Open AccessThe secreted glycolytic enzyme GPI/AMF stimulates glioblastoma cell migration and invasion in an autocrine fashion but can have anti-proliferative effects
Author(s) -
Annegret Kathagen-Buhmann,
Cécile L. Maire,
Jonathan Weller,
Alexander Schulte,
Jakob Matschke,
Mareike Holz,
Keith L. Ligon,
Markus Glatzel,
Manfred Westphal,
Katrin Lamszus
Publication year - 2018
Publication title -
neuro-oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.005
H-Index - 125
eISSN - 1523-5866
pISSN - 1522-8517
DOI - 10.1093/neuonc/noy117
Subject(s) - autocrine signalling , gene knockdown , downregulation and upregulation , pentose phosphate pathway , cancer research , anaerobic glycolysis , cell growth , biology , motility , cell migration , glycolysis , paracrine signalling , microbiology and biotechnology , cell , cell culture , receptor , biochemistry , enzyme , genetics , gene
Aerobic glycolysis confers several advantages to tumor cells, including shunting of metabolites into anabolic pathways. In glioblastoma cells, hypoxia induces a flux shift from the pentose phosphate pathway toward glycolysis and a switch from proliferation to migration. The mechanistic link between glycolysis and migration is poorly understood. Since glucose-6-phosphate isomerase (GPI) is identical to the secreted cytokine autocrine motility factor (AMF), we investigated whether GPI/AMF regulates glioblastoma cell invasion.
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