Cited by 34Glioma Diagnosis and TreatmentCellular Mechanics and InteractionsProtein Kinase Regulation and GTPase Signaling

Actin cytoskeleton organization, cell surface modification and invasion rate of 5 glioblastoma cell lines differing in PTEN and p53 status

Djuzenova, Cholpon S., Fiedler, Vanessa, Memmel, Simon, Katzer, Astrid, Hartmann, Susanne, Krohne, Georg, Zimmermann, Heiko, Scholz, Claus-Jürgen +3 more·2015·Experimental Cell Research

Abstract

Glioblastoma cells exhibit highly invasive behavior whose mechanisms are not yet fully understood. The present study explores the relationship between the invasion capacity of 5 glioblastoma cell lines differing in p53 and PTEN status, expression of mTOR and several other marker proteins involved in cell invasion, actin cytoskeleton organization and cell morphology. We found that two glioblastoma lines mutated in both p53 and PTEN genes (U373-MG and SNB19) exhibited the highest invasion rates through the Matrigel or collagen matrix. In DK-MG (p53wt/PTENwt) and GaMG (p53mut/PTENwt) cells, F-actin mainly occurred in the numerous stress fibers spanning the cytoplasm, whereas U87-MG (p53wt/PTENmut), U373-MG and SNB19 (both p53mut/PTENmut) cells preferentially expressed F-actin in filopodia and lamellipodia. Scanning electron microscopy confirmed the abundant filopodia and lamellipodia in the PTEN mutated cell lines. Interestingly, the gene profiling analysis revealed two clusters of cell lines, corresponding to the most (U373-MG and SNB19, i.e. p53 and PTEN mutated cells) and less invasive phenotypes. The results of this study might shed new light on the mechanisms of glioblastoma invasion.

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Crossref · 10.1016/j.yexcr.2014.08.013

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  • p53 inactivation in glioblastoma is correlated with a more invasive, less apoptotic, more proliferative, and more stem-like phenotype.

    “p53 inactivation is correlated with a more invasive [30], less apoptotic [31], more proliferative [27], and more stem-like [28] phenotype.”

    From The p53 Pathway in Glioblastoma (2018) · cites this paper as [30]

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Authors
Djuzenova, C. S., Fiedler, V., Memmel, S., Katzer, A., Hartmann, S., Krohne, G., Zimmermann, H., Scholz, C.-J., Polat, B., Flentje, M., & Sukhorukov, V. L.
Affiliations
  • Universitätsklinikum Würzburg (DE)
  • University of Würzburg (DE)
  • Fraunhofer Institute for Biomedical Engineering (DE)
Corresponding author
Djuzenova, Cholpon S.
Venue
Experimental Cell Research
Publisher
Elsevier BV
Published
2015-01
Volume
330
Issue
2
Pages
346-357
ISSN
0014-4827 (ISSN-L)
OpenAlex
W2020026579
Cited by
34
References
59
Citations by year
2025: 3 · 2024: 5 · 2023: 1 · 2022: 3 · 2021: 3 · 2020: 8 · 2019: 2 · 2018: 4 · 2017: 4 · 2016: 1
FWCI
0.84
Type
journal article
Language
en
Open access
closed
Locations
  • Experimental Cell Research (publishedVersion)
  • PubMed (publishedVersion)
  • Fraunhofer-Publica (Fraunhofer-Gesellschaft) (submittedVersion)
Topics
  • Health Sciences › Medicine › Genetics › Glioma Diagnosis and Treatment
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
Keywords
glioblastoma, tumor invasion, actin cytoskeleton, TP53 mutation, PTEN mutation, stress fibers, filopodia, lamellipodia, F-actin, mTOR, cell morphology, cell surface modification, gene expression profiling, U87MG
MeSH terms
Actins, Brain Neoplasms, Cell Adhesion, Cell Movement, Glioblastoma, Humans, Actin Cytoskeleton, Neoplasm Invasiveness, Toluene, Tumor Suppressor Protein p53, Phosphatidylinositol 3-Kinases, MAP Kinase Signaling System, RNA Interference, RNA, Small Interfering, Cell Line, Tumor, Proto-Oncogene Proteins c-akt, PTEN Phosphohydrolase, Benzothiazoles, TOR Serine-Threonine Kinases

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