Cancer cell death
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.
Cancer Cell Death team is focused right now on investigating how cell death is actually fuelling the oncogenic process by either promoting the proliferation of bystander cancer cells (Roumane et al., BMC Cell Biology, 2018), boosting the aggressiveness of cancer cells undergoing failed apoptosis (Berthenet et al., Cell Reports, 2020) or by sustaining glioblastoma stem cells survival (Fanfone et al., Cancers, 2020). The team also recently showed how lethal caspase activation in cancer cells can be weakened by tumor-relevant mechanical stress, uncovering yet another mechanism of treatment resistance (Fanfone et al., eLife, 2022).
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