Journal Article

DKFZ-2019-02273

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Glutamatergic synaptic input to glioma cells drives brain tumour progression.

Venkataramani, V. (First author) ; Tanev, D. I.DKFZ* ; Strahle, C. ; Studier-Fischer, A.DKFZ* ; Fankhauser, L.DKFZ* ; Kessler, T.DKFZ* ; Körber, C. ; Kardorff, M. ; Ratliff, M.DKFZ* ; Xie, R.DKFZ* ; Horstmann, H. ; Messer, M.DKFZ* ; Paik, S. P. ; Knabbe, J. ; Sahm, F.DKFZ* ; Kurz, F. T. ; Acikgöz, A. A.DKFZ* ; Herrmannsdörfer, F. ; Agarwal, A. ; Bergles, D. E. ; Chalmers, A. ; Miletic, H. ; Turcan, S. ; Mawrin, C. ; Hänggi, D. ; Liu, H.-K.DKFZ* ; Wick, W.DKFZ* ; Winkler, F. (Last author)DKFZ* ; Kuner, T.

2019
Nature Publ. Group52462 London [u.a.]

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Please use a persistent id in citations: doi:10.1038/s41586-019-1564-x

Abstract: A network of communicating tumour cells that is connected by tumour microtubes mediates the progression of incurable gliomas. Moreover, neuronal activity can foster malignant behaviour of glioma cells by non-synaptic paracrine and autocrine mechanisms. Here we report a direct communication channel between neurons and glioma cells in different disease models and human tumours: functional bona fide chemical synapses between presynaptic neurons and postsynaptic glioma cells. These neurogliomal synapses show a typical synaptic ultrastructure, are located on tumour microtubes, and produce postsynaptic currents that are mediated by glutamate receptors of the AMPA subtype. Neuronal activity including epileptic conditions generates synchronised calcium transients in tumour-microtube-connected glioma networks. Glioma-cell-specific genetic perturbation of AMPA receptors reduces calcium-related invasiveness of tumour-microtube-positive tumour cells and glioma growth. Invasion and growth are also reduced by anaesthesia and the AMPA receptor antagonist perampanel, respectively. These findings reveal a biologically relevant direct synaptic communication between neurons and glioma cells with potential clinical implications.

Note: DKFZ-ZMBH Alliance

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Contributing Institute(s):

1. KKE Neuroonkologie (B320)
2. KKE Neuropathologie (B300)
3. A240 Molekulare Neurogenetik (A240)
4. DKTK Heidelberg (L101)

Research Program(s):

1. 312 - Functional and structural genomics (POF3-312) (POF3-312)

Appears in the scientific report 2019

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Database coverage:
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