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AMOG/β2 and glioma invasion: does loss of AMOG make tumour cells run amok?
Author(s) -
Senner V.,
Schmidtpeter S.,
Braune S.,
Püttmann S.,
Thanos S.,
Bartsch U.,
Schachner M.,
Paulus W.
Publication year - 2003
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1046/j.1365-2990.2003.00473.x
Subject(s) - glioma , matrigel , malignancy , biology , astrocyte , in vitro , pathology , cell adhesion molecule , cell culture , cancer research , cell adhesion , cell , microbiology and biotechnology , medicine , central nervous system , neuroscience , biochemistry , genetics
The β2 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/β2 in human gliomas and its effect on glioma cell adhesion and migration. Compared to normal astrocytes of human brain, AMOG/β2 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/β2, its expression was re‐established by transfecting an expression plasmid into AMOG/β2‐negative C6 rat glioma cells. In vitro assays revealed increased adhesion and decreased migration on matrigel of AMOG/β2‐positive cells as compared to their AMOG/β2‐negative counterparts. We conclude that increasing loss of AMOG/β2 during malignant progression parallels and may underlie the extensive invasion pattern of malignant gliomas.