TO BETTER UNDERSTAND TREATMENT RESISTANCE AND CANCER PROGRESSION, OUR LAB STUDIES HOW CELL DEATH PATHWAYS ARE REGULATED UNDER STRESS.
Cells constantly face stimuli that disrupt homeostasis and have evolved mechanisms to survive such challenges. We investigate these responses using 2D/3D models and advanced microscopy.
A core focus is the multifunctional role of BCL2 family proteins. Beyond intrinsic apoptosis, these proteins regulate mitochondrial metabolism and other processes. We aim to define their non-canonical roles in cancer cells and how they support stress adaptation and therapy resistance.
We also study entosis, a form of cell death where one cell actively internalizes another. This process can benefit the host cell while eliminating the internalized one. We seek to determine its role in cancer progression, identify stressors that induce it, and discover compounds to modulate it.
Additionally, we investigate resistance driven by therapy-induced senescence in breast cancer. CDK4/6 inhibitors induce a senescent state, but senescent cells may persist and promote relapse through secretory and metabolic changes. Our goal is to dissect the molecular features of this state and identify vulnerabilities that can be targeted to improve therapeutic outcomes.
PRESENTATION
GET TO KNOW US BETTER
RESEARCH STAFF
THE PEOPLE WHO MAKE IT ALL POSSIBLE
Federico Lucantoni
flucantoni@cipf.es
Carolina Gandía Ventura
cgandia@cipf.es
PUBLICATIONS
OUR SCIENTIFIC CONTRIBUTIONS
Implication of autophagy in the antifibrogenic effect of Rilpivirine: when more is less.
Cell Death & Disease 2022 Apr, DOI: 10.1038/s41419-022-04789-7, Vol. 13, pag. 385-385
BCL(X)L and BCL2 increase mitochondrial dynamics in breast cancer cell: Evidence from functional and genetic studies.
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH 2021 Sep, DOI: 10.1016/j.bbamcr.2021.119095, Vol. 1868, pag. 119095-119095
BCL(X)L and BCL2 increase the metabolic fitness of breast cancer cells: a single-cell imaging study.
CELL DEATH AND DIFFERENTIATION 2021 May, DOI: 10.1038/s41418-020-00683-x, Vol. 28, pag. 1512-1531
