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  1. Article ; Online: Bone Morphogenic Proteins in Pediatric Diffuse Midline Gliomas: How to Make New Out of Old?

    Berthelot, Clément / Huchedé, Paul / Bertrand-Chapel, Adrien / Beuriat, Pierre-Aurélien / Leblond, Pierre / Castets, Marie

    International journal of molecular sciences

    2024  Volume 25, Issue 6

    Abstract: The BMP pathway is one of the major signaling pathways in embryonic development, ontogeny and homeostasis, identified many years ago by pioneers in developmental biology. Evidence of the deregulation of its activity has also emerged in many cancers, with ...

    Abstract The BMP pathway is one of the major signaling pathways in embryonic development, ontogeny and homeostasis, identified many years ago by pioneers in developmental biology. Evidence of the deregulation of its activity has also emerged in many cancers, with complex and sometimes opposing effects. Recently, its role has been suspected in Diffuse Midline Gliomas (DMG), among which Diffuse Intrinsic Pontine Gliomas (DIPG) are one of the most complex challenges in pediatric oncology. Genomic sequencing has led to understanding part of their molecular etiology, with the identification of histone H3 mutations in a large proportion of patients. The epigenetic remodeling associated with these genetic alterations has also been precisely described, creating a permissive context for oncogenic transcriptional program activation. This review aims to describe the new findings about the involvement of BMP pathway activation in these tumors, placing their appearance in a developmental context. Targeting the oncogenic synergy resulting from this pathway activation in an H3K27M context could offer new therapeutic perspectives based on targeting treatment-resistant cell states.
    MeSH term(s) Humans ; Child ; Glioma/metabolism ; Histones/metabolism ; Diffuse Intrinsic Pontine Glioma/genetics ; Diffuse Intrinsic Pontine Glioma/metabolism ; Diffuse Intrinsic Pontine Glioma/pathology ; Mutation ; Signal Transduction ; Bone Morphogenetic Proteins/metabolism
    Chemical Substances Histones ; Bone Morphogenetic Proteins
    Language English
    Publishing date 2024-03-15
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms25063361
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: The TLR3 L412F polymorphism prevents TLR3-mediated tumor cell death induction in pediatric sarcomas.

    Bisaccia, Joseph / Meyer, Swann / Bertrand-Chapel, Adrien / Hecquet, Quentin / Barbet, Virginie / Kaniewski, Bastien / Léon, Sophie / Gadot, Nicolas / Rochet, Isabelle / Fajnorova, Iveta / Leblond, Pierre / Cordier-Bussat, Martine / Corradini, Nadège / Vasiljevic, Alexandre / Billaud, Marc / Picard, Cécile / Broutier, Laura / Gallerne, Cindy / Dutour, Aurélie /
    Blay, Jean-Yves / Castets, Marie

    Cell death discovery

    2023  Volume 9, Issue 1, Page(s) 230

    Abstract: Toll-like receptor 3 (TLR3) is a pattern recognition receptor mainly known for its role in innate immune response to infection. Indeed, binding of double-stranded RNA (dsRNA) to TLR3 triggers a pro-inflammatory cascade leading to cytokine release and ... ...

    Abstract Toll-like receptor 3 (TLR3) is a pattern recognition receptor mainly known for its role in innate immune response to infection. Indeed, binding of double-stranded RNA (dsRNA) to TLR3 triggers a pro-inflammatory cascade leading to cytokine release and immune cell activation. Its anti-tumoral potential has emerged progressively, associated with a direct impact on tumor cell death induction and with an indirect action on immune system reactivation. Accordingly, TLR3 agonists are currently being tested in clinical trials for several adult cancers. Meanwhile, TLR3 variants have been linked to auto-immune disorders, and as risk factors of viral infection and cancers. However, aside from neuroblastoma, TLR3 role in childhood cancers has not been evaluated. Here, by integrating public transcriptomic data of pediatric tumors, we unveil that high TLR3 expression is largely associated with a better prognosis in childhood sarcomas. Using osteosarcomas and rhabdomyosarcomas as models, we show that TLR3 efficiently drives tumor cell death in vitro and induces tumor regression in vivo. Interestingly, this anti-tumoral effect was lost in cells expressing the homozygous TLR3 L412F polymorphism, which is enriched in a rhabdomyosarcomas cohort. Thus, our results demonstrate the therapeutic potential associated with the targeting of TLR3 in pediatric sarcomas, but also the need to stratify patients eligible for this clinical approach with respect to the TLR3 variants expressed.
    Language English
    Publishing date 2023-07-07
    Publishing country United States
    Document type Journal Article
    ISSN 2058-7716
    ISSN 2058-7716
    DOI 10.1038/s41420-023-01513-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: SMAD2/3 mediate oncogenic effects of TGF-β in the absence of SMAD4.

    Bertrand-Chapel, Adrien / Caligaris, Cassandre / Fenouil, Tanguy / Savary, Clara / Aires, Sophie / Martel, Sylvie / Huchedé, Paul / Chassot, Christelle / Chauvet, Véronique / Cardot-Ruffino, Victoire / Morel, Anne-Pierre / Subtil, Fabien / Mohkam, Kayvan / Mabrut, Jean-Yves / Tonon, Laurie / Viari, Alain / Cassier, Philippe / Hervieu, Valérie / Castets, Marie /
    Mauviel, Alain / Sentis, Stéphanie / Bartholin, Laurent

    Communications biology

    2022  Volume 5, Issue 1, Page(s) 1068

    Abstract: TGF-β signaling is involved in pancreatic ductal adenocarcinoma (PDAC) tumorigenesis, representing one of the four major pathways genetically altered in 100% of PDAC cases. TGF-β exerts complex and pleiotropic effects in cancers, notably via the ... ...

    Abstract TGF-β signaling is involved in pancreatic ductal adenocarcinoma (PDAC) tumorigenesis, representing one of the four major pathways genetically altered in 100% of PDAC cases. TGF-β exerts complex and pleiotropic effects in cancers, notably via the activation of SMAD pathways, predominantly SMAD2/3/4. Though SMAD2 and 3 are rarely mutated in cancers, SMAD4 is lost in about 50% of PDAC, and the role of SMAD2/3 in a SMAD4-null context remains understudied. We herein provide evidence of a SMAD2/3 oncogenic effect in response to TGF-β1 in SMAD4-null human PDAC cancer cells. We report that inactivation of SMAD2/3 in SMAD4-negative PDAC cells compromises TGF-β-driven collective migration mediated by FAK and Rho/Rac signaling. Moreover, RNA-sequencing analyses highlight a TGF-β gene signature related to aggressiveness mediated by SMAD2/3 in the absence of SMAD4. Using a PDAC patient cohort, we reveal that SMAD4-negative tumors with high levels of phospho-SMAD2 are more aggressive and have a poorer prognosis. Thus, loss of SMAD4 tumor suppressive activity in PDAC leads to an oncogenic gain-of-function of SMAD2/3, and to the onset of associated deleterious effects.
    MeSH term(s) Carcinogenesis/genetics ; Carcinoma, Pancreatic Ductal/metabolism ; Humans ; Pancreatic Neoplasms/metabolism ; RNA ; Smad2 Protein/genetics ; Smad2 Protein/metabolism ; Smad3 Protein/metabolism ; Smad4 Protein/genetics ; Smad4 Protein/metabolism ; Transforming Growth Factor beta/pharmacology ; Transforming Growth Factor beta1/metabolism ; Pancreatic Neoplasms
    Chemical Substances SMAD2 protein, human ; SMAD3 protein, human ; SMAD4 protein, human ; Smad2 Protein ; Smad3 Protein ; Smad4 Protein ; Transforming Growth Factor beta ; Transforming Growth Factor beta1 ; RNA (63231-63-0)
    Language English
    Publishing date 2022-10-07
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2399-3642
    ISSN (online) 2399-3642
    DOI 10.1038/s42003-022-03994-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Generation of a conditional Flpo/FRT mouse model expressing constitutively active TGFβ in fibroblasts.

    Cardot-Ruffino, Victoire / Chauvet, Véronique / Caligaris, Cassandre / Bertrand-Chapel, Adrien / Chuvin, Nicolas / Pommier, Roxane M / Valcourt, Ulrich / Vincent, David F / Martel, Sylvie / Aires, Sophie / Kaniewski, Bastien / Dubus, Pierre / Cassier, Philippe / Sentis, Stéphanie / Bartholin, Laurent

    Scientific reports

    2020  Volume 10, Issue 1, Page(s) 3880

    Abstract: Transforming growth factor (TGFβ) is a secreted factor, which accumulates in tissues during many physio- and pathological processes such as embryonic development, wound healing, fibrosis and cancer. In order to analyze the effects of increased ... ...

    Abstract Transforming growth factor (TGFβ) is a secreted factor, which accumulates in tissues during many physio- and pathological processes such as embryonic development, wound healing, fibrosis and cancer. In order to analyze the effects of increased microenvironmental TGFβ concentration in vivo, we developed a conditional transgenic mouse model (Flpo/Frt system) expressing bioactive TGFβ in fibroblasts, a cell population present in the microenvironment of almost all tissues. To achieve this, we created the genetically-engineered [Fsp1-Flpo;
    MeSH term(s) Animals ; Fibroblasts/metabolism ; Gene Expression ; Genetic Engineering ; Hep G2 Cells ; Humans ; Mice ; Mice, Transgenic ; Models, Animal ; Transforming Growth Factor beta/genetics
    Chemical Substances Transforming Growth Factor beta
    Language English
    Publishing date 2020-03-03
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-020-60272-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Generation of an Fsp1 (fibroblast-specific protein 1)-Flpo transgenic mouse strain.

    Cardot-Ruffino, Victoire / Chauvet, Véronique / Caligaris, Cassandre / Bertrand-Chapel, Adrien / Chuvin, Nicolas / Pommier, Roxane M / Valcourt, Ulrich / Vincent, David / Martel, Sylvie / Aires, Sophie / Kaniewski, Bastien / Dubus, Pierre / Cassier, Philippe / Sentis, Stéphanie / Bartholin, Laurent

    Genesis (New York, N.Y. : 2000)

    2020  Volume 58, Issue 5, Page(s) e23359

    Abstract: Recombination systems represent a major breakthrough in the field of genetic model engineering. The Flp recombinases (Flp, Flpe, and Flpo) bind and cleave DNA Frt sites. We created a transgenic mouse strain ([Fsp1-Flpo]) expressing the Flpo recombinase ... ...

    Abstract Recombination systems represent a major breakthrough in the field of genetic model engineering. The Flp recombinases (Flp, Flpe, and Flpo) bind and cleave DNA Frt sites. We created a transgenic mouse strain ([Fsp1-Flpo]) expressing the Flpo recombinase in fibroblasts. This strain was obtained by random insertion inside mouse zygotes after pronuclear injection. Flpo expression was placed under the control of the promoter of Fsp1 (fibroblast-specific protein 1) gene, whose expression starts after gastrulation at Day 8.5 in cells of mesenchymal origin. We verified the correct expression and function of the Flpo enzyme by several ex vivo and in vivo approaches. The [Fsp1-Flpo] strain represents a genuine tool to further target the recombination of transgenes with Frt sites specifically in cells of mesenchymal origin or with a fibroblastic phenotype.
    MeSH term(s) Animals ; Cells, Cultured ; DNA Nucleotidyltransferases/genetics ; DNA Nucleotidyltransferases/metabolism ; Fibroblasts/metabolism ; Gastrula/metabolism ; Gene Targeting/methods ; HaCaT Cells ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Promoter Regions, Genetic ; S100 Calcium-Binding Protein A4/genetics ; Zygote/metabolism
    Chemical Substances S100 Calcium-Binding Protein A4 ; S100a4 protein, mouse ; DNA Nucleotidyltransferases (EC 2.7.7.-) ; FLP recombinase (EC 2.7.7.-)
    Language English
    Publishing date 2020-03-19
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2004544-X
    ISSN 1526-968X ; 1526-954X
    ISSN (online) 1526-968X
    ISSN 1526-954X
    DOI 10.1002/dvg.23359
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Correction: Schwann cells support oncogenic potential of pancreatic cancer cells through TGFβ signaling.

    Roger, Elodie / Martel, Sylvie / Bertrand-Chapel, Adrien / Depollier, Arnaud / Chuvin, Nicolas / Pommier, Roxane M / Yacoub, Karam / Caligaris, Cassandre / Cardot-Ruffino, Victoire / Chauvet, Véronique / Aires, Sophie / Mohkam, Kayvan / Mabrut, Jean-Yves / Adham, Mustapha / Fenouil, Tanguy / Hervieu, Valérie / Broutier, Laura / Castets, Marie / Neuzillet, Cindy /
    Cassier, Philippe A / Tomasini, Richard / Sentis, Stéphanie / Bartholin, Laurent

    Cell death & disease

    2020  Volume 11, Issue 1, Page(s) 57

    Abstract: The original version of this article contained an error in the name of one of the co-authors (Kayvan Mohkam). This has been corrected in the PDF and HTML versions. ...

    Abstract The original version of this article contained an error in the name of one of the co-authors (Kayvan Mohkam). This has been corrected in the PDF and HTML versions.
    Language English
    Publishing date 2020-01-23
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/s41419-020-2262-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Schwann cells support oncogenic potential of pancreatic cancer cells through TGFβ signaling.

    Roger, Elodie / Martel, Sylvie / Bertrand-Chapel, Adrien / Depollier, Arnaud / Chuvin, Nicolas / Pommier, Roxane M / Yacoub, Karam / Caligaris, Cassandre / Cardot-Ruffino, Victoire / Chauvet, Véronique / Aires, Sophie / Mohkam, Kayvan / Mabrut, Jean-Yves / Adham, Mustapha / Fenouil, Tanguy / Hervieu, Valérie / Broutier, Laura / Castets, Marie / Neuzillet, Cindy /
    Cassier, Philippe A / Tomasini, Richard / Sentis, Stéphanie / Bartholin, Laurent

    Cell death & disease

    2019  Volume 10, Issue 12, Page(s) 886

    Abstract: Pancreatic ductal adenocarcinoma (PDAC) is one of the solid tumors with the poorest prognosis. The stroma of this tumor is abundant and composed of extracellular matrix and stromal cells (including cancer-associated fibroblasts and immune cells). Nerve ... ...

    Abstract Pancreatic ductal adenocarcinoma (PDAC) is one of the solid tumors with the poorest prognosis. The stroma of this tumor is abundant and composed of extracellular matrix and stromal cells (including cancer-associated fibroblasts and immune cells). Nerve fibers invading this stroma represent a hallmark of PDAC, involved in neural remodeling, which participates in neuropathic pain, cancer cell dissemination and tumor relapse after surgery. Pancreatic cancer-associated neural remodeling is regulated through functional interplays mediated by physical and molecular interactions between cancer cells, nerve cells and surrounding Schwann cells, and other stromal cells. In the present study, we show that Schwann cells (glial cells supporting peripheral neurons) can enhance aggressiveness (migration, invasion, tumorigenicity) of pancreatic cancer cells in a transforming growth factor beta (TGFβ)-dependent manner. Indeed, we reveal that conditioned medium from Schwann cells contains high amounts of TGFβ able to activate the TGFβ-SMAD signaling pathway in cancer cells. We also observed in human PDAC samples that high levels of TGFβ signaling activation were positively correlated with perineural invasion. Secretome analyses by mass spectrometry of Schwann cells and pancreatic cancer cells cultured alone or in combination highlighted the central role of TGFβ in neuro-epithelial interactions, as illustrated by proteomic signatures related to cell adhesion and motility. Altogether, these results demonstrate that Schwann cells are a meaningful source of TGFβ in PDAC, which plays a crucial role in the acquisition of aggressive properties by pancreatic cancer cells.
    Language English
    Publishing date 2019-11-25
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/s41419-019-2116-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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