Ricardo Armisén

ORCID: 0000-0003-2567-0521
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About
Contact & Profiles
Research Areas
  • Cancer Genomics and Diagnostics
  • Lung Cancer Treatments and Mutations
  • RNA regulation and disease
  • RNA Research and Splicing
  • RNA modifications and cancer
  • Gastric Cancer Management and Outcomes
  • Ion Channels and Receptors
  • Ion channel regulation and function
  • Magnesium in Health and Disease
  • Genetic factors in colorectal cancer
  • Endoplasmic Reticulum Stress and Disease
  • Genomics and Rare Diseases
  • Cancer-related molecular mechanisms research
  • CRISPR and Genetic Engineering
  • Colorectal Cancer Treatments and Studies
  • PI3K/AKT/mTOR signaling in cancer
  • RNA and protein synthesis mechanisms
  • Neuroscience and Neuropharmacology Research
  • Wnt/β-catenin signaling in development and cancer
  • Cholangiocarcinoma and Gallbladder Cancer Studies
  • Microtubule and mitosis dynamics
  • Protein Kinase Regulation and GTPase Signaling
  • Laser-Plasma Interactions and Diagnostics
  • Cancer Immunotherapy and Biomarkers
  • Cardiac electrophysiology and arrhythmias

Universidad del Desarrollo
2020-2025

Clínica Alemana
2020-2025

Universidad del Desarrollo del Estado de Puebla
2024

University of Chile
2010-2020

Precision for Medicine (United States)
2018

University of Talca
2017

State University of New York
2004-2006

Stony Brook University
2004-2006

Howard Hughes Medical Institute
2004

Endothelial dysfunction is decisive in the progression of cardiovascular diseases. Lipopolysaccharide (LPS)-induced reactive oxygen species (ROS)-mediated endothelial cell death a main feature observed inflammation secondary to endotoxaemia, emerging as leading cause among critically ill patients intensive care units. However, molecular mechanism underlying LPS-induced not well understood. Transient receptor protein melastatin 4 (TRPM4) an ion channel associated with that expressed...

10.1093/cvr/cvr135 article EN Cardiovascular Research 2011-05-11

Increased expression of the TRPM 4 channel has been reported to be associated with progression prostate cancer. However, molecular mechanism underlying its effect remains unknown. This work found that decreasing levels leads reduced proliferation PC 3 cells. was a decrease in total β‐catenin protein and nuclear localization, significant reduction Tcf/Lef transcriptional activity. Moreover, silencing increases Ser33/Ser37/Thr41 phosphorylated population reduces phosphorylation GSK ‐3β at...

10.1002/1878-0261.12100 article EN cc-by Molecular Oncology 2017-06-14

Prion-related disorders (PrDs) are fatal neurodegenerative characterized by progressive neuronal impairment as well the accumulation of an abnormally folded and protease resistant form cellular prion protein, termed PrPRES. Altered endoplasmic reticulum (ER) homeostasis is associated with occurrence neurodegeneration in sporadic, infectious familial forms PrDs. The ER operates a major intracellular calcium store, playing crucial role pathological events related to dysfunction death. Here we...

10.1371/journal.pone.0015658 article EN cc-by PLoS ONE 2010-12-29

β-Catenin is a key protein in the canonical Wnt signaling pathway and many cancers alterations transcriptional activity of its components are observed. This up-regulated by kinase CK2, but underlying mechanism this change unknown. It has been demonstrated that CK2 hyperactivates AKT/PKB phosphorylation at Ser129, AKT phosphorylates β-catenin Ser552, which turn, promotes nuclear localization activity. However, consequences CK2-dependent hyperactivation on cell viability have not evaluated. We...

10.1002/jcp.22527 article EN Journal of Cellular Physiology 2010-11-16

Abstract Transient Receptor Potential Melastatin 4 (TRPM4) is a Ca 2+ ‐activated and voltage‐dependent monovalent cation channel, which depolarizes the plasma cell membrane, thereby modulating influx across ‐permeable pathways. TRPM4 involved in different physiological processes such as T activation migration of endothelial certain immune cells. Overexpression this channel has been reported various types tumors including prostate cancer. In study, significant overexpression was found only...

10.1002/jcp.27371 article EN Journal of Cellular Physiology 2018-10-21

Whole transcriptome RNA variant analyses have shown that adenosine deaminases acting on (ADAR) enzymes modify a large proportion of cellular RNAs, contributing to diversity and cancer evolution. Despite the advances in understanding ADAR function breast cancer, editing functional consequences are not fully addressed. We characterized A G(I) mRNA 81 cell lines, showing increased at 3'UTR exonic regions cells compared immortalized non-malignant lines. In addition, tumors from BRCA TCGA cohort...

10.1186/s40659-018-0185-4 article EN cc-by Biological Research 2018-10-05

Necrosis is associated with an increase in plasma membrane permeability, cell swelling, and loss of integrity subsequent release cytoplasmic constituents. Severe redox imbalance by overproduction reactive oxygen species one the main causes necrosis. Here we demonstrate that H2O2 induces a sustained activity TRPM4, Ca2+-activated, Ca2+-impermeant nonselective cation channel resulting increased vulnerability to death. In HEK 293 cells overexpressing was found eliminate dose-dependent manner...

10.1074/jbc.m110.155390 article EN cc-by Journal of Biological Chemistry 2010-10-01

Altered expression of some members the TRP ion channel superfamily has been associated with development pathologies like cancer. In particular, TRPM4 levels are reportedly elevated in diffuse large B-cell non-Hodgkin lymphoma, prostate, and cervical However, whether such changes may be relevant to genesis or progression cancer remains unknown. Here we show that reducing decreases proliferation HeLa cells, a cancer-derived cell line. this line, constitutive silencing promoted GSK-3β-dependent...

10.1002/jcp.22310 article EN Journal of Cellular Physiology 2010-07-12

Dysregulated A>I(G) RNA editing, which is mainly catalyzed by ADAR1 and a type of post-transcriptional modification, has been linked to cancer. A low response therapy in breast cancer (BC) significant contributor mortality. However, it remains unclear if there an association between RNA-edited sites sensitivity genotoxic drugs. To address this issue, we employed stringent bioinformatics approach identify differentially (DESs) associated with or high (FDR 0.1, log2 fold change 2.5)...

10.3390/biomedicines12040728 article EN cc-by Biomedicines 2024-03-25

Tobacco use is one of the main risk factors for Lung Cancer (LC) development. However, about 10–20% those diagnosed with disease are never-smokers. For Non-Small Cell (NSCLC) there clear differences in both clinical presentation and tumor genomic profiles between smokers example, Adenocarcinoma (LUAD) histological subtype never-smokers predominately found young women European, North American, Asian descent. While have been widely examined, usually underrepresented, especially a Latin...

10.1186/s12885-024-12737-1 article EN cc-by-nc-nd BMC Cancer 2024-08-03

Adenosine-to-inosine (A-to-I) RNA editing and alternative splicing occur co-transcriptionally can regulate influence each other. The enzymes ADAR1 ADAR2 catalyze A-to-I editing, where it has been shown that expression changes in both exert splicing. manipulation a significant impact on While many of those are related to their activity, we speculate may also an editing-independent manner. In this work, the protein-protein interactome revealed interacts with spliceosome co-factors auxiliary...

10.1101/2025.03.12.642916 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2025-03-12

Restrictions resulting from the COVID-19 pandemic abruptly reversed slow decline of diagnosis and mortality rates gastric cancer (GC). This scenario highlights importance developing cost-effective methods for mass screening evaluation treatment response. In this study, we evaluated a non-invasive method based on circulating methylated cell-free DNA (cfDNA) Reprimo (RPRM), tumor suppressor gene associated with development GC. Methylated RPRM cfDNA was analyzed in three de-identified cohorts:...

10.3390/ijms26073333 article EN International Journal of Molecular Sciences 2025-04-03

ABSTRACT The mechanism of how toxicant exposure leads to aggressive tumors remains unresolved. A genetic‐based hypothesis predicts that under stress, the transcription growth‐related genes will be inhibited by activation mitogenic pathways, redirecting energy toward stress response and increasing survival. This fails explain why epidemiological data suggest growth are activated, as patients exposed toxicants exhibit more than nonexposed individuals. co‐occurrence requires increased...

10.1002/jat.4790 article EN Journal of Applied Toxicology 2025-04-15

Abstract Motivation: Tumors of non-small cell lung cancer (NSCLC) patients are heterogeneous entities. Genomic landscapes influenced by genetic constitution, environmental exposures and the complex interaction between two. In particular, it has been reported that germline variability specific to Latin American (LA) populations play an important role modulating presence acquired somatic alterations in EGFR KRAS, two most clinically relevant actionable genes for (LC). The influence these...

10.1158/1538-7445.am2025-1005 article EN Cancer Research 2025-04-21

Aims: To assess the mechanisms involved in lipopolysaccharide (LPS)-induced neuronal cell death, we examined cellular consequences of LPS exposure differentiated PC12 neurons and primary hippocampal neurons. Results: Our data show that is able to induce death without participation glial cells. Neuronal was mediated by an increase reactive oxygen species (ROS) levels. Considering prevalent role specific ion channels mediating deleterious effect ROS, assessed their contribution this process....

10.1089/ars.2010.3825 article EN Antioxidants and Redox Signaling 2011-05-03
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