CONTACT

Team Leader

Gabriel Ichim, PhD
gabriel.ichim@lyon.unicancer.fr

ROUMANE Ahlima
EL FASSI Chaimaa

Master 2 student

Voir les objectifs et projets Voir les publications

Fundings

LabEX DEVweCAN

EMBO 

OBJECTIVES

Our lab studies apoptosis (the main form of programmed cell death) and it's effectors, mitochondria and caspases. Beside having an important role in development, apoptosis is often affected in several pathologies: in cancer, apoptosis is most of the time blocked allowing rapid tumour growth, while in neurodegenerative diseases there is an excess of apoptosis. 

The key player in apoptosis is the mitochondria, an organelle that on one side provides the energy needed for survival while it also holds the power to kill the same cell: this happens when the mitochondria permeabilise following a lethal stress and triggers caspase activation. Caspases are proteases that efficiently kill the cell within minutes. 

Our team is interested in non-canonical roles that mitochondria and caspases have in tumourigenesis and development. Since it was recently showed that only few mitochondria can permeabilise allowing non-lethal caspase activation, we currently investigate the role of this discrete caspase activation in various settings ranging from cancer cell migration and invasion to stemness or senescence. 

PUBLICATIONS

ICHIM, G., Tait S.W. (2016) A fate worse than death: apoptosis as an oncogenic process. Nature Reviews Cancer 16: 539-48 

Correia-Melo, C.*, ICHIM, G.*, Tait, S. W. and Passos, J. F. (2016) Depletion of mitochondria in mammalian cells through enforced mitophagy. Nature Protocols.

ICHIM, G., Lopez, J., Ahmed, S.U., Muthalagu, N., Giampazolias, E., Delgado, M.E., Haller, M., Riley, J.S., Mason, S.M., Athineos, D., Parsons, M. J.,van de Kooij, B., Bouchier-Hayes, L., Chalmers, A. J., Rooswinkel, R. W., Oberst, A., Blyth, K., Rehm, M., Murphy, D. J., Tait, S. W. (2015). Limited mitochondrial permeabilization causes DNA damage and genomic instability in the absence of cell death. Molecular Cell 57, 860-872. 

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