AMOG/β2 and glioma invasion: Does loss of AMOG make tumour cells run amok?

Volker Senner, S. Schmidtpeter, S. Braune, S. Püttmann, S. Thanos, U. Bartsch, M. Schachner, W. Paulus

Research output: Contribution to journalArticlepeer-review

32 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)370-377
Number of pages8
JournalNeuropathology and Applied Neurobiology
Issue number4
StatePublished - Aug 2003

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Histology
  • Neurology
  • Clinical Neurology
  • Physiology (medical)


  • AMOG (adhesion molecule on glia)
  • Adhesion
  • Glioma
  • Invasion
  • Na, K-ATPase


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