A5083085617- Renal cell carcinoma treatment
- Angiogenesis and VEGF in Cancer
- Cancer, Hypoxia, and Metabolism
- RNA Research and Splicing
- Melanoma and MAPK Pathways
- Renal and related cancers
- PI3K/AKT/mTOR signaling in cancer
- RNA modifications and cancer
- Ferroptosis and cancer prognosis
- Lymphatic System and Diseases
- Cancer Genomics and Diagnostics
- Cancer-related Molecular Pathways
- Glioma Diagnosis and Treatment
- Cancer Cells and Metastasis
- Vascular Tumors and Angiosarcomas
- Protein Tyrosine Phosphatases
- Cytokine Signaling Pathways and Interactions
- Protein Kinase Regulation and GTPase Signaling
- Kruppel-like factors research
- Immunotherapy and Immune Responses
- T-cell and B-cell Immunology
- Epigenetics and DNA Methylation
- Cancer Treatment and Pharmacology
- Ubiquitin and proteasome pathways
- Cancer-related molecular mechanisms research
Centre National de la Recherche Scientifique
2016-2025
Institut de Recherche sur le Cancer et le Vieillissement de Nice
2016-2025
Inserm
2016-2025
Université Côte d'Azur
2016-2025
Centre Antoine Lacassagne
2015-2025
Institut de Chimie de Nice
2002-2025
Observatoire de la Côte d’Azur
2020-2024
Hôpital Saint Roch
2022-2024
Scientific Centre of Monaco
2013-2023
International University of Monaco
2020-2023
The mitogen-activated protein kinases (MAP kinases) p42mapk and p44mapk are serine/threonine rapidly activated in cells stimulated with various extracellular signals by dual phosphorylation of tyrosine threonine residues. They thought to play a pivotal role integrating transmitting transmembrane required for growth differentiation. Here we demonstrate that activation these ubiquitously expressed MAP is essential growth. To specifically suppress kinase fibroblasts, transiently either the...
The p42 and p44 mitogen-activated protein kinases (MAPKs), also called Erk2 Erk1, respectively, have been implicated in proliferation as well differentiation programs. specific role of the MAPK isoform whole animal was evaluated by generation MAPK-deficient mice homologous recombination embryonic stem cells. –/– were viable, fertile, normal size. Thus, is apparently dispensable (Erk2) may compensate for its loss. However, −/− mice, thymocyte maturation beyond CD4 + CD8 stage reduced half,...
The serine protease alpha-thrombin (thrombin) potently stimulates G-protein-coupled signaling pathways and DNA synthesis in CCL39 hamster lung fibroblasts. To clone a thrombin receptor cDNA, selective amplification of mRNA sequences displaying homology to the transmembrane domains genes was performed by polymerase chain reaction. Using reverse transcribed poly(A)+ RNA from cells degenerate primers corresponding conserved regions several phospholipase C-coupled receptors, three novel putative...
Hyperplasia of adipose tissue is critical for the development obesity, but molecular mechanisms governing normal or pathological recruitment new adipocytes remain unclear. The extracellular signal–regulated kinase (ERK) pathway plays a pivotal role in many essential cellular functions, such as proliferation and differentiation. Using ERK1−/− mice, we investigated this isoform development. Mice lacking ERK1 have decreased adiposity fewer than wild-type animals. Furthermore, mice challenged...
Vascular EndothelialGrowth Factor (VEGF) is a potent mitogen for vascular endothelial cells that has been implicated in tumor neovascularization. We show that, hamster fibroblasts (CCL39 cells), VEGF mRNAs are expressed at low levels serum-deprived or exponentially growing cells, whereas it rapidly induced after stimulation of quiescent with serum. CCL39 derivatives, transformed Polyoma virus active members the p42/p44 mitogen-activated protein (MAP) kinase pathway, Gly/Val point mutant Ras...
Sp1 regulates activation of many genes implicated in tumor growth and cell cycle progression. We have previously demonstrated its implication the up-regulation vascular endothelial factor (VEGF) gene transcription following stimulation quiescent cells, a situation where p42/p44 mitogen-activate protein kinase (MAPK) activity is dramatically increased. Here we show that MAPK directly phosphorylates on threonines 453 739 both vitro vivo. Mutation these sites to alanines decreases by half...
Increased expression of vascular endothelial growth factor (VEGF) contributes to the many tumors by increasing angiogenesis. Although hypoxia is a potent inducer VEGF, we previously showed that epidermal receptor amplification and loss PTEN, both which can increase phosphatidylinositol-3-kinase (PI3K) activity, VEGF expression. Using adenoviral vectors cell line permanently expressing constitutively active myristoylated Akt (myrAkt), show activation Akt, downstream PI3K, increases in vitro...
Myocardial infarction causes a rapid and largely irreversible loss of cardiac myocytes that can lead to sudden death, ventricular dilation, heart failure. Members the mitogen-activated protein kinase (MAPK) signaling cascade have been implicated as important effectors myocyte cell death in response diverse stimuli, including ischemia-reperfusion injury. Specifically, activation extracellular signal-regulated kinases 1/2 (ERK1/2) has associated with cardioprotection, likely through antagonism...
In B16 melanoma cells, mitogen-activated protein (MAP) kinases are activated during cAMP-induced melanogenesis (Englaro, W., Rezzonico, R., Durand-Clément, M., Lallemand, D., Ortonne, J. P., and Ballotti, R. (1995) <i>J. Biol. Chem.</i>270, 24315–24320). To establish the role of MAP in melanogenesis, we studied effects a specific kinase (MEK) inhibitor PD 98059 on different melanogenic parameters. We showed that inhibits activation extracellular signal-regulated 1 by cAMP, but does not...
Satellite cells (SCs) are stem that mediate skeletal muscle growth and regeneration. Here, we observe adult quiescent SCs their activated descendants expressed the homeodomain transcription factor Six1. Genetic disruption of Six1 specifically in impaired myogenic cell differentiation, myofiber repair during regeneration, perturbed homeostasis niche, as indicated by an increase SC self-renewal. regulated expression regulatory factors MyoD Myogenin, but not Myf5, which suggests acts on...
Metastatic renal cell carcinomas (mRCC) are highly vascularized tumors that a paradigm for the treatment with antiangiogenesis drugs targeting vascular endothelial growth factor (VEGF) pathway. The available increase time to progression but not curative and patients eventually relapse. In this study we have focused our attention on molecular mechanisms leading resistance sunitinib, first line of mRCC. Because anarchic vascularization core mRCC receives only suboptimal concentrations drug. To...
Sunitinib is an antiangiogenic therapy given as a first-line treatment for renal cell carcinoma (RCC). While improves progression-free survival, most patients relapse. We hypothesized that patient relapse can stem from the development of lymphatic network driven by production main growth factor endothelial cells, VEGFC. In this study, we found sunitinib stimulate vegfc gene transcription and increase VEGFC mRNA half-life. addition, activated p38 MAPK, which resulted in upregulation/activity...
Abstract Background In clear cell renal carcinoma (ccRCC), first-line treatment combines nivolumab (anti-PD-1) and ipilimumab (anti-CTLA4), yielding long-term remissions but with only a 40% success rate. Our study explored the potential of enhancing ccRCC by concurrently using CXCR2 inhibitors alongside immunotherapies. Methods We analyzed ELR + CXCL levels their correlation patient survival during immunotherapy. RCT001, unique inhibitor, was examined for its mechanism action, particularly...