Deregulated human glioma cell motility: inhibitory effect of somatostatin.

Mol Cell Endocrinol

Department of Pharmacology, School of Medicine, University of Milano, Via Vanvitelli 32, 20129 Milano, Italy.

Published: August 2006

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.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.mce.2006.05.006DOI Listing

Publication Analysis

Top Keywords

glioma cell
20
cell motility
12
cell lines
12
human glioma
8
u87-mg cells
8
motility
7
glioma
6
cell
6
deregulated human
4
motility inhibitory
4

Similar Publications

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 PDF

Comprehensive analysis and experiments identified ANXA1 as an unfavorable prognosticator in glioma.

Transl 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.

View Article and Find Full Text PDF

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 PDF

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 PDF

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.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!