In conclusion, our study indicated that therapies targeting the ATP1A1 and p53 signaling-mediated mitochondrial apoptotic pathways regulated by bufalin might be potential treatments for human glioma, and these findings will provide molecular bases for developing bufalin into a drug candidate for the treatment of malignant glioma.
The effects of layilin-knockdown on the expression and protein levels of snail family transcriptional repressor 1 (SNAI1), a transcriptional factor involved in the acquisition and enhancement of invasive ability in malignant gliomas, and on the expression of its target genes, matrix metalloproteinase 2 (MMP2), MMP9, and collagen type I alpha 1 chain (COL1A1), were investigated by qPCR and/or western blotting.
Via bioinformatic analysis based on TCGA-LGG and TCGA-GBM data, we explored the mechanisms of GAS5 expression in LGG (grades II and III) and high-grade glioma (glioblastoma multiforme, grade IV).
Collectively, this research shed light on mechanisms of invasion and progression of malignant gliomas and suggested that SLK may be a potential therapeutic strategy for glioma.
In current study, we found a HMGB1 regulated lncRNA, Linc00320, is significantly decreased in Glioma malignant tissues and its low expression predicts poor prognosis.
These data also suggest that overexpression of HOTAIRM1 can be a negative prognostic factor for patient survival in malignant glioma and may be a promising potential therapeutic target.
Histology revealed a high-grade glioma adjacent to a low-grade glioneuronal component with abundant Rosenthal fibers, focal eosinophilic granular bodies, and CD34-positive neurons.
These findings enrich our understanding of gliomagenesis, highlight the prognostic value of miR-29a/b/c and TRAF4, and imply their potential therapeutic roles in malignant gliomas.
Moreover, the uptake ratios of Ga-NOTA-PRGD2 over F-FDG, normalized as lg100 * SUVmax (RGD / FDG), in the uncommon meningiomas were significantly higher than those in HGG (1.87 ± 1.36 vs 1.04 ± 0.87, P = 0.0001).
In the discovery cohort, decreased BRMS1L expression was significantly associated with high-grade glioma as well as the higher mortality in survival analysis (log-rank test, p< 0.01).
Population proportion of the CREB3L1<sup>+</sup>-presenting patients decreased from the control to the high-grade glioma and the population of the PTN<sup>+</sup>-presenting patients increased in low- and high-grade gliomas as compared with the control (both <i>P</i><0.05).
CXCL14 has a strong correlation with immune(T cells, Monocytic lineage and Neutrophils) and Fibroblasts within glioma environment. miR-17-5p and CXCL14 exhibited predictive values for high-grade glioma(HGG) patients: Higher miR-17-5p indicated significantly longer survival while lower CXCL14 indicated longer survival.
In 189 HGG patients, Sox7 expression was heterogeneous in tumor vessels, and high Sox7 levels correlated with poor survival, early recurrence, and impaired vascular function, emphasizing the clinical relevance of Sox7 in HGG.
We conducted a phase I study to determine the safety of plerixafor and bevacizumab in recurrent HGG.<b>Patients and Methods:</b> Part 1 enrolled 23 patients with a 3 × 3 dose escalation design to a maximum planned dose of plerixafor 320 μg/kg subcutaneously on days 1 to 21 and bevacizumab 10 mg/kg intravenously on days 1 and 15 of each 28-day cycle.
The findings provide evidence that miR-361-5p directly targets SND1 to degradation and then reduces MMP-2 gene transcription, thus inhibiting glioma migration and invasion. miR-361-5p is an important tumor suppressor and a novel diagnostic biomarker of glioma, and miR-361-5p and SND1 are potential therapeutic candidates for malignant gliomas.
Additionally, latent TGF‑β‑binding protein‑1 (LTBP‑1) modulates the activity of the TGF‑β‑mothers against decapentaplegic (Smad) signaling pathway in numerous diseases, including malignant glioma.