Glial Plasticity and Neuro-Oncology


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


Astrocyte, glioma, metabolism, epigenetic, proteomic


Assad Kahn S, Costa SL, Gholamin S, Nitta RT, Dubois LG, Fève 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 PKCδ-dependent inhibition of the AKT pathway.EMBO Mol Med. 2016 May 2;8(5):511-26. doi: 10.15252/emmm.201505421.

Turchi L, Debruyne DN, Almairac F, Virolle V, Fareh M, Neirijnck Y, Burel-Vandenbos F, Paquis P, Junier MP, Van Obberghen-Schilling E, Chneiweiss H,Virolle T. Tumorigenic Potential of miR-18A* in Glioma Initiating Cells Requires NOTCH-1 Signaling. Stem Cells. 2013 31:1252-65.

Thirant C, Galan-Moya EM, Dubois LG, Pinte S, Chafey P, Broussard C, Varlet P, Devaux B,Soncin F, Gavard J, Junier MP,Chneiweiss H. Differential proteomic analysis of human glioblastoma and neural stem cells reveals HDGF as a novel angiogenic secreted factor.Stem Cells. 2012 May;30(5):845-53.

Fareh M, Turchi L, Virolle V, Debruyne D, Almairac F, de-la-Forest Divonne S, Paquis P, Preynat-Seauve O, Krause KH, Chneiweiss H, Virolle T The. miR 302-367 cluster drastically affects self-renewal and infiltration properties of glioma-initiating cells through CXCR4 repression and consequent disruption of the SHH-GLI-NANOG network.Cell Death Differ. 2012 Feb;19(2):232-44.

Galan-Moya EM, Le Guelte A, Lima-Fernandes E, Thirant C, Dwyer J, Bidere N, Couraud PO, Scott M, Junier MP Chneiweiss H, Gavard J.?Brain endothelial cells maintain glioblastoma stem-like cell expansion through the mTOR pathway. EMBO Report 2011,12: 470-6.

Silvestre DC, Pineda Marti JR, Hoffschir F, Studler JM,Mouthon MA, Pflumio F, Junier MP, Chneiweiss H,Boussin FD. Alternative Lengthening of Telomeres in Human Glioma Stem Cells. Stem Cells. 2011 Mar;29(3):440-

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