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AMOG/beta2 and glioma invasion

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AMOG/beta2 and glioma invasion : does loss of AMOG make tumour cells run amok? / Senner, V; Schmidtpeter, S; Braune, S; Püttmann, S; Thanos, S; Bartsch, U; Schachner, M; Paulus, W.

in: NEUROPATH APPL NEURO, Jahrgang 29, Nr. 4, 08.2003, S. 370-7.

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

Harvard

Senner, V, Schmidtpeter, S, Braune, S, Püttmann, S, Thanos, S, Bartsch, U, Schachner, M & Paulus, W 2003, 'AMOG/beta2 and glioma invasion: does loss of AMOG make tumour cells run amok?', NEUROPATH APPL NEURO, Jg. 29, Nr. 4, S. 370-7.

APA

Senner, V., Schmidtpeter, S., Braune, S., Püttmann, S., Thanos, S., Bartsch, U., Schachner, M., & Paulus, W. (2003). AMOG/beta2 and glioma invasion: does loss of AMOG make tumour cells run amok? NEUROPATH APPL NEURO, 29(4), 370-7.

Vancouver

Senner V, Schmidtpeter S, Braune S, Püttmann S, Thanos S, Bartsch U et al. AMOG/beta2 and glioma invasion: does loss of AMOG make tumour cells run amok? NEUROPATH APPL NEURO. 2003 Aug;29(4):370-7.

Bibtex

@article{4035d47fb1c14789be661c5537a1a9b2,
title = "AMOG/beta2 and glioma invasion: does loss of AMOG make tumour cells run amok?",
abstract = "The beta2 subunit of Na,K-ATPase, initially described as adhesion molecule on glia (AMOG), has been shown to mediate neurone-astrocyte adhesion as well as neural cell migration in vitro. We have investigated the expression of AMOG/beta2 in human gliomas and its effect on glioma cell adhesion and migration. Compared to normal astrocytes of human brain, AMOG/beta2 expression levels of neoplastic astrocytes were down-regulated in biopsy specimens and inversely related to the grade of malignancy. One rat and four human glioma cell lines showed complete loss of AMOG. To investigate the function of AMOG/beta2, its expression was re-established by transfecting an expression plasmid into AMOG/beta2-negative C6 rat glioma cells. In vitro assays revealed increased adhesion and decreased migration on matrigel of AMOG/beta2-positive cells as compared to their AMOG/beta2-negative counterparts. We conclude that increasing loss of AMOG/beta2 during malignant progression parallels and may underlie the extensive invasion pattern of malignant gliomas.",
keywords = "Adenosine Triphosphatases, Animals, Astrocytoma, Brain Neoplasms, Cation Transport Proteins, Cell Adhesion, Cell Adhesion Molecules, Neuronal, Cell Movement, Down-Regulation, Gene Expression Regulation, Neoplastic, Humans, Rats, Recombinant Proteins, Tumor Cells, Cultured, Journal Article, Research Support, Non-U.S. Gov't",
author = "V Senner and S Schmidtpeter and S Braune and S P{\"u}ttmann and S Thanos and U Bartsch and M Schachner and W Paulus",
year = "2003",
month = aug,
language = "English",
volume = "29",
pages = "370--7",
journal = "NEUROPATH APPL NEURO",
issn = "0305-1846",
publisher = "Wiley-Blackwell",
number = "4",

}

RIS

TY - JOUR

T1 - AMOG/beta2 and glioma invasion

T2 - does loss of AMOG make tumour cells run amok?

AU - Senner, V

AU - Schmidtpeter, S

AU - Braune, S

AU - Püttmann, S

AU - Thanos, S

AU - Bartsch, U

AU - Schachner, M

AU - Paulus, W

PY - 2003/8

Y1 - 2003/8

N2 - The beta2 subunit of Na,K-ATPase, initially described as adhesion molecule on glia (AMOG), has been shown to mediate neurone-astrocyte adhesion as well as neural cell migration in vitro. We have investigated the expression of AMOG/beta2 in human gliomas and its effect on glioma cell adhesion and migration. Compared to normal astrocytes of human brain, AMOG/beta2 expression levels of neoplastic astrocytes were down-regulated in biopsy specimens and inversely related to the grade of malignancy. One rat and four human glioma cell lines showed complete loss of AMOG. To investigate the function of AMOG/beta2, its expression was re-established by transfecting an expression plasmid into AMOG/beta2-negative C6 rat glioma cells. In vitro assays revealed increased adhesion and decreased migration on matrigel of AMOG/beta2-positive cells as compared to their AMOG/beta2-negative counterparts. We conclude that increasing loss of AMOG/beta2 during malignant progression parallels and may underlie the extensive invasion pattern of malignant gliomas.

AB - The beta2 subunit of Na,K-ATPase, initially described as adhesion molecule on glia (AMOG), has been shown to mediate neurone-astrocyte adhesion as well as neural cell migration in vitro. We have investigated the expression of AMOG/beta2 in human gliomas and its effect on glioma cell adhesion and migration. Compared to normal astrocytes of human brain, AMOG/beta2 expression levels of neoplastic astrocytes were down-regulated in biopsy specimens and inversely related to the grade of malignancy. One rat and four human glioma cell lines showed complete loss of AMOG. To investigate the function of AMOG/beta2, its expression was re-established by transfecting an expression plasmid into AMOG/beta2-negative C6 rat glioma cells. In vitro assays revealed increased adhesion and decreased migration on matrigel of AMOG/beta2-positive cells as compared to their AMOG/beta2-negative counterparts. We conclude that increasing loss of AMOG/beta2 during malignant progression parallels and may underlie the extensive invasion pattern of malignant gliomas.

KW - Adenosine Triphosphatases

KW - Animals

KW - Astrocytoma

KW - Brain Neoplasms

KW - Cation Transport Proteins

KW - Cell Adhesion

KW - Cell Adhesion Molecules, Neuronal

KW - Cell Movement

KW - Down-Regulation

KW - Gene Expression Regulation, Neoplastic

KW - Humans

KW - Rats

KW - Recombinant Proteins

KW - Tumor Cells, Cultured

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

M3 - SCORING: Journal article

C2 - 12887597

VL - 29

SP - 370

EP - 377

JO - NEUROPATH APPL NEURO

JF - NEUROPATH APPL NEURO

SN - 0305-1846

IS - 4

ER -