A5078143556- Cellular Mechanics and Interactions
- Melanoma and MAPK Pathways
- Cytokine Signaling Pathways and Interactions
- Cell Adhesion Molecules Research
- Cutaneous lymphoproliferative disorders research
- Eosinophilic Disorders and Syndromes
- Hippo pathway signaling and YAP/TAZ
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Cancer-related molecular mechanisms research
- Synthesis of Tetrazole Derivatives
- Cancer Cells and Metastasis
- RNA modifications and cancer
- bioluminescence and chemiluminescence research
- Immune Cell Function and Interaction
- Immunotherapy and Immune Responses
- melanin and skin pigmentation
- Skin and Cellular Biology Research
- Cancer Genomics and Diagnostics
- PI3K/AKT/mTOR signaling in cancer
- Nail Diseases and Treatments
- Cholangiocarcinoma and Gallbladder Cancer Studies
- Cell death mechanisms and regulation
- Mycobacterium research and diagnosis
- Biochemical Analysis and Sensing Techniques
- Cancer Mechanisms and Therapy
Inserm
2019-2024
Centre Méditerranéen de Médecine Moléculaire
2021-2023
Université Côte d'Azur
2019-2023
La Ligue Contre le Cancer
2019-2023
Centre National de la Recherche Scientifique
2017-2023
Institut Jacques Monod
2020-2023
Université Paris Cité
2020-2023
Université Claude Bernard Lyon 1
2023
Centre Léon Bérard
2023
Centre de Recherche en Cancérologie de Lyon
2023
Rationale: Given the paucity of effective treatments for idiopathic pulmonary fibrosis (IPF), new insights into deleterious mechanisms controlling lung fibroblast activation, key cell type driving fibrogenic process, are essential to develop therapeutic strategies. TGF-β (transforming growth factor-β) is main profibrotic factor, but its inhibition associated with severe side effects because pleiotropic role. Objectives: To determine if downstream noncoding effectors in fibroblasts may...
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...
Article14 February 2022Open Access Source DataTransparent process Blockade of the pro-fibrotic reaction mediated by miR-143/-145 cluster enhances responses to targeted therapy in melanoma Serena Diazzi Université Côte d'Azur, INSERM, C3M, Nice, France CNRS, Institut de Pharmacologie Moléculaire et Cellulaire (IPMC), Sophia Antipolis, Equipe labellisée Ligue Contre le Cancer, Contribution: Conceptualization, Formal analysis, Investigation, Methodology, Writing - original draft, review &...
Fibroblastic reticular cells (FRC) are immunologically specialized myofibroblasts that control the elasticity of lymph node, in part through their contractile properties. Swelling tumor-draining nodes is a hallmark lymphophilic cancers such as cutaneous melanoma. Melanoma displays high intratumoral heterogeneity with coexistence melanoma variable differentiation phenotypes from melanocytic to dedifferentiated states. Factors secreted by promote premetastatic node reprograming and tumor...
Abstract Recent studies have unveiled unexpected connections between cell death and motility. While traditionally recognized for their pro-apoptotic roles, caspases emerged as regulators of physiological processes beyond death, including cellular differentiation In some particularly aggressive cancers like melanoma, caspase-3, a prominent executioner caspase, is unexpectedly inexplicably highly expressed. Here, we describe novel non-apoptotic role caspase-3 in melanoma Through comprehensive...
Abstract Extracellular matrix (ECM) stiffening, resulting from increased collagen deposition and cross-linking, is a key biophysical factor of the tumor microenvironment. Cutaneous melanoma deadly metastatic cancer. Its aggressiveness stems high intratumoral heterogeneity, plasticity cells, which transit melanocytic state to dedifferentiated therapy-resistant invasive phenotypes, characterized by mesenchymal and/or neural crest stem cell-like features. Phenotypic regulated stroma-derived...
The TGFβ family member NODAL, repeatedly required during embryonic development, has also been associated with tumour progression. Our aim was to clarify the controversy surrounding its involvement in melanoma We found that deletion of NODAL exon 2 a metastatic cell line impairs ability form tumours and colonize distant tissues. However, we show this phenotype does not result from absence but defect expression natural antisense transcript here called LADON. LADON is specifically activated...
Abstract Resistance to BRAF and MEK inhibitors in V600E mutant melanomas remains a major obstacle that limits patient benefit. Microenvironment components including the extracellular matrix (ECM) can support tumor cell adaptation tolerance targeted therapies, however underlying mechanisms remain poorly understood. Here, we investigated process of matrix-mediated drug resistance (MM-DR) response inhibition melanoma. We demonstrate physical structural cues from fibroblast-derived ECM abrogate...
Summary The TGFβ family member NODAL, known for its role during embryonic development, has also been associated with tumor progression in several cancers. Some of the evidence supporting involvement melanoma appeared contradictory, suggesting that NODAL this context might rely on a non-canonical signalling mode. We found inactivation metastatic cell line prevents cells from acquiring invasive behaviour. However, we show phenotype does not result absence but defect expression natural...
Dupuytren disease (DD) is a hand-localized fibrotic disorder characterized by scar-like, collagen-rich cord. Treatment usually comprises surgical removal of the cord, but associated with high relapse rate, in some cases requiring finger amputation. There currently no consensual medical approach for treating DD. Numerous preclinical studies have highlighted antifibrotic properties metformin, and aim this study was to assess potential role metformin Fibroblasts from DD cords (DF)...
Supplementary Figure from Secretion of IL1 by Dedifferentiated Melanoma Cells Inhibits JAK1-STAT3–Driven Actomyosin Contractility Lymph Node Fibroblastic Reticular
Supplementary Figure from Secretion of IL1 by Dedifferentiated Melanoma Cells Inhibits JAK1-STAT3–Driven Actomyosin Contractility Lymph Node Fibroblastic Reticular
<div>Abstract<p>Fibroblastic reticular cells (FRC) are immunologically specialized myofibroblasts that control the elasticity of lymph node, in part through their contractile properties. Swelling tumor-draining nodes is a hallmark lymphophilic cancers such as cutaneous melanoma. Melanoma displays high intratumoral heterogeneity with coexistence melanoma variable differentiation phenotypes from melanocytic to dedifferentiated states. Factors secreted by promote premetastatic node...
<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>