Florinda Meléndez‐Rodríguez

ORCID: 0000-0002-1990-569X
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About
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Research Areas
  • Cancer, Hypoxia, and Metabolism
  • Epigenetics and DNA Methylation
  • Erythropoietin and Anemia Treatment
  • Adipose Tissue and Metabolism
  • Diet, Metabolism, and Disease
  • Renal cell carcinoma treatment
  • Histone Deacetylase Inhibitors Research
  • Peroxisome Proliferator-Activated Receptors
  • Mitochondrial Function and Pathology
  • RNA modifications and cancer
  • Alcohol Consumption and Health Effects
  • Immune Cell Function and Interaction
  • CAR-T cell therapy research
  • Cancer-related Molecular Pathways
  • Metabolism and Genetic Disorders
  • Liver Disease Diagnosis and Treatment
  • Immune cells in cancer
  • Amino Acid Enzymes and Metabolism
  • Virus-based gene therapy research
  • Adipokines, Inflammation, and Metabolic Diseases

Hospital Universitario Santa Cristina
2012-2022

Universidad Autónoma de Madrid
2012-2022

Centro de Investigación en Red en Enfermedades Cardiovasculares
2019-2020

Hospital Universitario de La Princesa
2020

Centro de Investigación Biomédica en Red
2018-2020

Instituto de Salud Carlos III
2018-2019

Cellular aspartate drives cancer cell proliferation, but signaling pathways that rewire biosynthesis to control growth remain largely unknown. Hypoxia-inducible factor-1α (HIF1α) can suppress tumor proliferation. Here, we discovered HIF1α acts as a direct repressor of involving the suppression several key aspartate-producing proteins, including cytosolic glutamic-oxaloacetic transaminase-1 (GOT1) and mitochondrial GOT2. Accordingly, suppresses production from both glutamine oxidation well...

10.1016/j.celrep.2019.01.106 article EN cc-by-nc-nd Cell Reports 2019-02-01

Molecular mechanisms by which hypoxia might contribute to hepatosteatosis, the earliest stage in non-alcoholic fatty liver disease (NAFLD) pathogenesis, remain still be elucidated. We aimed assess impact of hypoxia-inducible factor 2α (HIF2α) on acid translocase CD36 expression and function vivo vitro.CD36 intracellular lipid content were determined hypoxic hepatocytes, CD36- or HIF2α -silenced human cells. Histological analysis, evaluated livers from animals von Hippel-Lindau (Vhl) gene is...

10.1111/liv.14519 article EN cc-by Liver International 2020-05-20

CD69 is an early activation marker on the surface of T lymphocytes undergoing by cognate antigen. We observed intense expression tumor-infiltrating T-lymphocytes that reside in hypoxic tumor microenvironment and hypothesized could be, at least partially, under control transcriptional hypoxia response. In line with this, human mouse CD3-stimulated cultured (1% O2) showed increased protein mRNA level. Consistent these findings, had recently undergone vivo, as denoted pimonidazole staining,...

10.1080/2162402x.2017.1283468 article EN OncoImmunology 2017-01-19

Summary Recombinant human erythropoietin (r H u EPO ) is an effective treatment for anaemia but concerns that it causes disease progression in cancer patients by activation of receptors ( EPOR tumour tissue have been controversial and restricted its clinical use. Initial studies were flawed because they used polyclonal antibodies, later shown to lack specificity . Moreover, multiple isoforms caused differential splicing reported cell lines at the m RNA level investigations these variants...

10.1111/bjh.13133 article EN British Journal of Haematology 2014-10-04

Cellular response to hypoxia is controlled by the hypoxia-inducible transcription factors HIF1α and HIF2α. Some genes are preferentially induced or HIF2α, as has been explored in some cell models for particular sets of genes. Here we have extended this analysis other HIF-dependent using vitro WT8 renal carcinoma cells vivo conditional Vhl-deficient mice models. Moreover, generated chimeric HIF1/2 study contribution HIF2α DNA binding/heterodimerization transactivation domains HIF target...

10.3390/ijms21249401 article EN International Journal of Molecular Sciences 2020-12-10

Erythropoietin receptor (EPOR) is widely expressed in healthy and malignant tissues. In certain malignancies, EPOR stimulates tumor growth. tissues, controls processes other than erythropoiesis, including mitochondrial metabolism. We hypothesized that also the metabolism cancer cells. To test this hypothesis, we generated EPOR-knockdown cells to grow xenografts mice analyzed cellular respiration via high-resolution respirometry. Furthermore, respiratory control, content, regulators of...

10.3389/fonc.2022.976961 article EN cc-by Frontiers in Oncology 2022-08-16
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