Malignant gliomas are highly invasive tumors which are lethal despite aggressive therapy. The motility behavior of two human glioma cell lines i.e. T98G and U87-MG cells was analysed. The glioma cells showed a high degree of basal motility (especially U87-MG cells) that may be related to the considerable local invasiveness of such tumours even in the absence of exogenous factors. The two cell lines responded equally well to platelet-derived growth factor (PDGF) as chemoattractant factor. The phosphatidylinositol 3-kinase (PI3-K) signaling, but not the extracellular signal-related kinase (ERK) signaling, was strongly involved in the PDGF-stimulated glioma cell motility. Somatostatin was capable of inhibiting the migration in both glioma cell lines without affecting crucial targets for motility control like PI3-K and Rac activity. These data suggest that somatostatin, by interfering with a target further downstream to Rac, negatively affects glioma cell motility, and may thus offer a pharmacological approach to controlling the deregulated motility of these aggressive tumoral cells.
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http://dx.doi.org/10.1016/j.mce.2006.05.006 | DOI Listing |
Neurochem Res
January 2025
Dept Intens Care Unit, Hangzhou TCM Hospital Affiliated to Zhejiang Chinese Medical University, No.453, Stadium Road, Hangzhou, Zhejiang, 310007, China.
Glioblastoma (GBM) is the most malignant type of glioma with a very poor prognosis. N6-methyladenosine (m6A) is well-documented to be involved in GBM progression, and FTO is a demethylase. GSTO1 is also associated with tumor progression.
View Article and Find Full Text PDFTransl Oncol
January 2025
Department of neurosurgery, Jiangnan university Medical Center, Wuxi, Jiangsu province, 214002, PR China; Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu province, 214002, PR China. Electronic address:
Background: ANXA1 was upregulated in gliomas in previous bulk sequencing studies. we examined the role of ANXA1 in glioma using bioinformatics analysis and experiments.
Methods: Two cohorts were adopted to validate the prognostic value of ANXA1 in gliomas.
J Mol Neurosci
January 2025
Department of Pediatric Neurosurgery, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200092, China.
Primary brain tumors that were the most severe and aggressive were called glioblastoma multiforme (GBM). Cancers are caused in part by aberrant expression of circular RNA. Often referred to as competitive endogenous RNA (ceRNA), circRNA molecules act as "miRNA sponges" in cells by decreasing the inhibitory impact of miRNA on their target genes and hence raising the expression levels of those genes.
View Article and Find Full Text PDFMol Biol Rep
January 2025
Department of Biotechnology, Jaypee Institute of Information Technology, A-10, Sector 62, Noida, UP, 201309, India.
Metabolic reprogramming stands out as a defining characteristic of cancer, including glioblastoma (GB), enabling tumor cells to overcome growth and survival challenges in adverse conditions. The dysregulation of metabolic processes in GB is crucial to its pathogenesis, influencing both tumorigenesis and the disease's invasive tendencies. This altered metabolism supplies essential energy substrates for uncontrolled cell proliferation and also creates an immunosuppressive microenvironment, complicating conventional therapies.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114.
Ependymoma (EPN) is a common form of brain tumor in children, often resistant to available cytotoxic therapies. Molecular profiling studies have led to a better understanding of EPN subtypes and revealed a critical role of oncogenes ZFTA-RELA fusion and EPHB2 in supratentorial ependymoma (ST-EPN). However, the immune system's role in tumor progression and response to therapy remains poorly understood.
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