Delphine Javelaud

ORCID: 0000-0002-7674-7739
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About
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Research Areas
  • TGF-β signaling in diseases
  • Connective Tissue Growth Factor Research
  • Hedgehog Signaling Pathway Studies
  • Kruppel-like factors research
  • Melanoma and MAPK Pathways
  • NF-κB Signaling Pathways
  • Bone Metabolism and Diseases
  • Cell Adhesion Molecules Research
  • Epigenetics and DNA Methylation
  • Cancer-related Molecular Pathways
  • Cell death mechanisms and regulation
  • Heterotopic Ossification and Related Conditions
  • melanin and skin pigmentation
  • Oral and Maxillofacial Pathology
  • Cytokine Signaling Pathways and Interactions
  • Bone health and treatments
  • Wnt/β-catenin signaling in development and cancer
  • Bacterial Genetics and Biotechnology
  • Chromatin Remodeling and Cancer
  • Tendon Structure and Treatment
  • Cancer Cells and Metastasis
  • Cellular Mechanics and Interactions
  • Cancer Mechanisms and Therapy
  • interferon and immune responses
  • Inflammatory mediators and NSAID effects

Centre National de la Recherche Scientifique
2010-2024

Inserm
2010-2024

Institut Curie
2010-2024

Université Paris Sciences et Lettres
2010-2024

Université Paris-Sud
2019-2024

Université Paris Cité
2003-2015

Université Paris-Saclay
2010-2015

La Ligue Contre le Cancer
2013

National Cancer Institute
2012

Center for Cancer Research
2012

Melanoma often metastasizes to bone where it is exposed high concentrations of TGF-β. Constitutive Smad signaling occurs in human melanoma. Because TGF-β promotes metastases by several types solid tumors including breast cancer, we hypothesized that pharmacologic blockade the pathway may interfere with capacity melanoma cells metastasize bone. In this study, tested effect a small molecule inhibitor receptor I kinase (TβRI), SD-208, on various parameters affecting development and progression...

10.1158/0008-5472.can-10-2651 article EN Cancer Research 2010-11-18

Melanoma has a propensity to metastasize bone, where it is exposed high concentrations of transforming growth factor-beta (TGF-beta). Because TGF-beta promotes bone metastases from other solid tumors, such as breast cancer, we tested the role in melanoma bone. 1205Lu cells, stably transfected overexpress natural TGF-beta/Smad signaling inhibitor Smad7, were studied an experimental model metastasis whereby tumor cells are inoculated into left cardiac ventricle nude mice. All mice bearing...

10.1158/0008-5472.can-06-3950 article EN Cancer Research 2007-03-01

Radiation-induced fibrosis is an untoward effect of high dose therapeutic and inadvertent exposure to ionizing radiation. Transforming growth factor-β (TGF-β) has been proposed be critical in tissue repair mechanisms resulting from radiation injury. Previously, we showed that interruption TGF-β signaling by deletion Smad3 results resistance radiation-induced In the current study, a small molecular weight molecule, halofuginone (100 nm), demonstrated reporter assays inhibit pathway, Northern...

10.1074/jbc.m309798200 article EN cc-by Journal of Biological Chemistry 2004-04-01

Summary There is growing evidence that the metastatic spread of melanoma driven not by a linear increase in tumorigenic aggressiveness, but rather switching back and forth between two different phenotypes potential. In vitro these are respectively defined characteristics strong proliferation/weak invasiveness weak proliferation/strong invasiveness. Melanoma cell phenotype tightly linked to gene expression. Taking advantage this, we have developed expression–based tool for predicting called...

10.1111/j.1755-148x.2012.00986.x article EN Pigment Cell & Melanoma Research 2012-02-15

Repression of activation c‐Jun N‐terminal kinase (JNK) participates in the anti‐apoptotic effect nuclear factor‐κB (NF‐κB) TNFα‐treated Ewing sarcoma cells. As oxidative stress is one most prominent activators JNK, we investigated relationship between TNFα‐induced NF‐κB and control stress. Inhibition resulted an increase ROS production, lipid peroxidation protein oxidation. Those peroxides were both involved apoptosis, whereas only elevation triggered sustained JNK activation. TNFα increased...

10.1016/j.febslet.2004.10.082 article EN FEBS Letters 2004-11-11

Abstract c-Ski is an important corepressor of transforming growth factor-β (TGF-β) signaling through its ability to bind and repress the activity Smad proteins. It was initially identified as oncogene that promotes anchorage-independent chicken quail embryo fibroblasts when overexpressed. Although increased Ski expression detected in many human cancer cells, roles mammalian carcinogenesis have yet be defined. Here, we report reducing breast lung cells does not affect tumor but enhances...

10.1158/0008-5472.can-07-6793 article EN Cancer Research 2008-05-01

Transforming growth factor-β (TGF-β) is a pleiotropic factor with broad tissue distribution that plays critical roles during embryonic development, normal homeostasis, and cancer.While its cytostatic activity on epithelial cells initially defined TGF-β signaling as tumor suppressor pathway, there ample evidence indicating potent pro-tumorigenic agent, acting via autocrine paracrine mechanisms to promote peri-tumoral angiogenesis, together cell migration, immune escape, dissemination...

10.5021/ad.2013.25.2.135 article EN cc-by-nc Annals of Dermatology 2013-01-01

p21WAF1 appears to be a major determinant of the cell fate in response anticancer therapy. It was shown previously that HCT116 human colon cancer cells growing vitro enter stable arrest upon DNA damage, whereas with defective undergo apoptosis. Here we report enhanced sensitivity HCT116/p21−/−cells chemotherapeutic drug-induced apoptosis correlates an increased expression p53 and modification their Bax/Bcl-2 ratio favor pro-apoptotic protein Bax. Treatment HCT116/p21−/− daunomycin resulted...

10.1074/jbc.m204497200 article EN cc-by Journal of Biological Chemistry 2002-09-27

Summary We recently identified GLI2, the most active of GLI transcription factors, as a direct TGF‐β/SMAD target, whose expression in melanoma cells is associated with increased invasiveness and metastatic capacity. In this work, we provide evidence that high GLI2 inversely correlated melanocyte‐specific factor M‐microphthalmia (M‐MITF) transcriptional program. GLI2‐expressing cell lines were characterized by loss M‐MITF‐dependent melanocytic differentiation markers reduced pigmentation. The...

10.1111/j.1755-148x.2011.00893.x article EN Pigment Cell & Melanoma Research 2011-08-01

TGF-β derived from bone fuels melanoma metastases by inducing tumor secretion of prometastatic factors that act on cells to change the skeletal microenvironment. Halofuginone is a plant alkaloid derivative blocks signaling with antiangiogenic and antiproliferative properties. Here, we show for first time halofuginone therapy decreases development progression metastasis caused through inhibition signaling. treatment human inhibited cell proliferation, phosphorylation SMAD proteins in response...

10.1158/0008-5472.can-12-1444 article EN Cancer Research 2012-09-21

JNK1/2 proteins belong to the family of stress-activated protein kinases. They play a complex role in growth regulation, inducing either cell death or support. In this report, we provide evidence that, human melanoma cells, JNK inhibition with small molecule inhibitor SP600125 induces predominantly G2/M arrest apoptosis depending on line. 1205Lu induced cycle through p53-dependent induction p21 Cip1/Waf1 expression, while WM983B by was accompanied p53, Bad and Bax induction, not Cip1/Waf1....

10.1111/j.1755-148x.2008.00466.x article EN Pigment Cell & Melanoma Research 2008-06-16

Abstract Background SKI and SnoN proteins have been shown to inhibit TGF-β signaling, acting both as transcriptional co-repressors in the cell nucleus, sequestrators of SMAD cytoplasm. TGF-β, on other hand, induces rapid, proteasome-mediated, degradation proteins. How elevated protein levels co-exist with active autocrine signaling cancer cells is yet be understood. Results In this study, we found a panel melanoma lines, compared normal melanocytes. There was no correlation between content...

10.1186/1476-4598-10-2 article EN cc-by Molecular Cancer 2011-01-06
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