guest ::
| Home > Publications database > Three-dimensional invasion of human glioblastoma cells remains unchanged by X-ray and carbon ion irradiation in vitro. |
| Journal Article | GSI-2016-01107 |
; ; ; ; ; ; ; ; ;
2012
Elsevier Science
Amsterdam [u.a.]
This record in other databases: 
Please use a persistent id in citations: doi:10.1016/j.ijrobp.2012.06.012
Abstract: Cell invasion represents one of the major determinants that treatment has failed for patients suffering from glioblastoma. Contrary findings have been reported for cell migration upon exposure to ionizing radiation. Here, the migration and invasion capability of glioblastoma cells on and in collagen type I were evaluated upon irradiation with X-rays or carbon ions.Migration on and invasion in collagen type I were evaluated in four established human glioblastoma cell lines exposed to either X-rays or carbon ions. Furthermore, clonogenic radiation survival, proliferation (5-bromo-2-deoxyuridine positivity), DNA double-strand breaks (γH2AX/53BP1-positive foci), and expression of invasion-relevant proteins (eg, β1 integrin, FAK, MMP2, and MMP9) were explored. Migration and invasion assays for primary glioblastoma cells also were carried out with X-ray irradiation.Neither X-ray nor carbon ion irradiation affected glioblastoma cell migration and invasion, a finding similarly observed in primary glioblastoma cells. Intriguingly, irradiated cells migrated unhampered, despite DNA double-strand breaks and reduced proliferation. Clonogenic radiation survival was increased when cells had contact with extracellular matrix. Specific inhibition of the β1 integrin or proliferation-associated signaling molecules revealed a critical function of JNK, PI3K, and p38 MAPK in glioblastoma cell invasion.These findings indicate that X-rays and carbon ion irradiation effectively reduce proliferation and clonogenic survival without modifying the migration and invasion ability of glioblastoma cells in a collagen type I environment. Addition of targeted agents against members of the MAPK and PI3K signaling axis to conventional chemoradiation therapy seems potentially useful to optimize glioblastoma therapy.
Keyword(s): Antigens, CD29 ; Collagen Type I ; H2AFX protein, human ; Histones ; Intracellular Signaling Peptides and Proteins ; TP53BP1 protein, human ; Carbon ; Phosphatidylinositol 3-Kinases ; p38 Mitogen-Activated Protein Kinases ; MAP Kinase Kinase 4 ; Bromodeoxyuridine
- ddc:610
Contributing Institute(s): Research Program(s):
Appears in the scientific report 2012
Database coverage:
; BIOSIS Previews ; Current Contents - Clinical Medicine ; IF < 5 ; JCR ; NCBI Molecular Biology Database ; Nationallizenz
; SCOPUS ; Science Citation Index ; Science Citation Index Expanded ; Thomson Reuters Master Journal List ; Web of Science Core Collection
|
The record appears in these collections: |