A5078968903- Melanoma and MAPK Pathways
- Cellular Mechanics and Interactions
- Cell Adhesion Molecules Research
- Ubiquitin and proteasome pathways
- Hippo pathway signaling and YAP/TAZ
- Peptidase Inhibition and Analysis
- Protein Degradation and Inhibitors
- Synthesis of Tetrazole Derivatives
- Histone Deacetylase Inhibitors Research
- melanin and skin pigmentation
- MicroRNA in disease regulation
- Circular RNAs in diseases
- Autophagy in Disease and Therapy
- Cancer-related molecular mechanisms research
- bioluminescence and chemiluminescence research
- Heat shock proteins research
- Glycosylation and Glycoproteins Research
- Cancer Immunotherapy and Biomarkers
- Chromosomal and Genetic Variations
- FOXO transcription factor regulation
- Biomarkers in Disease Mechanisms
Université Côte d'Azur
2018-2020
Inserm
2013-2020
La Ligue Contre le Cancer
2017-2020
Centre Méditerranéen de Médecine Moléculaire
2018
Institut Cochin
2013
Centre National pour la Recherche Scientifique et Technique (CNRST)
2013
Université Paris Cité
2013
Centre National de la Recherche Scientifique
2013
Aberrant extracellular matrix (ECM) deposition and stiffening is a physical hallmark of several solid cancers associated with therapy failure. BRAF-mutant melanomas treated BRAF MEK inhibitors almost invariably develop resistance that frequently transcriptional reprogramming de-differentiated cell state. Melanoma cells secrete their own ECM proteins, an event promoted by oncogenic inhibition. Yet, the contribution cancer cell-derived tumor mechanics to drug adaptation remains poorly...
Abstract Advanced cutaneous melanoma is one of the most challenging cancers to treat because its high plasticity, metastatic potential, and resistance treatment. New targeted therapies immunotherapies have shown remarkable clinical efficacy. However, such treatments are limited a subset patients relapses often occur, warranting validation novel therapies. Posttranslational modification proteins by ubiquitin coordinates essential cellular functions, including ubiquitin-proteasome system (UPS)...
O-GlcNAcylation on serine/threonine is a post-translational modification that controls the activity of nucleocytoplasmic proteins according to glucose availability. We previously showed FoxO1 in liver cells increases its transcriptional activity. In present study, we evaluated potential involvement context pancreatic β-cell glucotoxicity. was O-GlcNAcylated INS-1 832/13 β and isolated rat islets. resulted 2-fold increase toward reporter gene 3-fold expression insulin-like growth...
Abstract RNAs competition to bind miRNA has been proposed influence biological systems whether these are implicated in diseases onset is unclear. Here, we report that TYRP1 mRNA, addition encoding tyrosinase-related protein 1 (TYRP1), indirectly governs cell proliferation by sequestering miR-16 on non-canonical response elements (MREs). Consequently, sequestered no longer able repress its mRNA targets such as RAB17, which show involved melanoma and invasion. Restoration of tumor suppressor...
<div>Abstract<p>Advanced cutaneous melanoma is one of the most challenging cancers to treat because its high plasticity, metastatic potential, and resistance treatment. New targeted therapies immunotherapies have shown remarkable clinical efficacy. However, such treatments are limited a subset patients relapses often occur, warranting validation novel therapies. Posttranslational modification proteins by ubiquitin coordinates essential cellular functions, including...
<p>F-actin and fibronectin stainings in M238P M238R cells</p>
<p>BRAF inhibition drives collagen deposition and stiffening in M229 xenograft melanoma tumor</p>
<div>Abstract<p>Aberrant extracellular matrix (ECM) deposition and stiffening is a physical hallmark of several solid cancers associated with therapy failure. BRAF-mutant melanomas treated BRAF MEK inhibitors almost invariably develop resistance that frequently transcriptional reprogramming de-differentiated cell state. Melanoma cells secrete their own ECM proteins, an event promoted by oncogenic inhibition. Yet, the contribution cancer cell–derived tumor mechanics to drug...
<div>Abstract<p>Aberrant extracellular matrix (ECM) deposition and stiffening is a physical hallmark of several solid cancers associated with therapy failure. BRAF-mutant melanomas treated BRAF MEK inhibitors almost invariably develop resistance that frequently transcriptional reprogramming de-differentiated cell state. Melanoma cells secrete their own ECM proteins, an event promoted by oncogenic inhibition. Yet, the contribution cancer cell–derived tumor mechanics to drug...
<p>Mesenchymal signature of BRAFi resistant melanoma cells</p>
<p>Mesenchymal signature of BRAFi resistant melanoma cells</p>
<p>Supplementary Methods</p>
<p>Morphology and focal adhesions complexes of parental BRAFi-resistant cells on hydrogels various stiffness</p>
<p>F-actin and fibronectin stainings in M238P M238R cells</p>
<p>BRAF and MEK inhibition induces F-actin remodeling, YAP/MRTF activation focal adhesion assembly in BRAF-mutant melanoma cells</p>
<p>Morphology and focal adhesions complexes of parental BRAFi-resistant cells on hydrogels various stiffness</p>
<p>BRAF inhibition drives collagen deposition and stiffening in M229 xenograft melanoma tumor</p>
<p>Drug-protective effect of M229R melanoma cells-derived ECM</p>
<p>Supplementary Methods</p>
<p>BRAF and MEK inhibition induces F-actin remodeling, YAP/MRTF activation focal adhesion assembly in BRAF-mutant melanoma cells</p>
<p>Drug-protective effect of M229R melanoma cells-derived ECM</p>