Karine Belguise

ORCID: 0000-0003-3426-8040
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About
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Research Areas
  • Cancer Cells and Metastasis
  • TGF-β signaling in diseases
  • Liver Disease and Transplantation
  • Cell Adhesion Molecules Research
  • Retinoids in leukemia and cellular processes
  • Cellular Mechanics and Interactions
  • NF-κB Signaling Pathways
  • Protease and Inhibitor Mechanisms
  • Mesenchymal stem cell research
  • Extracellular vesicles in disease
  • Organ Transplantation Techniques and Outcomes
  • Cancer-related Molecular Pathways
  • Estrogen and related hormone effects
  • Pulmonary Hypertension Research and Treatments
  • MicroRNA in disease regulation
  • Cancer, Hypoxia, and Metabolism
  • Cytokine Signaling Pathways and Interactions
  • Cancer-related gene regulation
  • Genetic factors in colorectal cancer
  • FOXO transcription factor regulation
  • ATP Synthase and ATPases Research
  • Neurobiology and Insect Physiology Research
  • Neonatal Respiratory Health Research
  • Cancer-related molecular mechanisms research
  • Ubiquitin and proteasome pathways

Université de Toulouse
2012-2024

Centre National de la Recherche Scientifique
2012-2024

Université Toulouse III - Paul Sabatier
2012-2024

Centre de Biologie du Développement
2024

Laboratoire de Biologie Cellulaire et Moléculaire du Contrôle de la Prolifération
2015-2023

Army Medical University
2023

Southwest Hospital
2023

Inserm
2001-2016

Université de Montpellier
2012-2016

Institut de Recherche en Cancérologie de Montpellier
2012-2016

Abstract Previously, we showed that the bioactive green tea polyphenol epigallocatechin-3-gallate (EGCG) inhibits growth in soft agar of breast cancer cells with Her-2/neu overexpression. Using gene expression profiling, here show EGCG treatment Her-2/neu–driven mammary tumor alters key regulators epithelial to mesenchymal transition (EMT) pathway, reducing invasive phenotype. Specifically, genes E-cadherin, γ-catenin, MTA3, and estrogen receptor α (ERα) were up-regulated by EGCG, whereas...

10.1158/0008-5472.can-06-4327 article EN Cancer Research 2007-06-15

Induction of epithelial-to-mesenchymal transition (EMT) by TGF-β1 requires Ras signaling. We recently identified the transcriptional repressor Blimp-1 (PRDM1) as a downstream effector NF-κB, RelB/Bcl-2/Ras-driven pathway that promotes breast cancer cell migration. As RelB/Blimp-1 similarly required signaling activation, we tested whether plays role in TGF-β1-mediated EMT. Here, treatment untransformed NMuMG mammary epithelial and MDA-MB-231 cells was shown to induce expression, which...

10.1158/0008-5472.can-12-2270 article EN Cancer Research 2012-10-11

Abstract Pulsatile actomyosin contractility, important in tissue morphogenesis, has been studied mainly apical but less basal domains. Basal myosin oscillation underlying egg chamber elongation is regulated by both cell–matrix and cell–cell adhesions. However, the mechanism which these two adhesions govern unknown. Here we demonstrate that adhesion positively regulates junctional Rho1 activity medio-basal ROCK activities, thus strongly controlling elongation. Differently, governs through...

10.1038/ncomms14708 article EN cc-by Nature Communications 2017-04-13

Actomyosin networks constrict cell area and junctions to alter tissue shape. However, during expansion under mechanical stress, actomyosin are strengthened polarized relax stress. Thus, cells face a conflicting situation between the enhanced contractile properties behaviour of or tissue. To address this paradoxical situation, we study late Drosophila oogenesis reveal an unusual epithelial wave behaviour. Mechanistically, Rac1 Rho1 integrate basal pulsatile with ruffles focal adhesions...

10.1038/s41467-024-47236-1 article EN cc-by Nature Communications 2024-04-08

Activated estrogen receptor α (ERα) modulates transcription triggered by the factor activator protein-1 (AP-1), which consists of Jun-Jun homodimers and Jun-Fos heterodimers. Previous studies have demonstrated that interference occurs without binding ERα to DNA but probably results from protein·protein interactions. However, involvement a direct interaction between AP-1 is still debated. Using glutathioneS-transferase pull-down assays, we bound directly c-Jun JunB not FOS family members, in...

10.1074/jbc.m101806200 article EN cc-by Journal of Biological Chemistry 2001-09-01

Abstract Exposure to and bioaccumulation of lipophilic environmental pollutants, such as polycyclic aromatic hydrocarbons (PAHs), has been implicated in breast cancer. Treatment female rats with the prototypic xenobiotic PAH 7,12-dimethylbenz(a)anthracene (DMBA) induces mammary tumors an invasive phenotype. Here, we show that green tea prevents or reverses loss epithelial marker E-cadherin on surface DMBA-induced situ cancers. To investigate mechanism(s) leading a less phenotype, effects...

10.1158/0008-5472.can-07-2730 article EN Cancer Research 2007-12-15

Aberrant constitutive expression of NF-kappaB subunits, reported in more than 90% breast cancers and multiple other malignancies, plays pivotal roles tumorigenesis. Higher RelB subunit was demonstrated estrogen receptor alpha (ERalpha)-negative versus ERalpha-positive ones, due part to repression synthesis by ERalpha signaling. Notably, promoted a invasive phenotype ERalpha-negative via induction the BCL2 gene. We report here that reciprocally inhibits cancer cells, which contributes...

10.1128/mcb.00032-09 article EN Molecular and Cellular Biology 2009-05-12

The vast majority of primary human breast cancer tissues display aberrant nuclear NF-κB c-Rel expression. A causal role for in mammary tumorigenesis has been demonstrated using a transgenic mouse model; however, tumors developed with long latency, suggesting second event is needed to trigger tumorigenesis. Here we show that activity the gland repressed by estrogen receptor α (ERα) signaling, and identify an epigenetic mechanism mediated activation what believe novel PKCθ-Akt pathway leads...

10.1172/jci32424 article EN Journal of Clinical Investigation 2007-11-21

Abstract Integration of collective cell direction and coordination is believed to ensure guidance for efficient movement. Previous studies demonstrated that chemokine receptors PVR EGFR govern a gradient Rac1 activity essential Drosophila border cells, whose mechanistic insight unknown. By monitoring manipulating subcellular activity, here we reveal two switchable pools at protrusions supracellular cables, important structures responsible coordination. Rho1 form positive feedback loop guides...

10.1038/s41467-022-33727-6 article EN cc-by Nature Communications 2022-10-12

Abstract Hepatopulmonary syndrome (HPS) is a serious vascular complication in the setting of liver disease. Factors produced by are essential to regulate pulmonary angiogenesis pathogenesis HPS; however, pathogenic mechanisms not fully understood. We investigated role HPS rat serum exosomes (HEs) and sham-operated (SEs) regulation angiogenesis. found that HEs significantly enhance PMVEC proliferation, migration, tube formation. further identified miR-194 was most notably increased miRNA...

10.1038/s41419-019-2087-y article EN cc-by Cell Death and Disease 2019-11-07

The incidence of subarachnoid hemorrhage (SAH) and hazard ratio death increase with age. Overactivation microglia contributes to brain damage. This study aimed investigate the effects A3 adenosine receptors (A3R) activation on neurofunction microglial phenotype polarization in context SAH aged rats. A3R agonist (CI-IB-MECA) antagonist (MRS1523) were used model. Microglia cultured mimic presence or absence CI-IB-MECA and/or siRNA for A3R. status evaluated. P38 inhibitor SB202190 STAT6...

10.18632/aging.202178 article EN cc-by Aging 2020-11-27

The matrix metalloproteinase (MMP) family degrades the extracellular matrix. One member of this family, MMP‐1, initiates breakdown interstitial collagens. expression MMP‐1 is controlled by mitogen activated protein kinase (MAPK) pathway(s) via activity activator protein‐1 (AP‐1) and polyoma enhancing activity‐3/E26 virus (PEA3/ETS) transcription factors through consensus binding sites present in promoter. Another ETS site promoter created at −1607 bp a single nucleotide polymorphism (SNP),...

10.1046/j.1432-1033.2003.03821.x article EN European Journal of Biochemistry 2003-09-30

In the presence of estradiol, estrogen receptor-alpha (ERalpha) increases transcription triggered by activator protein-1 (AP-1). We have previously shown that induction is mediated direct interaction between c-Jun and ERalpha, which stabilizes a multiprotein complex containing coactivator GRIP1 (glucocorticoid receptor interacting protein 1). The effect receptor-interacting 140 (RIP140) in this regulation was assessed present study. report overexpression RIP140 inhibits estradiol-induced...

10.1210/me.2002-0324 article EN Molecular Endocrinology 2003-01-28

Actomyosin supracellular networks emerge during development and tissue repair. These cytoskeletal structures are able to generate large scale forces that can extensively remodel epithelia driving buckling, closure extension. How emerge, controlled mechanically work still remain elusive. During Drosophila oogenesis, the egg chamber elongates along anterior-posterior axis. Here we show a dorsal-ventral polarized F-actin network, running around on basal side of follicle cells, emerges from...

10.1038/s41467-020-15593-2 article EN cc-by Nature Communications 2020-04-21

Background/Aims: Pulmonary microvascular endothelial cell (PMVEC) proliferation and angiogenesis contribute to the development of hepatopulmonary syndrome (HPS). MicroRNA-199a-5p (miR-199a-5p) has emerged as a potent regulator angiogenesis, its expression levels significantly decrease in serum patients with hepatopathy. However, it not been reported about whether miR-199a-5p might control PMVEC proliferation. Here, we described governing HPS. Methods: PMVECs were treated rat from common bile...

10.1159/000430252 article EN cc-by-nc Cellular Physiology and Biochemistry 2015-01-01

Background and AimsHepatopulmonary syndrome (HPS) is characterized by arterial oxygenation defects due to pulmonary vascular dilation in liver disease. To date, transplantation remains the only effective treatment for HPS. This study aimed explore preventative role of baicalein HPS development.

10.14218/jcth.2023.00513 article EN Journal of Clinical and Translational Hepatology 2024-03-18

Background and AimsThe results of basic research implicate the vascular endothelial growth factor (VEGF) family as a potential target hepatopulmonary syndrome (HPS). However, negative anti-angiogenetic therapy in clinical studies have highlighted need for markers HPS. Therefore, we aimed to determine whether VEGF members their receptors can be biomarkers HPS through experimental studies.

10.14218/jcth.2022.00421 article EN Journal of Clinical and Translational Hepatology 2023-04-24

Abstract Hepatopulmonary syndrome (HPS) is a defective liver-induced pulmonary vascular disorder with massive microvascular dilation and excessive proliferation of endothelial cells (PMVECs). Growing evidence suggests that autophagy involved in diseases, protectively or detrimentally. Thus, it interesting important to explore whether might be critical HPS. In the present study, we report was activated common bile duct ligation (CBDL) rats cultured PMVECs induced by CBDL rat serum, two...

10.1038/srep30833 article EN cc-by Scientific Reports 2016-08-02
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