To advance our understanding of treatment resistance and cancer progression, we investigate how cell death pathways are modulated.

Cells are constantly exposed to various stimuli that can disrupt their homeostasis. In order to maintain their survival, cells have developed complex mechanisms to respond to different types of stress.

Our laboratory investigates cell death pathways through the use of 2D/3D models and various microscopy techniques. One of our primary research areas centers around exploring the alternative roles of BCL2 proteins in cellular physiology. Recent studies have shown that these proteins regulate multiple pathways beyond intrinsic apoptosis, including mitochondrial metabolism. Our aim is to characterize the different functions of BCL2 proteins in cancer cells, and determine their relevance in terms of treatment resistance and stress survival.

Another area of research focuses on entosis, a cell death pathway that allows cancer cells to actively invade other homotypic cancer cells. While entosis provides a survival advantage for the host cell, it selectively removes the internalized cell. Our objective is to investigate the significance of entosis and entotic cell death in the context of cancer, to identify novel stressors and stimuli that induce this process, and to discover chemical tools to modulate entosis.

Presentation

Get to know us better

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Research Staff

The people who make it all possible

Federico Lucantoni 
flucantoni@cipf.es

Alberto Hernandez Cano 
ahernandez@cipf.es

Domingo Gil 
dgil@cipf.es

Virginia Rejas
vrejas@cipf.es

Publications

Our scientific contributions

Implication of autophagy in the antifibrogenic effect of Rilpivirine: when more is less.
Lucantoni F, Benedicto AM, Gruevska A, Moragrega ÁB, Fuster-Martínez I, Esplugues JV, Blas-García A and Apostolova N
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.
Lucantoni F, Salvucci M, Dussmann H and Prehn JHM
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.
Lucantoni F, Salvucci M, Düssmann H, Lindner AU, Lambrechts D and Prehn JHM
CELL DEATH AND DIFFERENTIATION, 2021 May,  DOI:  10.1038/s41418-020-00683-x,  Vol. 28,  pag. 1512-1531

Metabolic Targeting of Breast Cancer Cells With the 2-Deoxy-D-Glucose and the Mitochondrial Bioenergetics Inhibitor MDIVI-1.
Lucantoni F, Dussmann H and Prehn JHM
Frontiers in Cell and Developmental Biology, 2018 Sep,  DOI:  10.3389/fcell.2018.00113,  Vol. 6,  pag. 113-113

Systems modeling accurately predicts responses to genotoxic agents and their synergism with BCL-2 inhibitors in triple negative breast cancer cells.
Lucantoni F, Lindner AU, O'Donovan N, Düssmann H and Prehn JHM
Cell Death & Disease, 2018 Jan,  DOI:  10.1038/s41419-017-0039-y,  Vol. 9,  pag. 42-42

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