Stéphane Garcia

Aix-Marseille Université

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Juan Iovanna

Inserm

Nelson Dusetti

Centre de Recherche en Cancérologie de Marseille

Véronique Secq

Inserm

Marie‐Noëlle Lavaut

Inserm

Sophie Vasseur

Centre de Recherche en Cancérologie de Marseille

Colette Charpin

Hôpital Nord

Vincent Moutardier

Assistance Publique Hôpitaux de Marseille

Céline Loncle

Centre de Recherche en Cancérologie de Marseille

Claude Allasia

Hôpital Nord

Mohamed Gasmi

Hôpital Nord

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Inserm

442

Aix-Marseille Université

322

Centre National de la Recherche Scientifique

274

Assistance Publique Hôpitaux de Marseille

169

Centre de Recherche en Cancérologie de Marseille

133

Hôpital Nord

118

Hôpital de la Timone

116

Institut Paoli-Calmettes

Hôpital de la Conception

Institut de Neurobiologie de la Méditerranée

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Collagen-derived proline promotes pancreatic ductal adenocarcinoma cell survival under nutrient limited conditions

Nature Communications (2017)

O. Porta Olivares Jared R. Mayers Victoire Gouirand Margaret E. Torrence Tristan Gicquel

Abstract Tissue architecture contributes to pancreatic ductal adenocarcinoma (PDAC) phenotypes. Cancer cells within PDAC form gland-like structures embedded in a collagen-rich meshwork where nutrients and oxygen are scarce. Altered metabolism is needed for tumour cells to survive in this environment, but the metabolic modifications that allow PDAC cells to endure these conditions are incompletely understood. Here we demonstrate that collagen serves as a proline reservoir for PDAC cells to use as a nutrient source when other fuels are limited. We show PDAC cells are able to take up collagen fragments, which can promote PDAC cell survival under nutrient limited conditions, and that collagen-derived proline contributes to PDAC cell metabolism. Finally, we show that proline oxidase (PRODH1) is required for PDAC cell proliferation in vitro and in vivo . Collectively, our results indicate that PDAC extracellular matrix represents a nutrient reservoir for tumour cells highlighting the metabolic flexibility of this cancer.

10.1038/ncomms16031

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Citations (344)

Supplementary Figure Legends 1-6 from Tumor Protein 53–Induced Nuclear Protein 1 Is a Major Mediator of p53 Antioxidant Function

Carla E. Cano Julien Gommeaux Sylvia Pietri Marcel Culcasi Stéphane Garcia

Supplementary Figure Legends 1-6 from Tumor Protein 53–Induced Nuclear Protein 1 Is a Major Mediator of p53 Antioxidant Function

Mediator

10.1158/0008-5472.22375848

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Supplementary Figures 1-6 from Tumor Protein 53–Induced Nuclear Protein 1 Is a Major Mediator of p53 Antioxidant Function

Carla E. Cano Julien Gommeaux Sylvia Pietri Marcel Culcasi Stéphane Garcia

Supplementary Figures 1-6 from Tumor Protein 53–Induced Nuclear Protein 1 Is a Major Mediator of p53 Antioxidant Function

Mediator

10.1158/0008-5472.22375845.v1

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Tumor protein 53-induced nuclear protein 1 expression is repressed by miR-155, and its restoration inhibits pancreatic tumor development

Proceedings of the National Academy of Sciences (2007)

Meritxell Gironella Mylène Seux Min-Jue Xie Carla E. Cano Richard Tomasini

Pancreatic cancer is a disease with an extremely poor prognosis. Tumor protein 53-induced nuclear protein 1 ( TP53INP1 ) is a proapoptotic stress-induced p53 target gene. In this article, we show by immunohistochemical analysis that TP53INP1 expression is dramatically reduced in pancreatic ductal adenocarcinoma (PDAC) and this decrease occurs early during pancreatic cancer development. TP53INP1 reexpression in the pancreatic cancer-derived cell line MiaPaCa2 strongly reduced its capacity to form s.c., i.p., and intrapancreatic tumors in nude mice. This anti-tumoral capacity is, at least in part, due to the induction of caspase 3-mediated apoptosis. In addition, TP53INP1 −/− mouse embryonic fibroblasts (MEFs) transformed with a retrovirus expressing E1A/ras V12 oncoproteins developed bigger tumors than TP53INP1 +/+ transformed MEFs or TP53INP1 −/− transformed MEFs with restored TP53INP1 expression. Finally, TP53INP1 expression is repressed by the oncogenic micro RNA miR-155, which is overexpressed in PDAC cells. TP53INP1 is a previously unknown miR-155 target presenting anti-tumoral activity.

miR-155

10.1073/pnas.0703942104

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Citations (550)

Genetic inactivation ofNupr1acts as a dominant suppressor event in a two-hit model of pancreatic carcinogenesis

Gut (2013)

Carla E. Cano Tewfik Hamidi María Noé Garcia Daniel Grasso Céline Loncle

Nuclear protein 1 (Nupr1) is a major factor in the cell stress response required for Kras(G12D)-driven formation of pancreatic intraepithelial neoplastic lesions (PanINs). We evaluated the relevance of Nupr1 in the development of pancreatic cancer. We investigated the role of Nupr1 in pancreatic ductal adenocarcinoma (PDAC) progression beyond PanINs in Pdx1-cre;LSL-Kras(G12D);Ink4a/Arf(fl/fl)(KIC) mice. Even in the context of the second tumorigenic hit of Ink4a/Arf deletion, Nupr1 deficiency led to suppression of malignant transformation involving caspase 3 activation in premalignant cells of KIC pancreas. Only half of Nupr1-deficient;KIC mice achieved PDAC development, and incident cases survived longer than Nupr1(wt);KIC mice. This was associated with the development of well-differentiated PDACs in Nupr1-deficient;KIC mice, which displayed enrichment of genes characteristic of the recently identified human classical PDAC subtype. Nupr1-deficient;KIC PDACs also shared with human classical PDACs the overexpression of the Kras-activation gene signature. In contrast, Nupr1(wt);KIC mice developed invasive PDACs with enriched gene signature of human quasi-mesenchymal (QM) PDACs. Cells derived from Nupr1-deficient;KIC PDACs growth in an anchorage-independent manner in vitro had higher aldehyde dehydrogenase activity and overexpressed nanog, Oct-4 and Sox2 transcripts compared with Nupr1(wt);KIC cells. Moreover, Nupr1-deficient and Nurpr1(wt);KIC cells differed in their sensitivity to the nucleoside analogues Ly101-4b and WJQ63. Together, these findings show the pivotal role of Nupr1 in both the initiation and late stages of PDAC in vivo, with a potential impact on PDAC cell stemness. According to Nupr1 status, KIC mice develop tumours that phenocopy human classical or QM-PDAC, respectively, and present differential drug sensitivity, thus becoming attractive models for preclinical drug trials.

Pancreatic Intraepithelial Neoplasia

10.1136/gutjnl-2013-305221

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Immediate or Delayed Transplantation of a Vein Conduit Filled with Nasal Olfactory Stem Cells Improves Locomotion and Axogenesis in Rats after a Peroneal Nerve Loss of Substance

International Journal of Molecular Sciences (2020)

M Bonnet G. Guiraudie‐Capraz Tanguy Marqueste Stéphane Garcia Charlotte Jaloux

Over the recent years, several methods have been experienced to repair injured peripheral nerves. Among investigated strategies, the use of natural or synthetic conduits was validated for clinical application. In this study, we assessed the therapeutic potential of vein guides, transplanted immediately or two weeks after a peroneal nerve injury and filled with olfactory ecto-mesenchymal stem cells (OEMSC). Rats were randomly allocated to five groups. A3 mm peroneal nerve loss was bridged, acutely or chronically, with a 1 cm long femoral vein and with/without OEMSCs. These four groups were compared to unoperated rats (Control group). OEMSCs were purified from male olfactory mucosae and grafted into female hosts. Three months after surgery, nerve repair was analyzed by measuring locomotor function, mechanical muscle properties, muscle mass, axon number, and myelination. We observed that stem cells significantly (i) increased locomotor recovery, (ii) partially maintained the contractile phenotype of the target muscle, and (iii) augmented the number of growing axons. OEMSCs remained in the nerve and did not migrate in other organs. These results open the way for a phase I/IIa clinical trial based on the autologous engraftment of OEMSCs in patients with a nerve injury, especially those with neglected wounds.

Peripheral nerve injury

10.3390/ijms21082670

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Citations (12)

Iconographies supplémentaires de l'article : Léiomyomatose œsophagienne diffuse et syndrome d’Alport : rapport d’un cas

Clémence Delteil Nicolas Macagno Laurent Daniel Xavier Benoît D’Journo Sophie Guisiano

Source

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Histological identification of nasopharyngeal mechanoreceptors

European Archives of Oto-Rhino-Laryngology (2016)

F. Salburgo Stéphane Garcia Aude Lagier Dominique Estève Jean‐Pierre Lavieille

Immunostaining

Ostium

10.1007/s00405-016-4069-3

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Citations (18)

Targeting Tissular Immune Response Improves Diagnostic Performance of Anti-Saccharomyces cerevisiae Antibodies (ASCA) in Crohn’s Disease

PLoS ONE (2013)

Daniel Bertin Jean–Charles Grimaud Nathalie Lesavre Chahine Benelmouloud Ariadne Desjeux

Antibodies against Saccharomyces cerevisiae (ASCA) and Escherichia coli outer membrane porin C (anti-OmpC) are known to be detectable in the serum of patients with Crohn's disease (CD) but display a very poor sensitivity for the disease especially in forms with isolated colonic involvement. In this study we aimed at evaluating performances of these markers in supernatant of cultured colonic biopsies. Patients with colonic CD (n = 67), ulcerative colitis (UC) (n = 35) and control individuals (n = 37) were prospectively recruited for colonoscopy pinch biopsies and blood sampling. Serum and supernatant of culture tissues were analyzed for ASCA and anti-OmpC. Direct immunofluorescence was also performed on colonic tissues for total IgA detection. We detected for the first time ASCA IgA/IgG and anti-OmpC IgA in cultured colonic tissue supernatants. For both markers, sensitivities for diagnosing CD were better in supernatants (ASCA: 53.7%, anti-OmpC: 28.4%) than in serum (ASCA: 31.3%, anti-OmpC: 22.4%). Combination of results from a panel of these tests gave the greatest sensitivity ever described for CD diagnosis in colonic forms (70.2%). In this study, we described, for the first time, ASCA in supernatant of colonic tissue cultures. This assaying approach in CD diagnosis should be taken into consideration in the future especially in CD forms with isolated colonic involvement.

Immunofluorescence

10.1371/journal.pone.0080433

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Citations (6)

L’expression immunohistochimique de l’antigène PTEN : Un nouvel outil diagnostique dans les néoplasies débutantes de l’endomètre

Bulletin de l Académie Nationale de Médecine (2004)

Colette Taranger‐Charpin Séverine Carpentier Jean‐Philippe Dales Stéphane Garcia Amina Djemli

10.1016/s0001-4079(19)33772-0

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Citations (3)