Plasticité Gliale


Research center

9 Quai Saint-Bernard Université Pierre et Marie Curie, Campus Jussieu, Bâtiments A-B-C
75005 Paris
Michel Labouesse


Université Pierre et Marie Curie


Neuroscience Paris Seine
U1130 UMR8246 UMCR18

Mots clefs

Neural stem cells
Glial cells
Brain tumors
cellular biology
Available to host a PhD student


El-Habr EA, Dubois LG, Burel-Vandenbos F, Bogeas A, Lipecka J, Turchi L, Lejeune FX, Coehlo PL, Yamaki T, Wittmann BM, Fareh M, Mahfoudhi E, Janin M, Narayanan A, Morvan-Dubois G, Schmitt C, Verreault M, Oliver L, Sharif A, Pallud J, Devaux B, Puget S, Korkolopoulou P, Varlet P, Ottolenghi C, Plo I, Moura-Neto V, Virolle T, Chneiweiss H*, Junier MP*. A driver role for GABA metabolism in controlling stem and proliferative cell state through GHB production in glioma. Acta Neuropathol. 2017 Apr;133(4):645-660. doi: 10.1007/s00401-016-1659-5. [IF: 12.21] 

Fareh M, Almairac F, Turchi L, Burel-Vandenbos F, Paquis P, Fontaine D, Lacas-Gervais S, Junier MP, Chneiweiss H, Virolle T. Cell-based therapy using miR-302-367 expressing cells represses glioblastoma growth. Cell Death Dis. 2017 ;8(3):e2713. doi: 10.1038/cddis.2017.117. [IF: 5.97]


Debruyne DN, Turchi L, Burel-Vandenbos F, Fareh M, Almairac F, Virolle V, Figarella-Branger D, Baeza-Kallee N, Lagadec P, Kubiniek V, Paquis P, Fontaine D, Junier MP, Chneiweiss H, Virolle T.DOCK4 promotes loss of proliferation in glioblastoma progenitor cells through nuclear beta-catenin accumulation and subsequent miR-302-367 cluster expression.Oncogene. 2017 Sep 18. doi: 10.1038/onc.2017.323

 Assad Kahn S, Costa SL, Gholamin S, Nitta RT, Dubois LG, F√®ve M, Zeniou M, Coelho PL, El-Habr E, Cadusseau J, Varlet P, Mitra SS, Devaux B, Kilhoffer MC, Cheshier SH, Moura-Neto V, Haiech J, Junier MP*, Chneiweiss H*. The anti-hypertensive drug prazosin inhibits glioblastoma growth via the PKCdelta-dependent inhibition of the AKT pathway. EMBO Mol Med. 2016 May 2;8(5):511-26. doi: 10.15252/emmm.201505421. [IF: 9.25]

Hirsch F, Lévy Y, Chneiweiss H. CRISPR-Cas9: A European position on genome editing. Nature. 2017 Jan 4;541(7635):30. doi: 10.1038/541030c.

Fields of research

Neurophysiology / systems neuroscience

Research Theme

The main focus of our research is the plasticity and development of human brain tumors
We are interested in understanding how interactions between cell intrinsic and extrinsic signaling pathways control the stem and tumor-initiating properties of glioma stem cells.

Our project aims at characterizing intra- and extracellular molecular pathways that restrict the stem-like potential, and consequently the tumorigenicity of human glioma stem cells (GSC), as compared to human neural stem cells (NSC). It takes advantage of the unique model offered by the couple formed by GSC and their non-tumorigenic counterparts miR-302-367-GSC. Recent advances show that the metabolic changes could be at the core of tumorigenesis. They have noteworthy led to the identification of mutations in metabolic enzymes that drive cancer pathogenesis, of metabolic markers of cancer progression, and to the recognition that metabolic changes may affect the cell phenotype. In light of these discoveries, we postulate that a change in cell phenotype as radical as that induced by miR-302-367 should result in metabolic alterations instrumental in the loss of tumorigenic and stem-like properties

We will specifically:
1. Determine the mechanism and functional consequences of the metabolite rearrangements accompanying the irreversible
repression of GSC stem and tumor-initiating properties.
2. Extend the identification of compounds targeting GSC and and transfer