Dynamic determination of human glioma invasion in vitro

Nygaard, Svein Jacob Tjoflaat; Haugland, Hans Kristian; Lærum, Ole Didrik; Lund‐Johansen, Morten; Bjerkvig, Rolf; Tysnes, Ole‐Bjørn

doi:10.3171/jns.1998.89.3.0441

Cited by 22 publications

(22 citation statements)

References 34 publications

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“…To further con®rm the e ect of p16 transfer on invasion, we utilized a three-dimensional co-culture model that closely mimics in vivo invasion into a complex and intact extracellular matrix synthesized by fetal rat-brain aggregates under confocal laser scanning microscopy (Nygaard et al, 1995), which gives the added advantage of observing tumor-cell invasion at di erent depths by optical sectioning. As in the Matrigel assays, SNB19 spheroids treated with p16 failed to invade the fetal rat-brain aggregates.…”

Section: Discussionmentioning

confidence: 99%

“…Invasion of the tumor spheroids into fetal rat-brain aggregates was analysed by confocal Laser Scanning Microscopy (Zeiss LSM210, Thornwood, NY; Nygaard et al, 1995). Brie¯y, DiO-stained tumor spheroids and DiIstained fetal rat-brain aggregates were washed in the medium and transferred in quadruplicate to individual wells of a 96-well plate, base-coated with agar.…”

Section: Confocal Laser Scanning Microscopymentioning

confidence: 99%

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Adenovirus-mediated p16/CDKN2 gene transfer suppresses glioma invasion in vitro

et al. 1997

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Malignant gliomas extensively in®ltrate the surrounding normal brain, and their di use invasion is one of the most important barriers to successful therapy. Recent studies indicate that the progression of gliomas from lowgrade to high-grade may depend on the acquisition of a new phenotype and the subsequent addition of genetic defects. One of the most frequent abnormalities in the progression of gliomas is the inactivation of tumorsuppressor gene p16, suggesting that loss of p16 is associated with acquisition of malignant characteristics. Consistent with this hypothesis, our previous studies showed that restoring wild-type p16 activity into p16-null malignant glioma cells modi®ed their phenotype. In order to understand whether the biological consequences of p16 inactivation in high-grade gliomas included facilitating invasiveness, we used a recombinant replication-de®cient adenovirus carrying the cDNA of the p16/CDKN2 gene to infect and express high levels of p16 protein in p16-null SNB19 glioma cells. Invasion of SNB19 glioma cells was tested into two models: invasion of glioma cells through Matrigel-coated transwell inserts and invasion of tumor-cell spheroids into fetal rat-brain aggregates in a co-culture system. Matrigel invasion assays showed that the SNB19 cells expressing exogenous p16 exhibited signi®cantly reduced invasion. Similarly, invasion of p16-treated SNB19 cells into fetal rat-brain aggregates was reduced during a 72 h time period compared to invasion of the adenovirus-control and mock-infected cells. Expression of matrix metalloproteinase-2 (MMP-2), an enzyme involved in tumor-cell invasion, in SNB19 cells expressing p16 was signi®cantly reduced compared to that of parental SNB19 and vector-infected cells. Our results show that restoring wild-type p16 activity into p16-null SNB19 glioma cells signi®cantly inhibits tumorcell invasion, thus suggesting a novel function of the p16 gene.

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Section: Discussionmentioning

confidence: 99%

Section: Confocal Laser Scanning Microscopymentioning

confidence: 99%

Adenovirus-mediated p16/CDKN2 gene transfer suppresses glioma invasion in vitro

et al. 1997

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“…malignant cells could easily be discriminated from each other and the invasion rate was measured quantitatively over a period of up to ten days. The result was that the rate of invasion varied considerably with the individual tumours, as tested with spheroids from primary brain tumour biopsies (Nygaard, Haugland, Laerum, Lund-Johansen, Bjerkvig and Tysnes, 1998).…”

Section: Could You Modify the Invasiveness By Addition Of Growth Factmentioning

confidence: 98%

“…Nygaard, Haugland, Laerum, Lund-Johansen, Bjerkvig and Tysnes, (1998). malignant cells could easily be discriminated from each other and the invasion rate was measured quantitatively over a period of up to ten days.…”

Section: Could You Modify the Invasiveness By Addition Of Growth Factmentioning

confidence: 99%

Brain tumour development and invasion. An interview with Ole Didrik Laerum

Hülser¹

2004

Int. J. Dev. Biol.

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“…Glioma accounts for 50% of all intracranial tumors. 1 Glioma has high capacity of proliferation and invasion into healthy brain tissue. 2 The current standard of care for gliomas is surgery, radiotherapy, and alkylating agent chemotherapy, which result in a 2-year survival rate of 15%-26% and extremely frequent tumor recurrence.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of CPEB4 in glioma indicates a poor prognosis by promoting cell migration and invasion

Liu

Jiang

et al. 2017

Tumour Biol.

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Glioma is an aggressive malignancy with limited effective treatment and poor prognosis. Cytoplasmic polyadenylation element binding protein 4 is a regulator of gene transcription and has been reported to be associated with biological malignancy in cancers. However, the mechanisms that cytoplasmic polyadenylation element binding protein 4 contributes to tumor migration and invasion remain unknown. Here, cytoplasmic polyadenylation element binding protein 4 expression was assessed using immunohistochemistry, and the results were compared with clinicopathological parameters, including survival. Using glioma cell lines (SKMG-4 and T98G), we measured cytoplasmic polyadenylation element binding protein 4 messenger RNA and protein expression and studied the effects of cytoplasmic polyadenylation element binding protein 4 expression on cell migration and invasion. Cytoplasmic polyadenylation element binding protein 4 expression was significantly higher in tumor tissues than that in normal brain tissues. Clinicopathological analysis showed that cytoplasmic polyadenylation element binding protein 4 expression was significantly correlated with advanced World Health Organization grade (p < 0.001) and lower Karnofsky Performance Status (KPS) score (p = 0.001). Cytoplasmic polyadenylation element binding protein 4 positive as opposed to the cytoplasmic polyadenylation element binding protein 4 negative patients had lower overall survival (p < 0.001). Multivariate analysis suggested that cytoplasmic polyadenylation element binding protein 4 expression might be an independent prognostic indicator (hazard ratio = 2.091, 95% confidence interval: 1.093-3.999, p = 0.026) for glioma patients. Moreover, upregulated cytoplasmic polyadenylation element binding protein 4 expression could promote T98G cell migration and invasion, and downregulated cytoplasmic polyadenylation element binding protein 4 expression could inhibit SKMG-4 cell migration and invasion. Furthermore, downregulated cytoplasmic polyadenylation element binding protein 4 could reduce the protein expression of matrix metalloproteinase-2 and matrix metalloproteinase-9. In conclusion, our studies indicated that positive cytoplasmic polyadenylation element binding protein 4 expression predicted a worse prognosis in glioma patients, and cytoplasmic polyadenylation element binding protein 4 could represent a useful biomarker or therapeutic target for glioma.

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Dynamic determination of human glioma invasion in vitro

Abstract: The present work provides a model for quick and efficient assessment of dynamic interactions between tumor and normal brain tissue shortly after surgery.

Cited by 22 publications

References 34 publications

Adenovirus-mediated p16/CDKN2 gene transfer suppresses glioma invasion in vitro

Adenovirus-mediated p16/CDKN2 gene transfer suppresses glioma invasion in vitro

Brain tumour development and invasion. An interview with Ole Didrik Laerum

Overexpression of CPEB4 in glioma indicates a poor prognosis by promoting cell migration and invasion

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