Upregulation of the canonical signaling pathway of interferon-gamma is associated with glioblastoma progression

Background Glioblastoma is a brain malignant tumor grade IV, highly invasive. Alterations in several signaling pathways are involved in glioblastoma development. In this work, we evaluated the IFN-γ canonical signaling pathway in glioblastoma cells and its effect on cell viability and migration. Met...

Full description

Saved in:
Bibliographic Details
Published in:Molecular biology reports 2024-12, Vol.51 (1), p.64-64, Article 64
Main Authors: Zamora-Salas, Sayra Ximena, Macías-Silva, Marina, Tecalco-Cruz, Angeles C.
Format: Article
Language:English
Subjects:
Animal Anatomy
Animal Biochemistry
B7-H1 Antigen - metabolism
Biomedical and Life Sciences
Brain cancer
Brain tumors
Calcein
Cell activation
Cell Line, Tumor
Cell migration
Cell viability
Gene expression
Glioblastoma
Glioblastoma - genetics
Glioblastoma cells
Histology
Humans
Interferon regulatory factor 1
Interferon-gamma - metabolism
Life Sciences
Morphology
PD-L1 protein
Propidium iodide
Short Communication
Signal Transduction
Stat1 protein
Up-Regulation
Western blotting
Wound healing
γ-Interferon
Citations: Items that this one cites
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Background Glioblastoma is a brain malignant tumor grade IV, highly invasive. Alterations in several signaling pathways are involved in glioblastoma development. In this work, we evaluated the IFN-γ canonical signaling pathway in glioblastoma cells and its effect on cell viability and migration. Methods The levels of STAT1/pSTAT1, IRF1, and PD-L1 in LN-18 glioblastoma cells were analyzed using western blotting. Cell viability was evaluated by calcein-AM/propidium iodide assays, and a wound healing assay was used to study the migration of glioblastoma cells treated with IFN-γ. Our aim was to determine the expression of IFN-γ signaling elements in cell lines and tissue from glioblastoma samples and examine the relationship between these elements and the survival of glioblastoma patients. The following platforms were utilized for analysis: the CCLE (Cancer Cell Line Encyclopedia), UALCAN (University of Alabama at Birmingham Cancer data analysis Portal), GEPIA (Gene Expression Profiling Interactive Analysis), and GENT2 (Gene Expression patterns across Normal and Tumor tissues). Results Our results evidenced that IFN-γ signaling increases non-phosphorylated and phosphorylated STAT1 levels and promotes the upregulation of IRF1 and PD-L1 in glioblastoma cells. The activation of IFN-γ signaling increased cell migration without affecting the viability of glioblastoma cells. Furthermore, in silico analysis showed that the elements of IFN-γ signaling pathways ( IFNGR1/IFNGR2/STAT1/IRF1 ) are upregulated in human glioblastoma samples. The upregulation of IFN-γ signaling was associated with shorter survival in glioblastoma patients. Conclusion IFN-γ signaling pathway is upregulated in glioblastoma, displaying pro-tumor activity. Thus, IFN-γ signaling elements may be potential biomarkers and targets for treating glioblastoma.
ISSN:0301-4851
1573-4978
DOI:10.1007/s11033-023-09062-4