Ras-related protein 25 (Rab25) is a member of the Rab family, and it has been reported to play an important role in tumorigenesis. However, its direct involvement in human glioblastoma multiforme (GBM) is still unclear. The aim of the current study was to investigate the potential role of Rab25 in the growth, proliferation, invasion, and migration of human GBM. Our results showed that Rab25 expression was significantly higher in human GBM cell lines compared with a normal astrocyte cell line. In vitro functional studies revealed that knockdown of Rab25 reduced cell proliferation and inhibited invasion and migration of GBM cells. In vivo experiments showed that knockdown of Rab25 attenuated the tumor growth in nude mice. Finally, knockdown of Rab25 significantly inhibited the phosphorylation levels of PI3K and AKT in GBM cells. Taken together, these findings indicate that Rab25 may act as a tumor promoter in human GBM and that approaches to target Rab25 may provide a novel strategy to treat this disease.
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http://dx.doi.org/10.3727/096504016X14736286083065 | DOI Listing |
Eur J Med Res
January 2025
Department of Neurosurgery, Institute of Brain Diseases, Nanfang Hospital, Southern Medical University, Guangzhou Avenue North No.1838, Guangzhou, 510515, Guangdong, People's Republic of China.
The identification of oncogenic gene fusions in diffuse gliomas may serve as potential therapeutic targets and prognostic indicators, representing a novel strategy for treating gliomas consistent with the principles of personalized medicine. This study identified detectable oncogene fusions in glioma patients through an integrated analysis of genomic and transcriptomic data, which encompassed whole exon sequencing and next-generation RNA sequencing. In addition, this study also conducted a comparison of the genetic characteristics, tumor microenvironment, mutation burden and survival between glioma patients with or without gene fusions.
View Article and Find Full Text PDFAJNR Am J Neuroradiol
January 2025
From the Department of Neuroradiology (G.B., N.H., F.D.v.D., A.B., Z.K.), University Hospital Zürich, Zürich, Switzerland.
Background And Purpose: Whether differences in the O-methylguanine-DNA methyltransferase () promoter methylation status of glioblastoma (GBM) are reflected in MRI markers remains largely unknown. In this work, we analyze the ADC in the perienhancing infiltration zone of GBM according to the corresponding status by using a novel distance-resolved 3D evaluation.
Materials And Methods: One hundred one patients with wild-type GBM were retrospectively analyzed.
Front Immunol
January 2025
Department of Neurological Care Unit, The First Affiliated Hospital of YangTze University, Jingzhou, Hubei, China.
Background: Recent years have seen persistently poor prognoses for glioma patients. Therefore, exploring the molecular subtyping of gliomas, identifying novel prognostic biomarkers, and understanding the characteristics of their immune microenvironments are crucial for improving treatment strategies and patient outcomes.
Methods: We integrated glioma datasets from multiple sources, employing Non-negative Matrix Factorization (NMF) to cluster samples and filter for differentially expressed metabolic genes.
Chron Respir Dis
January 2025
The Woolcock Institute of Medical Research, The University of Sydney, Sydney, Australia.
Individuals with Preserved Ratio Impaired Spirometry (PRISm), defined as FEV/FVC ≥0.7 and FEV1 <80% predicted, are at higher risk of developing COPD. However, data for Australian adults are limited.
View Article and Find Full Text PDFExpert Rev Mol Med
January 2025
Centre for Gene Therapy and Regenerative Medicine, King's College London, London, United Kingdom.
Background: Glioblastoma multiforme (GBM) is the most prevalent primary brain tumour, with an incidence of 2 per 100,000. The standard clinical treatments do not sufficiently target cell migration and invasion, leading to recurrence after surgical resection and resistance after chemotherapy and radiotherapy. Pre-clinical studies are being conducted to construct artificial substrates that can mimic the tumour microenvironment (TME) to prevent GBM cells from migrating along their primary route through blood vessels and white matter tracts.
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