NES (Nestin)

In addition, treatment enhanced odontoblast differentiation and mineralization, as evidenced by the upregulated expression of Nestin, collagen type I alpha-1, transforming growth factor beta 1, runt-related transcription factor 2, osteopontin, and osteocalcin. Moreover, at 42 days, MG132-treated samples exhibited distinct dentin bridge formation.

However, chrysin significantly reversed the effects of MTX on these parameters. In conclusion, chrysin exhibits neuroprotective effects against MTX-induced neurogenesis impairment by upregulating antioxidant enzyme activity, reducing oxidative stress, and improving protein expression related to neurogenesis.

Propidium iodide (PI) staining revealed increased membrane permeability in cells treated with the combination, which was accompanied by an increase in p53 expression, supporting the induction of apoptosis. Collectively, these findings demonstrate that HCE increases the cytotoxic effects of TMZ by inhibiting Wnt/β-catenin signalling, reducing tumour stemness, and promoting apoptotic pathways in GB cells.

For instance, CAN-3110, a Nestin-promoter-driven herpes simplex virus-1 (HSV-1), demonstrated a median overall survival of 14.9 months in patients with recurrent GBM, with HSV-1 seropositive patients achieving more prolonged survival (14.2 versus 7.8 months in seronegative patients). This review aims to synthesize the current evidence on clinical outcomes in patients with recurrent GBM receiving oncolytic virotherapy, with a specific focus on safety profiles, therapeutic efficacy, and survival outcomes.

Overall, our results demonstrate that in addition to its known nuclear localization, McIdas also localizes to centrioles, affecting centriole duplication. This novel, direct role of McIdas in centriole duplication connects its functions in cell cycle regulation and multiciliogenesis.

Supratentorial ependymomas with ZFTA-RELA fusions represent a highly aggressive pediatric brain tumor subtype, yet the post-transcriptional mechanisms driving their malignancy remain unclear. This study fills a critical gap by systematically profiling miRNA expression in fusion-positive and fusion-negative supratentorial ependymomas, revealing a distinct fusion-associated miRNA signature. The identification of hsa-miR-138-5p upregulation and hsa-miR-135b-5p/hsa-miR-216a-3p downregulation, converging on key oncogenic nodes such as TERT, YAP1, RELA, and TP53, provides novel mechanistic insight into how fusion-driven miRNA dysregulation enhances epithelial-mesenchymal transition and stemness. The findings suggest that miRNA-fusion interactions play an important role in tumor aggressiveness and highlight hsa-miR-138-5p as a potential biomarker for disease progression. Clinically, the work advances understanding of fusion-driven ependymoma biology and lays the foundation for developing miRNA-based diagnostic and therapeutic strategies targeting molecular mechanisms of tumor progression.

In addition, the use of a JAK2 inhibitor (WP1066) and agonist (C-A1) verified that Mel exerted its protective effects by down-regulating the JAK2/STAT3 pathway. Morris water maze further confirmed that Mel improved spatial learning and memory function in neonatal rats with HIBD. Multimodal MRI offers a visual basis for monitoring metabolic changes and therapeutic effects, while Mel enhances neurogenesis and mitigates brain injury through inhibition of the JAK2/STAT3 pathway, thus providing a theoretical basis for the clinical application of Mel in HIBD in neonates.

Using a conditional mouse model, we demonstrate that driving the expression of Spy1, in the Nestin-enriched NSC population of the brain, increases stemness characteristics, decreases differentiation, and increases susceptibility to oncogenic transformation. This study contributes to better understanding of intricate cell cycle mechanisms that lead to deviation from the homeostatic state, promoting aberrant changes in adult NSCs.

This review further provides insights for future research by proposing a hierarchical regulatory network of methylation in GSCs to deepen understanding of their unique characteristics. Furthermore, this review highlights the potential for developing additional methylation-related clinical markers to enhance diagnostic approaches.

The accumulating evidence on PASCs highlights their pivotal role in PitNET tumorigenesis, progression, and therapy resistance. Their molecular and functional overlap with normal pituitary stem cells underscores the need for further lineage-tracing and in vivo validation.

Temozolomide acts on more differentiated glioma cells and enriches stem cells. iNOS inhibition reduces the stem cell niche, enhancing TMZ sensitization.

Although lenalidomide/bortezomib/dexamethasone (RVd) and cyclophosphamide/bortezomib/dexamethasone (CyBorD) are clinically effective, their precise impacts on PC/B-cell maturation remain unclear. RVd responders further downregulated CD56, CD269, and CD329, and increased CD243. These shared and divergent modulations elucidate the molecular underpinnings of RVd and CyBorD efficacy and inform precision regimen selection.