Our findings provide valuable insights into the roles of m6A demethylation-mediated upregulation of SH3RF3-AS1 in supporting glioma proliferation and demonstrate the potential of NanoPCPT/siRNA@U251 as an innovative chemotherapeutic strategy for glioma.
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RAC1 (Rac Family Small GTPase 1) • ALKBH5 (AlkB Homolog 5, RNA Demethylase)
Additionally, CMA is involved in epigenetic silencing of the cGAS-STING pathway, promoting tumor immune escape via lysosomal degradation of the DNA demethylase TET3. Inhibition of CMA synergizes with immune checkpoint therapy in glioblastoma models, highlighting a potential therapeutic target.
Conversely, miR-101-mediated suppression of METTL3 disrupts EIF3J-AS1-FOXG1 binding, restoring MIF expression and promoting autophagy. These findings highlight EIF3J-AS1 and METTL3 as potential therapeutic targets, with disruption of EIF3J-AS1-FOXG1 interactions representing a novel autophagy-modulating strategy for glioma treatment.
The study we conducted establishes the groundwork for comprehending the function of anoikis genes in glioma, and recognizes PLAU as a potential biomarker for glioma.
In vivo, NRTL-24 demonstrated superior tumor-targeting ability, significantly prolonging median survival compared to untreated and temozolomide-treated groups while maintaining favorable safety. This NQO1-responsive linker technology enables precise payload activation in tumor while minimizing off-target effects, establishing NRTL-24 as a promising therapeutic candidate. The strategy provides a blueprint for enzyme-targeted ADC development through tumor- selective linker design.
This well-characterized model provides a physiologically and functionally relevant platform for further dissecting the reciprocal interactions present between various brain cancer cells and vascular endothelial cells, supporting the development of targeted therapeutic strategies and advancing our understanding of brain tumor biology.
Noninvasive imaging parameters extracted from QSM images can reflect glioma WHO grade, molecular markers, prognosis, and recurrence risk. These preliminary findings showed that the QSM might be a noninvasive imaging biomarker for comprehensive evaluation of adult-type diffuse gliomas.
These findings highlight the diagnostic and therapeutic relevance of Kisspeptin-10-associated molecular regulation in GB. This is the first study to integrate transcriptomics, miRNA-mRNA network analysis, and experimental validation to elucidate Kisspeptin-10-mediated modulation of GB progression.
TLR7 suppresses glioblastoma by inhibiting cell progression via the PI3K/AKT/mTOR signaling pathway and promoting an anti-tumoral immune microenvironment. These findings suggest the potential of TLR7 as a promising therapeutic target for GBM.
Our findings suggest that targeting cytokine mRNAs to PBs could be a potential strategy to manage inflammation in activated astroglia in neurodegenerative diseases. At the same time, PB isolation from detergent-permeabilized cells can be an effective, simplified method for studying PB-RNA dynamics in eukaryotic cells.
Importantly, TNFR2 knockdown increased intracranial tumabstor cell apoptosis and prolonged survival in the brain metastasis mouse model. These findings collectively demonstrate that TAAs in lung cancer brain metastasis promote tumor cell survival through a TNFR2-NF-κB-dependent mechanism mediated by TNF-α secretion.