Eventos

12:00 – 12:30 – Anna Labernadie
Study of tumor/stroma mechanobiology in cancer

Abstract:  Our research focuses on understanding processes of cellular mechanosensing (how cells sense and respond to mechanical cues from their environment) involved during tumor dissemination and the immune response in cancer. For those projects, we use or design 2D and 3D on-chip models to mimic the tissue/tumor-like physical constraints, composition, and spatial organization of the tumor and its tumor microenvironment. Those approaches enable the study of tumor and stromal cell motility, interaction, and mechanosensing in controlled microenvironments and specific cellular organization, and address the impact of anti-cancer therapies on those cellular behaviors. In this seminar, we will present our ongoing projects and preliminary results related to NK cell trafficking, cytotoxicity, and mechanosensing using on-chip tumor models.

12:30 – 13:00 – Salvador Meseguer
Mitochondrial G-actin modulates the tumor mitochondrial metabolism and communication with the microenvironment

Abstract: Several studies have reported the presence of actin in mitochondria (mt). The interactions between the actin cytoskeleton and the mt control essential functions of this organelle, including mtDNA expression. The tumor suppressor gene APC, frequently mutated in colorectal cancer, has also been found at the mt and nucleates actin filaments. In this project, we have used a specific mutant of APC which is impaired in actin nucleation, APC-m4, to investigate the role of the G-actin in the mt and links with the mtDNA transcription machinery.
We observed that increased G-actin levels in the mutant cells results in a greater presence of actin at the mtDNA promoter, and an increase of the mitochondrial expression and the oxygen consumption rate without affecting the mitochondrial mass. Using RNASeq data we constructed a condition-specific modelling (in silico) approach that revealed a metabolic rewiring – from glucose oxidation to fatty acid synthesis – in the mutant versus wild type cancer cells. We hypothesize that such metabolic reorganization in the mutant cancer cells stimulates gene expression of FFAR receptors and the ability to polarize and migrate of RAW macrophages.