

The integration of bioinformatics and machine learning in this study underscores a strong correlation between FRG expression patterns and BRCA prognosis, affirming their potential as precise biomarkers for personalized immunotherapy.

In HT22 neuronal cells subjected to OGD/R, pretreated with NAD+ (100 μM) for 12 h significantly increased the cell viability, decreased the LDH levels, and inhibited the ferroptosis evidenced by the changes in redox-related parameters including concentrations of Fe2+, GSH, MDA, H2O2 as well as the expression of GPX4 and SLC7A11. CPLX2 knockdown in HT22 neuronal cells blocked the protective effects of NAD+ as in HI mice, whereas CPLX2 overexpression enhanced the inhibitory effects of NAD+ on ferroptosis in HT22 neuronal cells.

The constructed prognostic model showed promise in predicting the survival of LUAD patients. Notably, KCTD12 and CCT6A might be candidate biomarkers for improving diagnostic performance and guiding individualized therapy for EGFR-TKI-resistant LUAD patients.

Our data indicated that CPLX2 functions as a tumor suppressor and could be used as a potential prognostic marker in glioma.

Upregulation of ZNF777, TCOF1, CPLX2, and ABL1 was associated with a poor prognosis, whereas upregulation of ZER1, VPS53, and RRBP1 was associated with a good prognosis. This study provides potential therapeutic targets for LUAD and a basis for further studies on the mechanism underlying the effects of ALKBH5.

In summary, our study constructed a risk model composed of ARGs, which could be used as a solid model for predicting the survival and prognosis of BC patients. Moreover, this model also played an important role in tumor immunity, providing a new direction for patient immune status assessment and immunotherapy selection.