A5058075716- Wnt/β-catenin signaling in development and cancer
- Cancer-related gene regulation
- Bone and Dental Protein Studies
- Cancer-related Molecular Pathways
- Mechanisms of cancer metastasis
- Immune cells in cancer
- NF-κB Signaling Pathways
- Cancer Cells and Metastasis
- Cytokine Signaling Pathways and Interactions
- Protein Tyrosine Phosphatases
- Telomeres, Telomerase, and Senescence
- Signaling Pathways in Disease
- Peptidase Inhibition and Analysis
- Digestive system and related health
- Cancer Research and Treatments
- Protease and Inhibitor Mechanisms
- Ion channel regulation and function
- Antimicrobial Peptides and Activities
- RNA Interference and Gene Delivery
- Cancer Mechanisms and Therapy
- RNA Research and Splicing
- Immunotherapy and Immune Responses
- Epigenetics and DNA Methylation
- Genomics and Chromatin Dynamics
- Genetic factors in colorectal cancer
Consorci Institut D'Investigacions Biomediques August Pi I Sunyer
2010-2023
Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas
2013-2023
Hospital Clínic de Barcelona
2023
Universitat de Barcelona
2003-2021
Hospital Universitario HM Sanchinarro
2019
University of Louisville
2013
Hospital Universitario Miguel Servet
2012
Instituto de Investigación Sanitaria Aragón
2012
Institute for Research in Biomedicine
2007-2010
Instituto de Agroquímica y Tecnología de Alimentos
2010
In most carcinomas, invasion of malignant cells into surrounding tissues involves their molecular reprogramming as part an epithelial-to-mesenchymal transition (EMT). Mutation the APC gene in colorectal carcinomas (CRCs) contributes to nuclear translocation oncoprotein β-catenin that upon binding T-cell and lymphoid enhancer (TCF-LEF) factors triggers EMT a proinvasive expression profile. A key inducer is ZEB1 transcription factor whose promotes tumorigenesis metastasis carcinomas. As...
Earlier work has shown that the transcription factor C/EBPalpha induced a transdifferentiation of committed lymphoid precursors into macrophages in process requiring endogenous PU.1. Here we have examined effects PU.1 and on fibroblasts, cell type distantly related to blood cells akin myoblasts, adipocytes, osteoblasts, chondroblasts. The combination two factors, as well C/EBPbeta, up-regulation macrophage/hematopoietic surface markers large proportion NIH 3T3 cells. They also up-regulated...
Murine bone marrow macrophages were able to recognize gold nanoparticle peptide conjugates, while peptides or nanoparticles alone not recognized. Consequently, in the presence of macrophage proliferation was stopped and pro-inflammatory cytokines such as TNF-α, IL-1β, IL-6, well nitric oxide synthase (NOS2) induced. Furthermore, activation by conjugated different appeared be rather independent length polarity, but dependent on pattern at surface. Correspondingly, biochemical type response...
Voltage-dependent K+ channels (VDPC) are expressed in most mammalian cells and involved the proliferation activation of lymphocytes. However, role VDPC macrophage responses is not well established. This study was undertaken to characterize macrophages determine their physiological during activation. Macrophages proliferate until an endotoxic shock halts cell growth they become activated. By inducing a schedule that similar pattern, we have identified non-transformed bone marrow-derived...
Abstract Macrophages perform essential functions in the infection and resolution of inflammation. IFN-γ is main endogenous macrophage Th1 type activator. The classical signaling pathway involves activation Stat-1. However, has also capability to activate members MAPK family. In primary bone marrow-derived macrophages, we have observed strong p38 at early time points stimulation, whereas weak ERK-1/2 JNK-1 was detected a more delayed stage. parallel, exerted repressive effects on expression...
Abstract Purpose: Carcinoma cells enhance their invasive capacity through dedifferentiation and dissolution of intercellular adhesions. A key activator this process is the ZEB1 transcription factor, which induced in invading cancer by canonical Wnt signaling (β-catenin/TCF4). Tumor invasiveness also entails proteolytic remodeling peritumoral stroma. This study aimed to investigate potential regulation plasminogen system constituted urokinase (uPA), its inhibitor, inhibitor-1 (PAI-1)....
Skeletal muscle development is orchestrated by the myogenic regulatory factor MyoD, whose activity blocked in myoblasts proteins preventing its nuclear translocation and/or binding to G/C-centered E-boxes target genes. Recent evidence indicates that gene expression also regulated at cis level differential affinity for DNA between MyoD and other E-box during myogenesis. binds E-boxes, enriched differentiation genes, myotubes but not myoblasts. Here, we used cell-based vivo Drosophila, Xenopus...
Macrophages proliferate in the presence of their growth factor, macrophage colony-stimulating factor (M-CSF), a process that is dependent on early and short ERK activation. Lipopolysaccharide (LPS) induces activation, stops proliferation, delays phosphorylation, thereby triggering an inflammatory response. Proliferating or activating responses are balanced by kinetics inactivation which correlates with Mkp1 induction. Here we show transcriptional induction this phosphatase M-CSF LPS depends...
<h3>Objective</h3> Understand the role of ZEB1 in tumour initiation and progression beyond inducing an epithelial-to-mesenchymal transition. <h3>Design</h3> Expression transcription factor associates with a worse prognosis most cancers, including colorectal carcinomas (CRCs). The study uses survival analysis, vivo mouse transgenic xenograft models, gene expression arrays, immunostaining protein regulation assays. <h3>Results</h3> poorer determined by <i>ZEB1</i> CRCs depended on simultaneous...
Abstract Background Bipolar disorder (BD) is a chronic and recurrent disease characterized by acute mood episodes periods of euthymia. The available literature postulates that biphasic dysregulation mitochondrial bioenergetics might underpin the neurobiology BD. However, most studies focused on inter‐subject differences rather than intra‐subject variations between different states. To test this hypothesis, in preliminary proof‐of‐concept study, we measured vivo respiration patients with BD...
Mouse bone marrow-derived macrophages proliferate in the presence of macrophage colony-stimulating factor (M-CSF), granulocyte-macrophage factor, or IL-3, but undergo apoptosis their absence. Inhibition extracellular signal-regulated kinases (ERK)-1/2 blocks growth factor-dependent proliferation not survival, indicating that two processes require independent signaling pathways. Although M-CSF induces activation other kinase pathways, such as c-Jun N-terminal kinase, p38, and...
Abstract MAPK phosphatase‐1 (MKP‐1) is a protein phosphatase that plays crucial role in innate immunity. This inactivates ERK1/2, which are involved two opposite functional activities of the macrophage, namely proliferation and activation. Here we found although macrophage activation induce MKP‐1 with different kinetics, gene expression mediated by proximal promoter sequences localized between −380 −180 bp. Mutagenesis experiments element determined CRE/AP‐1 required for LPS‐ or...
BCL6 is essential for normal antibody responses and highly expressed in germinal centre B-cells. Constitutive expression due to chromosomal translocations or mutations of cis-acting regulatory elements contributes diffuse large B-cell lymphoma. therefore tightly regulated a lineage- developmental-stage-specific manner, disruption controls can contribute lymphomagenesis. In order discover potential control regions we carried out DNase I-hypersensitive site mapping. Gel-shift assays chromatin...
Despite being in the same pathway, mutations of KRAS and BRAF colorectal carcinomas (CRCs) determine distinct progression courses. ZEB1 induces an epithelial-to-mesenchymal transition (EMT) is associated with worse most carcinomas. Using samples from patients CRC, mouse models KrasG12D BrafV600E a Zeb1-deficient mouse, we show that had opposite functions KRAS- BRAF-mutant CRCs. In CRCs, was correlated prognosis higher number larger undifferentiated (mesenchymal or EMT-like) tumors....
Rb1 restricts cell cycle progression, and it imposes contact inhibition to suppress tumor outgrowth. It also triggers oncogene-induced senescence block Ras mutation. Loss of the pathway, which is a hallmark cancer cells, then provides permissive environment for mutation, sufficient invasive formation in family mutant mouse embryo fibroblasts (MEFs). These results demonstrate that sequential mutation pathways comprises initiation axis. Both regulate expression transcription factor ZEB1,...