Auswahl der wissenschaftlichen Literatur zum Thema „Voie Wnt/b-Catenine“
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Zeitschriftenartikel zum Thema "Voie Wnt/b-Catenine"
Lefèvre, L., H. Omeiri, L. Drougat, S. Rodriguez, K. Perlemoine, M. Rizk-Rabin, J. Bertherat und B. Ragazzon. „AFF3, une nouvelle cible de la voie Wnt/b-catenin impliquée dans la tumorigenèse cortico-surrénalienne“. Annales d'Endocrinologie 74, Nr. 4 (September 2013): 267. http://dx.doi.org/10.1016/j.ando.2013.07.101.
Der volle Inhalt der QuelleLefèvre, L., S. Gaujoux, C. Hantel, M. P. Launay, S. Bonnet, K. Perlemoine, M. Guillaud-Bataille et al. „L’invalidation de la voie Wnt/b-catenin in vitro et in vivo dans des cellules tumorales cortico-surrénaliennes inhibe la prolifération et augmente l’apoptose cellulaire“. Annales d'Endocrinologie 73, Nr. 4 (September 2012): 265. http://dx.doi.org/10.1016/j.ando.2012.07.099.
Der volle Inhalt der QuelleDissertationen zum Thema "Voie Wnt/b-Catenine"
Berenguier, Camille. „Exploration de la fonction du canal potassique KCNQ1 dans l'homéostasie de la crypte colique“. Electronic Thesis or Diss., Université Côte d'Azur, 2023. http://www.theses.fr/2023COAZ6025.
Der volle Inhalt der QuelleIn recent years, the role of ion channels in cancer processes has emerged and the field continues to expand. It has been shown that 1) the expression of certain ion channels is deregulated in cancers, and 2) ion channels can regulate various signalling pathways. In physiology, the balance of signalling pathways must be maintained. In the epithelium of the colon, maintaining this balance is particularly crucial as cells undergo rapid renewal which relies on the combined action of multiple signalling pathways. Dysregulated activation of the Wnt/β-catenin signalling pathway, promoting cell proliferation, is a major driver of tumour development in the colon. In most cases of colorectal cancer, patients harbour mutations on the component of this pathway, contributing to its overactivation. The potassium channel KCNQ1 has diverse functions. In the colonic epithelium, it enables water secretion and maintains epithelial integrity by exerting its tumour suppressor activity through the repression of the Wnt/β-catenin pathway. Despite the impact of somatic mutations in cancers, there are no studies, to this day, exploring mutations of ion channels in this context. Therefore, we hypothesized that colorectal cancer patients carry pathogenic mutations on KCNQ1. By analysing publicly available databases, we identified 36 different mutations harboured by KCNQ1 in various cancers. We found that the most common mutations were loss-of-function. In colorectal cancer cells, the loss-of-function mutations were associated with increased Wnt/β-catenin pathway activity, independently of the canonical pathway receptors. We also observed an activation of several tyrosine kinase receptors that could directly mediate β-catenin activation. In the more physiological model of murine colonoids, loss-of-function mutations in KCNQ1 also seem to increase Wnt/β-catenin pathway activity. Furthermore, these mutations had an impact on the expression of Wnt/β-catenin pathway regulators, favouring a permissive state for the pathway overactivation. KCNQ1 thus appears to restrict the signalling pathway at multiple levels: directly by sequestering β-catenin at adherens junctions, preventing its activity as a transcription factor, and indirectly by allowing the expression of regulatory proteins that inhibit the Wnt/β-catenin pathway. Our results highlight, for the first time, that ion channels can carry somatic mutations in cancers, altering channel function. Moreover, our findings demonstrate that these mutations directly influence the activity of signaling pathways involved in cancer processes. Additionally, given that KCNQ1 expression levels can be used for classifying colorectal cancers, these mutations could potentially aid in the prognosis and stratification of patients. Altogether, these findings open a new avenue of investigations to better understand the diversity of mechanisms involved in cancer processes. Numerous other ion channels or their associated subunits may carry somatic mutations in cancers, deregulating their activity and the processes they govern
Cacheux, Wulfran. „Analyse moléculaire des conséquences de l’activation de la voie Wnt/b-caténine : mise en évidence del’autophagie au cours de la carcinogenèse intestinale“. Thesis, Paris 11, 2011. http://www.theses.fr/2011PA11T071.
Der volle Inhalt der QuelleOver 80% of colorectal cancers are linked to an Apc mutation. To identify new therapeutic targets, we used mouse models with Apc mutations and performed microarray experiments to identify key molecular events involved in intestinal carcinogenesis. This approach allowed usto identify an activation of the Notch signaling all along tumor progression. However, this induction is dispensable for tumor development since its inhibition did not prevent the Apc phenotype. In addition, we have identified an induction of autophagy throughout intestinal carcinogenesis which appears to be an attractive therapeutic target in the treatment of CRC patients
St-Jean, Guillaume. „Élucidation des rôles des voies Wnt et Hippo dans le développement et la fonction du tractus reproducteur femelle chez la souris“. Thesis, 2019. http://hdl.handle.net/1866/24240.
Der volle Inhalt der QuelleThe development of the female reproductive tract arises from the coordination of numerous signaling pathways regulating processes such as proliferation, differentiation and apoptosis during embryogenesis. The Wnt and Hippo pathways are known to be involved in these processes. Wnt pathway activation, via its specific ligands, results in the stabilisation and increased transcriptional activity of β-catenin. The Hippo pathway does not possess any specific ligands. In contrast to Wnt, inactivation of the Hippo pathway (via Lats1 and Lats2 kinases) is required for the stabilization and increased activity of the transcriptional coactivators YAP and TAZ. The Wnt pathway is known to be involved in the development of the female reproductive tract. Further evidence also suggests the possibility of functional redundancy amongst certain WNT ligands such as Wnt4 and Wnt5a. The Hippo pathway is not known to be implicated in the development of the female reproductive tract. However, numerous interactions have been reported between both pathways, suggesting a possible unknown role of Hippo in that context. The objective of this project was to elucidate the roles of Wnt4, Wnt5a, Lats1 and Lats2 in the Müllerian mesenchyme and the development of the uterus. Results from our first study confirmed the partially redundant roles of Wnt4 and Wnt5a in the development of the uterus. Our model was notably characterized by developmental abnormalities and loss of uterine functions resulting in in vivo decidualization defects and loss of conceptus viability. Results from our second study confirmed the redundant roles of Lats1 and Lats2 in the maintenance of Müllerian mesenchymal cell multipotency. We observed premature differentiation of Müllerian mesenchymal cells into myofibroblasts in absence of both Lats1 and Lats2. These changes were in part due to the increased expression of the target gene Ctgf. Our additional results could not demonstrate any potential interactions between the Wnt and Hippo pathways that could explain the phenotypic changes. In conclusion, our studies confirmed and further discovered novel roles of these pathways in the development of the Müllerian ducts. These models could also lead to better understanding of the pathophysiology of certain uterine diseases and the discovery of potential therapeutic approaches.