PortalPublikationenCRN2 enhances the invasiveness of glioblastoma cells

CRN2 enhances the invasiveness of glioblastoma cells

Standard

CRN2 enhances the invasiveness of glioblastoma cells. / Ziemann, Anja; Hess, Simon; Bhuwania, Ridhirama; Linder, Stefan; Kloppenburg, Peter; Noegel, Angelika A; Clemen, Christoph S.

in: NEURO-ONCOLOGY, Jahrgang 15, Nr. 5, 01.05.2013, S. 548-61.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Ziemann, A, Hess, S, Bhuwania, R, Linder, S, Kloppenburg, P, Noegel, AA & Clemen, CS 2013, 'CRN2 enhances the invasiveness of glioblastoma cells', NEURO-ONCOLOGY, Jg. 15, Nr. 5, S. 548-61. https://doi.org/10.1093/neuonc/nos388

APA

Ziemann, A., Hess, S., Bhuwania, R., Linder, S., Kloppenburg, P., Noegel, A. A., & Clemen, C. S. (2013). CRN2 enhances the invasiveness of glioblastoma cells. NEURO-ONCOLOGY, 15(5), 548-61. https://doi.org/10.1093/neuonc/nos388

Vancouver

Ziemann A, Hess S, Bhuwania R, Linder S, Kloppenburg P, Noegel AA et al. CRN2 enhances the invasiveness of glioblastoma cells. NEURO-ONCOLOGY. 2013 Mai 1;15(5):548-61. https://doi.org/10.1093/neuonc/nos388

Bibtex

@article{5c86fbb63b38442ca5d26f8ce5385b46,
title = "CRN2 enhances the invasiveness of glioblastoma cells",
abstract = "BACKGROUND: Movement of tumor cells involves dynamic remodeling of the actin cytoskeleton, which is regulated by actin binding proteins, such as CRN2 (synonyms: coronin 1C, coronin 3). In vitro, CRN2 participates in secretion, matrix degradation, protrusion formation, and cell migration. Furthermore, expression of CRN2 correlates with the malignant phenotype of human diffuse gliomas. CRN2's effects on actin polymerization and F-actin bundling are abolished by protein kinase 2 (CK2) dependent phosphorylation at serine 463.METHODS: We generated human U373 glioblastoma cell lines with knock-down of CRN2 or over-expression of CRN2 variants and studied their behavior in vitro and ex vivo in organotypic brain slice cultures.RESULTS: CRN2 over-expression and expression of the S463A phospho-resistant CRN2 variant increase proliferation, matrix degradation, and invasion but decrease adhesion and formation of invadopodia-like extensions in vitro. Knock-down of CRN2 and expression of S463D phospho-mimetic CRN2 generally have opposite effects. Analysis of invadopodia-like cell extensions shows a diffuse relocalization of F-actin in CRN2 knockdown cells, whereas expression of S463A and S463D mutant CRN2 causes enrichments of F-actin structures at the center and rime zone, respectively. Fluorescence recovery after photobleaching studies of CRN2 and F-actin in lamellipodia show that both CRN2 variants decrease the turnover of actin filaments. Glioblastoma cells over-expressing wild-type or S463A CRN2, which were transplanted onto brain slices, characteristically developed into tumors with an invasive phenotype.CONCLUSIONS: Overall, our data indicate that CRN2 participates in cancer progression via modulation of the actin cytoskeleton.",
keywords = "Actin Cytoskeleton, Actins, Animals, Apoptosis, Blotting, Western, Cell Adhesion, Cell Movement, Cell Proliferation, Cell Surface Extensions, Glioblastoma, Humans, Mice, Mice, Inbred C57BL, Microfilament Proteins, Neoplasm Invasiveness, Organ Culture Techniques, Phosphorylation, Pseudopodia, RNA, Small Interfering, Tumor Cells, Cultured",
author = "Anja Ziemann and Simon Hess and Ridhirama Bhuwania and Stefan Linder and Peter Kloppenburg and Noegel, {Angelika A} and Clemen, {Christoph S}",
year = "2013",
month = may,
day = "1",
doi = "10.1093/neuonc/nos388",
language = "English",
volume = "15",
pages = "548--61",
journal = "NEURO-ONCOLOGY",
issn = "1522-8517",
publisher = "Oxford University Press",
number = "5",

}

RIS

TY - JOUR

T1 - CRN2 enhances the invasiveness of glioblastoma cells

AU - Ziemann, Anja

AU - Hess, Simon

AU - Bhuwania, Ridhirama

AU - Linder, Stefan

AU - Kloppenburg, Peter

AU - Noegel, Angelika A

AU - Clemen, Christoph S

PY - 2013/5/1

Y1 - 2013/5/1

N2 - BACKGROUND: Movement of tumor cells involves dynamic remodeling of the actin cytoskeleton, which is regulated by actin binding proteins, such as CRN2 (synonyms: coronin 1C, coronin 3). In vitro, CRN2 participates in secretion, matrix degradation, protrusion formation, and cell migration. Furthermore, expression of CRN2 correlates with the malignant phenotype of human diffuse gliomas. CRN2's effects on actin polymerization and F-actin bundling are abolished by protein kinase 2 (CK2) dependent phosphorylation at serine 463.METHODS: We generated human U373 glioblastoma cell lines with knock-down of CRN2 or over-expression of CRN2 variants and studied their behavior in vitro and ex vivo in organotypic brain slice cultures.RESULTS: CRN2 over-expression and expression of the S463A phospho-resistant CRN2 variant increase proliferation, matrix degradation, and invasion but decrease adhesion and formation of invadopodia-like extensions in vitro. Knock-down of CRN2 and expression of S463D phospho-mimetic CRN2 generally have opposite effects. Analysis of invadopodia-like cell extensions shows a diffuse relocalization of F-actin in CRN2 knockdown cells, whereas expression of S463A and S463D mutant CRN2 causes enrichments of F-actin structures at the center and rime zone, respectively. Fluorescence recovery after photobleaching studies of CRN2 and F-actin in lamellipodia show that both CRN2 variants decrease the turnover of actin filaments. Glioblastoma cells over-expressing wild-type or S463A CRN2, which were transplanted onto brain slices, characteristically developed into tumors with an invasive phenotype.CONCLUSIONS: Overall, our data indicate that CRN2 participates in cancer progression via modulation of the actin cytoskeleton.

AB - BACKGROUND: Movement of tumor cells involves dynamic remodeling of the actin cytoskeleton, which is regulated by actin binding proteins, such as CRN2 (synonyms: coronin 1C, coronin 3). In vitro, CRN2 participates in secretion, matrix degradation, protrusion formation, and cell migration. Furthermore, expression of CRN2 correlates with the malignant phenotype of human diffuse gliomas. CRN2's effects on actin polymerization and F-actin bundling are abolished by protein kinase 2 (CK2) dependent phosphorylation at serine 463.METHODS: We generated human U373 glioblastoma cell lines with knock-down of CRN2 or over-expression of CRN2 variants and studied their behavior in vitro and ex vivo in organotypic brain slice cultures.RESULTS: CRN2 over-expression and expression of the S463A phospho-resistant CRN2 variant increase proliferation, matrix degradation, and invasion but decrease adhesion and formation of invadopodia-like extensions in vitro. Knock-down of CRN2 and expression of S463D phospho-mimetic CRN2 generally have opposite effects. Analysis of invadopodia-like cell extensions shows a diffuse relocalization of F-actin in CRN2 knockdown cells, whereas expression of S463A and S463D mutant CRN2 causes enrichments of F-actin structures at the center and rime zone, respectively. Fluorescence recovery after photobleaching studies of CRN2 and F-actin in lamellipodia show that both CRN2 variants decrease the turnover of actin filaments. Glioblastoma cells over-expressing wild-type or S463A CRN2, which were transplanted onto brain slices, characteristically developed into tumors with an invasive phenotype.CONCLUSIONS: Overall, our data indicate that CRN2 participates in cancer progression via modulation of the actin cytoskeleton.

KW - Actin Cytoskeleton

KW - Actins

KW - Animals

KW - Apoptosis

KW - Blotting, Western

KW - Cell Adhesion

KW - Cell Movement

KW - Cell Proliferation

KW - Cell Surface Extensions

KW - Glioblastoma

KW - Humans

KW - Mice

KW - Mice, Inbred C57BL

KW - Microfilament Proteins

KW - Neoplasm Invasiveness

KW - Organ Culture Techniques

KW - Phosphorylation

KW - Pseudopodia

KW - RNA, Small Interfering

KW - Tumor Cells, Cultured

U2 - 10.1093/neuonc/nos388

DO - 10.1093/neuonc/nos388

M3 - SCORING: Journal article

C2 - 23410663

VL - 15

SP - 548

EP - 561

JO - NEURO-ONCOLOGY

JF - NEURO-ONCOLOGY

SN - 1522-8517

IS - 5

ER -