A5033639948- Ubiquitin and proteasome pathways
- Liver physiology and pathology
- PI3K/AKT/mTOR signaling in cancer
- Glioma Diagnosis and Treatment
- Neuroblastoma Research and Treatments
- Cell Adhesion Molecules Research
- Hepatocellular Carcinoma Treatment and Prognosis
- FOXO transcription factor regulation
- Platelet Disorders and Treatments
- Cancer Mechanisms and Therapy
- Peptidase Inhibition and Analysis
- Cancer Cells and Metastasis
- Cancer Research and Treatments
- Melanoma and MAPK Pathways
- Cancer, Hypoxia, and Metabolism
- Blood Coagulation and Thrombosis Mechanisms
- Antiplatelet Therapy and Cardiovascular Diseases
- Signaling Pathways in Disease
- Immune cells in cancer
- Cell death mechanisms and regulation
- NF-κB Signaling Pathways
- Microtubule and mitosis dynamics
- Histone Deacetylase Inhibitors Research
- Phagocytosis and Immune Regulation
- Glycosylation and Glycoproteins Research
Universidad Complutense de Madrid
2014-2025
Centre National de la Recherche Scientifique
2020-2025
Inserm
2025
Centre de Recherche en Cancérologie de Marseille
2025
Instituto de Investigación Sanitaria del Hospital Clínico San Carlos
2016-2022
Institut de Biologie du Développement Marseille
2020-2022
Abstract Enhanced activation of the transcription factor MYC and receptor tyrosine kinase MET are among events frequently occurring in hepatocellular carcinoma (HCC). Both genes individually act as drivers liver cancer initiation progression. However, their concomitant alteration HCC has not been explored, nor functionally documented. Here, we analysed databases five independent human cohorts found a subset patients with high levels ( /MET ) characterised by poor prognosis. This clinical...
Primary liver cancer usually occurs in the context of chronic disease (CLD), association with fibrosis. Platelets have emerged as important regulators CLD and cancer, although their precise function mechanism action need to be clarified. C3G (RapGEF1) regulates platelet activation, adhesion, secretion. Here we evaluate role chemically induced fibrosis associated using genetically modified mouse models. We found that while overexpression full-length platelets decreased by treatment CCl4,...
// Víctor Martín-Granado 1, 2 , Sara Ortiz-Rivero Rita Carmona 3 Gutiérrez-Herrero Mario Barrera 1 Laura San-Segundo Celia Sequera 4 Pedro Perdiguero 2, 5 Francisco Lozano 6 Martín-Herrero José Ramón González-Porras 7 Muñoz-Chápuli Almudena Porras and Carmen Guerrero 8 Instituto de Biología Molecular y Celular del Cáncer, USAL-CSIC, Salamanca, Spain Investigación Biomédica Salamanca (IBSAL),...
// Neibla Priego 1,2,* , María Arechederra Celia Sequera 1,2 Paloma Bragado 3 Ana Vázquez-Carballo Álvaro Gutiérrez-Uzquiza 1,7 Víctor Martín-Granado 4 Juan José Ventura 5 Marcelo G. Kazanietz 6 Carmen Guerrero and Almudena Porras 1 Departamento de Bioquímica y Biología Molecular II, Facultad Farmacia, Universidad Complutense Madrid, Spain 2 Instituto Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS),...
Abstract Glioblastoma (GBM) is the most aggressive tumor from central nervous system (CNS). The current lack of efficient therapies makes essential to find new treatment strategies. C3G, a guanine nucleotide exchange factor for some Ras proteins, plays dual role in cancer, but its function GBM remains unknown. Database analyses revealed reduced C3G mRNA expression patient samples. protein levels were also decreased panel human cell lines as compared astrocytes. Based on this, we...
Previous data indicate that C3G (RapGEF1) main isoform is highly expressed in liver progenitor cells (or oval cells) compared to adult mature hepatocytes, suggesting it may play an important role cell biology. Hence, we have explored function the regulation of properties by permanent gene silencing using shRNAs. We found knock-down enhanced migratory and invasive ability promoting a partial epithelial mesenchymal transition (EMT). This likely mediated upregulation mRNA expression...
The complexity of hepatocellular carcinoma (HCC) challenges the identification disease-relevant signals. C3G, a guanine nucleotide exchange factor for Rap and other Ras proteins, plays dual role in cancer acting as either tumor suppressor or promoter depending on type stage. potential relevance C3G upregulation HCC patients suggested by database analysis remains unknown. We have explored function underlying mechanisms using public patient data vitro vivo human mouse models. found that is...
Compelling evidence points to the MET receptor tyrosine kinase as a key player during liver development and regeneration. Recently, role of in pathophysiology insulin resistance obesity is emerging. Herein, we aimed determine whether regulates hepatic sensitivity. To achieve this, mice which expression wild-type hepatocytes slightly enhanced above endogenous levels (Alb-R26Met mice) were analyzed document glucose homeostasis, energy balance, signaling hepatocytes. We found that Alb-R26Met...
TWEAK regulates multiple physio-pathological processes in fibroblasts such as fibrosis. It also induces migration and invasion tumors it can activate p38 MAPK various cell types. Moreover, p38α promotes several cancer cells types mouse embryonic (MEFs). However, remains unknown if could promote whether might play a role. Our results reveal that activates ERKs, Akt, p38α/β MAPKs reduces secreted Fibulin 3 MEFs. increases wt deficient MEFs, which indicates is not required to mediate these...
Hepatoma Research is an open access journal and focuses on all topics related to hepatoma. The following articles are especially welcome: pathogenesis, clinical examination early diagnosis of hepatoma, complications their preventions treatments, etc.
Abstract C3G is a guanine-nucleotide exchange factor (GEF) for Rap1, although it can act through GEF-independent mechanisms. plays dual role in cancer, acting as either tumor suppressor or inducer depending on the type/stage. It regulates different key aspects of tumorigenic process such invasion, apoptosis proliferation. In colon carcinoma, represses invasion down-regulation p38αMAPK activity and promotes growth. We have now analyzed glioblastoma (GBM), characterized by its aggressiveness...