Loss of cell-matrix contact increases hypoxia-inducible factor-dependent transcriptional activity in glioma cells.

Affiliation

Dr. Senckenberg Institute of Neurooncology, University Hospital Frankfurt, Goethe University, Schleusenweg 2-16, 60528, Frankfurt am Main, Germany; University Cancer Center Frankfurt (UCT), University Hospital Frankfurt, Goethe University, Theodor-Stern-Kai 7, 60590, Frankfurt am Main, Germany; German Cancer Consortium (DKTK), Partner Site Frankfurt/Mainz, Theodor-Stern-Kai 7, 60590, Frankfurt am Main, Germany. Electronic address: [Email]

Abstract

In a variety of malignomas, the acquisition of a mesenchymal phenotype has been linked with anchorage-independent growth and invasiveness. To some extent, glioma cells are able to survive a loss of cell-matrix contact. We here describe that non-adherent culture of glioma cells was accompanied by an increase in hypoxia-inducible factor (HIF)-dependent, but not β-catenin/TCF-induced transcription. Levels of reactive oxygen species decreased in suspension and knockdown of HIF-1α enhanced cell death following detachment. By promoting the adaptation to non-adherent conditions, mechanisms driven by HIF-1α may considerably contribute to the biology and aggressiveness of glioblastoma.

Keywords

Anoikis,Epithelial-mesenchymal transition,Glioblastoma,Hypoxia-inducible factor,Reactive oxygen species,

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