Irradiation differentially affects substratum-dependent survival, adhesion, and invasion of glioblastoma cell lines

Cordes, Nils; Hansmeier, B; Beinke, Christina; Meineke, Viktor; Beuningen, D. van

doi:10.1038/sj.bjc.6601429

Cited by 102 publications

(91 citation statements)

References 51 publications

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“…Cell division is a highly regulated process that is modulated in response to adverse conditions including ionizing radiation [40,41]. Signaling via adhesion of integrins to laminin 5 is known to be involved in progression through the G1 phase of the cell cycle [32,33,42] and other integrin/ligand interactions in the G2/M transition [35,43]. Our data support adhesion-mediated regulation of the G2 phase through the integrin ligand laminin 5.…”

Section: Discussionsupporting

confidence: 73%

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Integrin‐dependent amplification of the G2 arrest induced by ionizing radiation

2005

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The progressive loss of laminin 5 and the α6β4 integrin is a characteristic of the transition of prostatic intraepithelial neoplasia (PIN) to invasive human prostate cancer. Our objective was to determine if the loss of the interaction with laminin 5 would influence the ability of human epithelial cells to respond to DNA damage. Three cellular damage responses to ionizing radiation (IR) were analyzed including G2 progression, cdc2 phosphorylation, and cell survival. The adhesion of normal human prostate epithelial cells to laminin 5 amplified the G2 arrest induced by IR, and depends on a known cell binding domain of laminin 5. The alteration of G2 arrest was confirmed by an inhibition of phospho-cdc2 nuclear translocation. In contrast, a prostate epithelial cancer cell line blocked in G2 independent of adhesion to laminin 5. The survival of these cell lines in response to IR was unaffected by adhesion to laminin 5. These results suggest that cell adhesion to laminin 5 in normal cells will amplify the IR induced G2 cell cycle progression block without altering cell survival. The loss of laminin 5 and the α6β4 integrin in PIN lesions may contribute to the selection and progression of genetically unstable cell types via attenuation of a DNA damage induced G2 arrest.

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Section: Discussionsupporting

confidence: 73%

“…However, it has been reported that in some cell lines, adhesion does not confer increased survival after DNA damage [43] and G2 arrest responses can occur without altering cell survival [55]. In our study, adhesion to laminin 5 did not influence cell survival in PrEC, PC3, and MCF10A cells exposed to ionizing radiation.…”

Section: Discussioncontrasting

confidence: 66%

Integrin‐dependent amplification of the G2 arrest induced by ionizing radiation

2005

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“…For instance, x-ray irradiation increases expression of functional integrins β1 and β3 in glioma cell lines in a dose-dependent manner [8]. In lung adenocarcinoma A549 and SKMES1 cells, x-ray irradiation also induces expression of functional integrin β1 [9].…”

Section: Introductionmentioning

confidence: 99%

Integrin β1-dependent invasive migration of irradiation-tolerant human lung adenocarcinoma cells in 3D collagen matrix

Ishihara

Haga

Yasuda

et al. 2010

Biochemical and Biophysical Research Communications

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Radiotherapy is one of the effective therapies used for treating various malignant tumors.However, the emergence of tolerant cells after irradiation remains problematic due to their high metastatic ability, sometimes indicative of poor prognosis. In this study, we showed that subcloned human lung adenocarcinoma cells (A549P-3) that are irradiation-tolerant indicate high invasive activity in vitro, and exhibit an integrin β1 activity-dependent migratory pattern.In collagen gel overlay assay, majority of the A549P-3 cells displayed round morphology and low migration activity, whereas a considerable number of A549P-3IR cells surviving irradiation displayed a spindle morphology and high migration rate. Blocking integrin β1 activity reduced the migration rate of A549P-3IR cells and altered the cell morphology allowing them to assume a round shape. These results suggest that the A549P-3 cells surviving irradiation acquire a highly invasive integrin β1-dependent phenotype, and integrin β1 might be a potentially effective therapeutic target in combination with radiotherapy.

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“…10,14,15 Further, increasing migration at low doses has been described, followed by a decrease at higher doses. 2,9 On the other hand, irradiation-induced reduction of migration and invasion was shown for colon carcinoma, glioblastoma and lung carcinoma 3,4,16 as well as reduction of plating efficiency in irradiated hepatocarcinoma and mouse mammary carcinoma.…”

Section: Introductionmentioning

confidence: 99%

“…The irradiation-induced impairment of cellular viability, proliferation and clonal survival was analyzed in many different tumor entities, among them were glioblastoma, non-small-cell lung cancer, colon carcinoma and melanoma. [2][3][4] The influence of irradiation on human melanoma cells was analyzed by Ristic-Fira and colleagues who found a dose-dependent decrease of cell proliferation 7 d after irradiation with gamma rays. 5 In a previous study we analyzed the impact of irradiation on mouse melanoma cells and also found decreased viability and proliferation, respectively, which persisted for at least two weeks.…”

Section: Introductionmentioning

confidence: 99%