دورية أكاديمية

Autocrine control of glioma cells adhesion and migration through IRE1 -mediated cleavage of SPARC mRNA

التفاصيل البيبلوغرافية
العنوان: Autocrine control of glioma cells adhesion and migration through IRE1 -mediated cleavage of SPARC mRNA
المؤلفون: Dejeans, N., Pluquet, O., Lhomond, S., Grise, F., Bouchecareilh, M., Juin, A., Meynard-Cadars, M., Bidaud-Meynard, A., Gentil, C., Moreau, V., Saltel, F., Chevet, E.
المساهمون: Physiopathologie du cancer du foie, Université Bordeaux Segalen - Bordeaux 2-Institut National de la Santé et de la Recherche Médicale (INSERM), Faculté de Médecine Purpan, This work was supported by the Avenir program of Institut National de la Santé et de la Recherche Médicale, Institut national du cancer, Ligue Contre le Cancer to E.C., the French Association pour la Recherche contre le Cancer to O.P., La Ligue contre le Cancer to N.D., and the Cancéropôle Grand Sud-Ouest to C.G., We thank the Chevet lab for critical reading of the manuscript. We are indebted to Sebastien Marais (Bordeaux Imaging Center, Bordeaux, France) for help with the ImageJ program.
المصدر: ISSN: 0021-9533.
بيانات النشر: HAL CCSD
Company of Biologists
سنة النشر: 2012
المجموعة: Archive ouverte HAL (Hyper Article en Ligne, CCSD - Centre pour la Communication Scientifique Directe)
مصطلحات موضوعية: IRE1, Cell adhesion, cell migration, Endoplasmic reticulum, SPARC, MESH: Actin Cytoskeleton/metabolism, MESH: Autocrine Communication*/genetics, MESH: Extracellular Matrix Proteins/metabolism, MESH: Gene Expression Profiling, MESH: Gene Expression Regulation, Neoplastic, MESH: Glioma/genetics, MESH: Glioma/pathology, MESH: Humans, MESH: Models, Biological, MESH: Osteonectin/genetics, MESH: Osteonectin/metabolism, MESH: Protein-Serine-Threonine Kinases/metabolism, MESH: Brain Neoplasms/genetics, MESH: RNA, Messenger/genetics, Messenger/metabolism, MESH: Signal Transduction/genetics, MESH: Spheroids, Cellular/pathology, MESH: Tumor Cells, Cultured, MESH: rhoA GTP-Binding Protein/metabolism, MESH: Brain Neoplasms/pathology
الوصف: International audience ; The endoplasmic reticulum (ER) is an organelle specialized for the folding and assembly of secretory and transmembrane proteins. ER homeostasis is often perturbed in tumor cells because of dramatic changes in the microenvironment of solid tumors, thereby leading to the activation of an adaptive mechanism named the unfolded protein response (UPR). The activation of the UPR sensor IRE1α has been described to play an important role in tumor progression. However, the molecular events associated with this phenotype remain poorly characterized. In the present study, we examined the effects of IRE1α signaling on the adaptation of glioma cells to their microenvironment. We show that the characteristics of U87 cell migration are modified under conditions where IRE1α activity is impaired (DN_IRE1). This is linked to increased stress fiber formation and enhanced RhoA activity. Gene expression profiling also revealed that loss of functional IRE1α signaling mostly resulted in the upregulation of genes encoding extracellular matrix proteins. Among these genes, Sparc, whose mRNA is a direct target of IRE1α endoribonuclease activity, was in part responsible for the phenotypic changes associated with IRE1α inactivation. Hence, our data demonstrate that IRE1α is a key regulator of SPARC expression in vitro in a glioma model. Our results also further support the crucial contribution of IRE1α to tumor growth, infiltration and invasion and extend the paradigm of secretome control in tumor microenvironment conditioning.
نوع الوثيقة: article in journal/newspaper
اللغة: English
العلاقة: info:eu-repo/semantics/altIdentifier/pmid/22718352; hal-02400377; https://hal.archives-ouvertes.fr/hal-02400377Test; PUBMED: 22718352
DOI: 10.1242/jcs.099291
الإتاحة: https://doi.org/10.1242/jcs.099291Test
https://hal.archives-ouvertes.fr/hal-02400377Test
رقم الانضمام: edsbas.58A87141
قاعدة البيانات: BASE