Auswahl der wissenschaftlichen Literatur zum Thema „Wnt/b-Catenin pathway“
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Zeitschriftenartikel zum Thema "Wnt/b-Catenin pathway"
Yu, Fujun, Yong Guo, Bicheng Chen, Liang Shi, Peihong Dong, Mengtao Zhou und Jianjian Zheng. „LincRNA-p21 Inhibits the Wnt/β-Catenin Pathway in Activated Hepatic Stellate Cells via Sponging MicroRNA-17-5p“. Cellular Physiology and Biochemistry 41, Nr. 5 (2017): 1970–80. http://dx.doi.org/10.1159/000472410.
Der volle Inhalt der QuelleAdjei-Fremah, Sarah, Emmanuel Kwaku Asiamah, Kingsley Ekwemalor, Louis Jackai, Keith Schimmel und Mulumebet Worku. „Modulation of Bovine Wnt Signaling Pathway Genes by Cowpea Phenolic Extract“. Journal of Agricultural Science 8, Nr. 3 (16.02.2016): 21. http://dx.doi.org/10.5539/jas.v8n3p21.
Der volle Inhalt der QuelleLi, Xinyu, Lingyu Geng, Xiangxiang Zhou, Kang Lu, Peipei Li und Xin Wang. „5-Aza-2-Deoxycytidine Regulates Wnt Beta-Catenin Pathway in B Cell Lymphoma“. Blood 126, Nr. 23 (03.12.2015): 4810. http://dx.doi.org/10.1182/blood.v126.23.4810.4810.
Der volle Inhalt der QuelleLanghammer, Tina-Susann, Catrin Roolf, Saskia Krohn, Christin Kretzschmar, Rayk Huebner, Arndt Rolfs, Mathias Freund und Christian Junghanss. „PI3K/Akt Signaling Interacts With Wnt/β-Catenin Signaling But Does Not Induce An Accumulation Of β-Catenin In The Nucleus Of Acute Lymphoblastic Leukemia Cell Lines“. Blood 122, Nr. 21 (15.11.2013): 4886. http://dx.doi.org/10.1182/blood.v122.21.4886.4886.
Der volle Inhalt der QuelleFachel, Angela A., Ashlesha Shrikant Muley, Cem Meydan, Xabier Agirre, Leandro Cerchietti, Ari Melnick und Kristy L. Richards. „Targeting ß-Catenin Signaling in DLBCL with ICG-001 and PAM-1 Suppresses Cell Proliferation and Induces Apoptosis“. Blood 128, Nr. 22 (02.12.2016): 5382. http://dx.doi.org/10.1182/blood.v128.22.5382.5382.
Der volle Inhalt der QuelleTran, Bang Manh, Dustin James Flanagan, Gregor Ebert, Nadia Warner, Hoanh Tran, Theodora Fifis, Georgios Kastrappis et al. „The Hepatitis B Virus Pre-Core Protein p22 Activates Wnt Signaling“. Cancers 12, Nr. 6 (31.05.2020): 1435. http://dx.doi.org/10.3390/cancers12061435.
Der volle Inhalt der QuelleRogaczewski, Patryk, Michał Janiak, Kamil Borysewicz, Tadeusz Głos, Navid Ahmadi und Łukasz Szylberg. „Clinical significancy of WNT pathway inhibition in various cancers“. Journal of Education, Health and Sport 12, Nr. 11 (03.11.2022): 183–91. http://dx.doi.org/10.12775/jehs.2022.12.11.024.
Der volle Inhalt der QuelleThanendrarajan, S., Y. Kim und I. G. H. Schmidt-Wolf. „Understanding and Targeting the Wnt/β-Catenin Signaling Pathway in Chronic Leukemia“. Leukemia Research and Treatment 2011 (04.12.2011): 1–7. http://dx.doi.org/10.4061/2011/329572.
Der volle Inhalt der QuelleShi, Chong-Shan, Ning-Na Huang, Kathleen Harrison, Sang-Bae Han und John H. Kehrl. „The Mitogen-Activated Protein Kinase Kinase Kinase Kinase GCKR Positively Regulates Canonical and Noncanonical Wnt Signaling in B Lymphocytes“. Molecular and Cellular Biology 26, Nr. 17 (01.09.2006): 6511–21. http://dx.doi.org/10.1128/mcb.00209-06.
Der volle Inhalt der QuelleQiang, Ya-Wei, Bo Hu, Yu Chen, Wei Qiang, Christoph Heuck, Bart Barlogie und John D. Shaughnessy. „Bortezomib Induces Activation of b-Catenin/TCF Signaling Pathway in Multiple Myeloma“. Blood 118, Nr. 21 (18.11.2011): 1851. http://dx.doi.org/10.1182/blood.v118.21.1851.1851.
Der volle Inhalt der QuelleDissertationen zum Thema "Wnt/b-Catenin pathway"
Ferreira, Catarina Domingues. „WNT/ß-catenin and Hedgehog signaling pathways as therapeutic targets in B cell neoplasms“. Master's thesis, Universidade de Aveiro, 2018. http://hdl.handle.net/10773/22676.
Der volle Inhalt der QuelleAs neoplasias de células B são caracterizadas por um grupo heterogéneo de doenças que incluem linfomas de células B e doenças de células plasmáticas, entre outras. O mieloma múltiplo (MM) é uma neoplasia maligna originada pela proliferação de células plasmáticas monoclonais que permanece incurável. Esta proliferação de células plasmáticas malignas no microambiente da medula óssea produz proteína monoclonal no sangue ou na urina e está associada a sinais malignos. Representa aproximadamente 1% das doenças neoplásicas e 10% a 15% das neoplasias hematológicas. O linfoma difuso de grandes células B (DLBCL) é a forma mais comum de linfoma não-Hodgkin, representando 31% dos linfomas não-Hodgkin, e sendo fatal se não for tratado. DLBCL é um linfoma agressivo e de crescimento rápido que pode surgir nos gânglios linfáticos ou fora do sistema linfático, no trato gastrointestinal, testículos, tiroide, pele, mama, osso ou cérebro. A ativação inadequada de vias de sinalização embrionárias, como WNT/β-catenina e Hedgehog, vias críticas de autorrenovação das células estaminais e diferenciação das células hematopoiéticas, tem sido implicada nestas neoplasias de células B. Neste sentido, essas vias podem constituir potenciais novos alvos terapêuticos para tratar o MM e o DLBCL. O objetivo principal deste estudo foi avaliar o potencial terapêutico de inibidores das vias WNT/β-catenina e Hedgehog, respetivamente IWR-1 e vismodegib, isolados e em combinação um com o outro, usando linhas celulares de MM e DLBCL. Para avaliar o efeito dos inibidores IWR-1 e vismodegib no MM e no DLBCL foram utilizadas linhas celulares H929 (MM) e FARAGE (DLBCL), submetidas a diferentes concentrações dos inibidores. A atividade metabólica foi avaliada utilizando o ensaio de resazurina, a morte celular por microscopia ótica (coloração de May-Grunwald) e citometria de fluxo (FC) (marcação com anexina V/7-AAD e quantificação de BCL-2 e caspases, proteínas relacionadas com a apoptose). A análise do ciclo celular foi avaliada por FC, utilizando a solução PI/RNAse. Também por FC, foi avaliada a expressão de β-catenina e ERK fosforilado, moléculas relacionadas com as vias de sinalização WNT/β-catenina e HH. Os resultados mostraram que IWR-1 e vismodegib reduziram a atividade metabólica celular de modo dependente do tempo, da linha celular e da concentração, em monoterapia ou em combinação. O IC50 do IWR-1 nas células H929 e Farage foi de 40 μM e 75 μM, respetivamente, enquanto que o IC50 do vismodegib foi de 70 μM para as células H929 e 57 μM para as células Farage, após 24 horas de tratamento. Estes resultados mostram que as células H929 são mais sensíveis ao IWR-1 e, contrariamente, as células Farage são mais sensíveis ao vismodegib. Estes compostos induzem a morte celular predominantemente por apoptose e induzem bloqueio do ciclo celular em G1. Em conclusão, os resultados sugerem que IWR-1 e vismodegib são potenciais novas terapias direcionadas que poderão ser eficientes no tratamento de MM e DLBCL. No entanto, IWR-1 é mais indicado para a terapêutica do MM e o vismodegib para a terapêutica do DLBCL.
B-cell neoplasms are characterized by a heterogeneous group of diseases that include, B-cell lymphomas and plasma cell disorders, among others. Multiple myeloma (MM) is a malignant neoplasm originated by proliferation of monoclonal plasma cells that remains incurable. This clonal proliferation of malignant plasma cells occurs in the bone marrow microenvironment, leads to the production of monoclonal protein in the blood or urine and is associated with malignant signals. It accounts for approximately 1% of neoplastic diseases and 10% to 15% of hematologic neoplasms. Diffuse large B-cell lymphoma (DLBCL) is the most common form of non-Hodgkin lymphoma, representing 31% of the non-Hodgkins lymphomas, being fatal if untreated. DLBCL is an aggressive, fast-growing lymphoma, that can arise in lymph nodes or outside of the lymphatic system, in the gastrointestinal tract, testicles, thyroid, skin, breast, bone, or brain. Inappropriate activation of conserved embryonic signaling pathways, such as WNT/β-catenin and Hedgehog (HH), critical for stem cell self-renewal and differentiation of hematopoietic cells, has been implicated in these B-cell neoplasms. In this sense, these pathways may constitute new potential therapeutic targets to treat MM and DLBCL. The main goal of this study was to evaluate the therapeutic potential of a WNT/ β-catenin and a Hedgehog inhibitor, respectively, the IWR-1 and vismodegib, alone and in combination, using MM and DLBCL cell lines. To evaluate the effect of IWR-1 and vismodegib in MM and in DLBCL, H929 (MM) and FARAGE (DLBCL) cell lines were submitted to different concentrations of the inhibitors. Metabolic activity was evaluated using resazurin assay and cell death was evaluated by optical microscopy (May-Grunwald staining) and flow cytometry (FC) (Annexin V/7-AAD staining and by quantification of BCL-2 and caspases expression, apoptosis-related proteins). Cell cycle analysis was evaluated by FC, using a PI/RNAse solution. Also by FC the expression of β-catenin and phosphorylated ERK, molecules related to the WNT/β-catenin and HH signaling pathways, were tested. Results showed that IWR-1 and vismodegib reduced cell metabolic activity in a time-, cell line- and dose-dependent manner, when administrated in monotherapy or in combination. The IC50 of IWR-1 in H929 and Farage cells was 40 μM and 75 μM, respectively, and the IC50 of vismodegib was 70 μM for H929 cells and 57 μM in Farage cells, after 24h of treatment. These results show that H929 cells are more sensitive to IWR-1 and, contrarily, Farage cells are more sensitive to vismodegib. These compounds induce cell death mainly by apoptosis and showed an arrest in cell cycle at G1. In conclusion, results suggest that IWR-1 and vismodegib are potential new targeted therapies that could be efficient in MM and DLBCL treatment in the future. However, IWR-1 is more indicated for MM therapy and vismodegib for DLBCL therapy
Dias, Neto Domingos Pedro Manuel. „The wnt/b-catenin signalling pathway and anterior posterior patterning in the vertebrate central nervous system“. Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368691.
Der volle Inhalt der QuelleFiore, Donatella. „In vitro and in vivo study of cannabinoids as modulators of Wnt/β-catenin pathway in human colorectal cancer“. Doctoral thesis, Universita degli studi di Salerno, 2017. http://hdl.handle.net/10556/2485.
Der volle Inhalt der QuelleColorectal cancer (CRC) is the second most common cause of cancer death. Molecular events in CRC has been extensively studied and several data suggest that Wnt/β-catenin signaling deregulation play a pivotal role in colorectal carcinogenesis. Majority of both familial syndromes (FAP) and sporadic colon cancers, arise from APC or β-catenin genes alterations, leading to Wnt signaling hyperactivation. According to the cancer stem cells (CSCs) theory, some cancer-initiating cells, harboring stem-cell like properties, evade standard chemotherapies, resulting in recurrent and metastatic tumors. Wnt/β-catenin signaling and its deregulation is involved in the recurrence and maintenance of CSCs. In recent years, understanding of molecular mechanisms underlying CSCs biology, led to development of novel strategies to completely eradicate colorectal cancer. Some evidences suggest a potential crosstalk between the endocannabinoid system and the Wnt pathway, also in cancer stem cells, in several tumor types. This could represent a key mechanism in the control of the anti-cancer activity of cannabinoids, as well as a novel putative site for pharmacological intervention. Results from this work led to identification of Rimonabant, originally an inverse agonist of CB1 cannabinoids receptor, as modulator of Wnt/β-catenin pathway in CRC, able to control colon cancer stemness, without toxicity toward cells from healty tissue. Moreover, for the first time, we proposed a novel epigenetic mechanism Rimonabant-mediated. [edited by author]
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Vadnais, Charles. „Transcriptional regulation by CUX1 and its implication in the DNA damage response and Wnt/b-Catenin pathway activation“. Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116915.
Der volle Inhalt der QuelleL'objectif global de ma thèse était d'étudier et de caractériser l'activité transcriptionelle du facteur de transcription CUX1, autant de façon globale que dans le contexte de processus cellulaires spécifiques. J'ai effectué des expériences de localisation génomiques à grande échelle afin d'identifier un grand nombre de cibles potentielles directes de transcription de CUX1 et j'ai analysé leur régulation par CUX1 en effectuant des expériences de profilage d'expression génétique à la suite de la surexpression de l'isoform p110CUX1 ainsi qu'à la suite de la répression de CUX1 par shRNA. Cette étude a démontré que CUX1 peut activer ou réprimer l'expression de ces cibles, même lorsqu'il se lie à une distance considérable du promoteur de ces gènes, et que la séquence consensus de liaison de CUX1 joue un rôle dans sa liaison à l'ADN mais n'est pas nécessaire pour celle-ci dans plusieurs cas. L'analyse de cibles potentielles de CUX1 identifiées par des expériences de localisation génomique a grande échelle ont fortement suggéré l'implication de CUX1 dans la réponse des cellules au dommage à l'ADN. J'ai utilisé diverses techniques de biologie moléculaire pour étudier ce phénomène et j'ai démontré que l'activité transcriptionelle de CUX1 est nécessaire au maintien de niveaux suffisants de nombreuses protéines constituant la machinerie essentielle à la réponse des cellules au dommage à l'ADN. Les cellules n'exprimant pas ou peu de CUX1 sont déficientes dans leur capacité d'arrêt du cycle cellulaire et de réparation du dommage à l'ADN, sont plus sensibles au dommage et montrent un phénotype d'instabilité génomique accrue. Des études précédentes de tumeurs des glandes mammaires dans un modèle de souris ont montré qu'une partie des tumeurs provenant de souris surexprimant p110 ou p75 CUX1 montraient une activation du processus de signalement Wnt/β-Catenin. Cependant, le mécanisme par lequel seule une partie des tumeurs montrait ce phénotype n'était pas connu. J'ai donc effectué du profilage d'expression génétique sur ces tumeurs afin de caractériser l'effet transcriptionel de CUX1 dans celles-ci et d'identifier d'autres facteurs qui collaborent dans l'activation de Wnt/β-Catenin. J'ai ainsi identifié des membres de la famille de facteurs de transcription GLI comme étant requis pour l'activation de Wnt/β-Catenin dans ces tumeurs. J'ai aussi observé des caractéristiques de transition épithélio-mésenchymateuse dans ces tumeurs, ce qui pourrait avoir des implications sur la capacité d'invasion et la sévérité de celles-ci. La coopération entre CUX1 et les gènes GLI a été confirmée par une méta-analyse de données de profilage d'expression de tumeurs humaines ainsi qu'avec des expériences cellulaires testant la capacité de chacun de ces deux facteurs à activer Wnt/β-Catenin, individuellement et en combinaison.
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
Armstrong, Victoria Janetta. „Involvement of the WNT/b-catenin signalling pathway and the estrogen receptor in bone cells' adaptive responses to mechanical strains“. Thesis, Royal Veterinary College (University of London), 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.500028.
Der volle Inhalt der QuelleUsongo, Macalister. „Characterization of the WNT/B-catenin signaling pathway in the development of mouse ovarian surface epithelium (MOSE) and follicular ovulatory capability“. Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116973.
Der volle Inhalt der QuelleLes Wnts sont des molécules de signalisation sécrétées dans l'espace extracellulaire pour réagir localement et contrôler divers processus du développement comme la spécification, la prolifération et la différenciation des cellules. Trois voies de signalisation WNTS ont été identifiées. La plus connue est la voie canonique appelée aussi la voie WNT/β-catenin. Récemment des études ont montré que la voie de signalisation WNT serait impliquée dans le développement et la différenciation ovarienne. Malgré ces études, peu est connu sur l'expression et la fonction de l'activité β-catenin/Tcf dans les différents compartiments d'ovaire. Pour clarifier les mécanismes moléculaires responsables dans le développement d'ovaire, j'ai étudié le rôle de la signalisation WNT/β-catenin durant la formation d'épithélium superficiel ovarien et dans la capacité ovulatoire des follicules. Pour visualiser l'implication de la voie canonique dans l'activation ovarienne, nous avons utilisé des souris transgéniques qui expriment la protéine β-galactosidase (lacZ) en réponse des protéines β-catenin/Tcf.Le premier article que je présente (Manuscrit I) décrit l'activation spatiotemporal de β-catenin/Tcf dans l'épithélium superficiel ovarien au cours du développement de la souris. Au jour E11.5, la gonade non-différenciée est marquée positivement pour LacZ indiquant que β-catenin/Tcf est activée. Au cours de la différenciation sexuelle de la souris, l'expression de LacZ disparait dans les testicules. Par contre, dans l'ovaire embryonnaire l'expression de LacZ est maintenue. À la maturation sexuelle de la souris femelle, l'expression de LacZ est devenue plus diffuse et la quantité de cellules qui expriment LacZ a diminué. Une analyse de cytométrie en flux a indiqué que la population de cellules positive pour LacZ démontre des mécanismes cytoprotecteurs. En conclusion, les résultats suggèrent que l'épithélium superficiel ovarien est constitué d'une population de cellules hétérogène et mais aussi de cellules progénitrices. Le deuxième article que je présente (Manuscrit II) étudie la stabilisation de β-catenin, les gènes induit par le complexe de β-catenin/Tcf et la prolifération d'épithélium superficiel ovarien. β-catenin est localisée dans les membranes latérales d'épithélium ovarien. J'ai démontré que la stimulation des cellules d'épithélium superficiel ovarien avec une agoniste Wnt stabilise β-catenin mais n'induit pas l'expression de lacZ dans les souris transgéniques. En plus, le niveau d'expression du gène E-cadherin a baissé et la prolifération des cellules d'épithélium superficiel ovarien a augmenté. Des quatre lignées cellulaires de cellules ovariennes cancéreuses qu'on a examinées, seulement la lignée HEY avait une réponse transcriptionelle à la stimulation de protéines WNT canoniques. Nos études révèlent que la localisation nucléaire de β-catenin n'est pas suffisante pour induire l'expression de ces gènes cibles dans l'épithélium superficiel ovarien. Dans les cellules cancereuses la voie de signalisation WNT est altèrée de sorte que l'inhibition de GSK-3β est augmentée et β-catenin est activée ce que contrôle la prolifération et la transition d'éptihelium à mésenchyme durant la tumorigenèse.Le troisième article que je présente (Manuscrit III) examine le rôle de la voie canonique durant le développement folliculaire. Les ovocytes des follicules primordiaux et primaires ne montraient aucune activation de la signalisation WNT. L'activation de β-catenin/Tcf était présente dans les follicules secondaires et la proportion de follicules positifs pour l'expression de lacZ a augmenté durant la maturation des follicules. Au contraire, la majorité (>90%) d'ovocytes retrouvés dans les oviductes durant l'oestrus et aprés un traitement hormonal n'exprimait pas le gène lacZ. Nos résultats indiquent que la voie de signalisation canonique de WNT est activée durant la croissance des ovocytes et peut identifier les follicules non-ovulatoires.
Spadoni, I. „IDENTIFICATION AND CHARACTERIZATION OF THE 'GUT VASCULAR BARRIER'“. Doctoral thesis, Università degli Studi di Milano, 2014. http://hdl.handle.net/2434/234155.
Der volle Inhalt der QuelleSammarco, Alessandro. „Study on normal and tumoral cell subpopulations and their interactions in the mammary gland cancer of humans and animals“. Doctoral thesis, Università degli studi di Padova, 2018. http://hdl.handle.net/11577/3425737.
Der volle Inhalt der QuelleHuman breast cancer (HBC), canine (CMT), and feline mammary tumors (FMT) are extremely common and are characterized by a remarkable both inter- and intra-tumor heterogeneity. Intra-tumor heterogeneity is due to the coexistence of cancer cells that differ between each other in terms of phenotypic, genetic, behavioral characteristics, and metastatic potential. Cancer stem cells (CSCs) are thought to be responsible for such heterogeneity, resistance to therapy, and metastasis development. Several pathways are altered in CSCs, such as the oncogenic Wnt/-catenin and Hippo pathways, and CSCs are associated to the epithelial-to-mesenchymal transition (EMT) process. The aims of this study were to i) isolate and characterized mammary CSCs; ii) investigate EMT process and Wnt/-catenin and Hippo pathways in mammary cancer of the three species; iii) establish a metastatic mouse model of breast cancer seeking for genes responsible of metastatic dissemination; iv) isolate and characterize extracellular vesicles (EVs), which is one of the main forms of intercellular communication, from canine and feline mammary tumors as well as study the role that EVs play during tumor development. CSC-like cells were isolated from established canine and feline mammary tumor cell lines (CYPp and FMCp, respectively) and phenotypically and molecularly characterized for common CSC markers: CD44, CD24, CD133, SOX2, OCT4. Moreover, gene (qPCR) and protein (IHC and WB) expression of Wnt/-catenin and Hippo pathways-related molecules (-catenin, CCND1, YAP, TAZ, CTGF, ANKRD1) as well as protein expression (IHC) of EMT-related molecules (E-cadherin, SNAIL, TWIST, ZEB) were evaluated in a subset of human, canine, and feline mammary cancer tissues, that were also phenotypically characterized for the following markers: CK8/18, CK5/6, CK14, CD44, and vimentin. Additionally, triple negative breast cancer (TNBC) cell line MDA-MB-231 was used to establish a clinically relevant in vivo metastatic model. Finally, EVs were isolated and characterized from CYPp and FMCp and human glioblastoma-derived EVs were used to study tumor angiogenesis. We found that CD44, CD133, SOX2, and OCT4 expression increase in CSC-like cells (mammospheres) compared to parental adherent cells, therefore they could be used as useful markers in CMTs and FMTs. Wnt/-catenin and Hippo pathways seem to be deregulated at a post-transcriptional level in HBCs, CMTs, and FMTs. Interesting similarities were confirmed between TNBCs and FMTs, as well as between ER+ HBC and CMTs. In our metastatic model, mice developed distant metastases and we found a few genes that might play a role during metastatic dissemination. Among these, caspase 3 seems to be involved in brain metastases. Additionally, EVs were isolated from CYPp and FMCp, visualized by transmissible electron microscopy, counted using nanoparticle tracking analysis, and characterized by immunogold and WB (Alix, CD63, TSG101). Finally, using a human glioblastoma cell line (GBM8) we demonstrated that EVs are directly involved in tumor angiogenesis. Overall, this study confirms the use of dogs and cats as spontaneous models of mammary cancer development due to highly interesting biological similarities among the three species. Also, identification of EVs in CMTs and FMTs opens an interesting unexplored field in veterinary medicine.
Lima, Ana Paula Calheiros de. „Efeitos in vitro de soro de pacientes com nefrite lúpica ativa em células de linhagem osteoblástica humana hFOB 1.19“. Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-20032019-084434/.
Der volle Inhalt der QuelleINTRODUCTION: Bone loss is a common finding in Lupus Nephritis (LN) patients even in those recently diagnosed. Some evidences indicate an increased osteoclastogenesis as the main disturb of the bone remodeling process. The aim of this study was to investigate some pathways (RANK-L/OPG, Wnt/?-catenin and Th17/IL-17) possibly involved in the abnormal osteoclastogenesis detected in women at the diagnosis of proliferative LN as well as evaluating the action of vitamin D (vitD) in this scenario and their correlation with inflammatory factors. METHODS: We cultured the human osteoblastic cell line hFOB 1.19 (ATCC), and divided cultures into those supplemented with serum from healthy controls (HC) (n=15) and LN patients (n=15) instead of fetal bovine serum (FBS). Then 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] was added in two subgroups at the concentrations of 10-9M e 10-7M while vitD was absent in one subgroup in both HC and LN cultures (HC, HC+vitD 10-9M, HC+vitD 10-7M, LN, LN+vitD 10-9M, LN+vitD 10-7M) . After 48h of vitD addition, hFOB cultures were trypsinized. Flow cytometry and multiplex assays were performed to test CD166, CD54, alkaline phosphatase, RANKL, OPG, CD14, TLR4, NF-KappaB, SOST, DKK-1, ?-catenin, IL-1Beta, IL-2, IL-6, TNF-alfa, IL-17A, IL-17F, IL-21 and IL-22 concentrations in the cell lysates. Polymerase reaction chain (RT-PCR) assays analyzed the expression of RANKL, SOST, OPG and Beta-catenin mRNA. RESULTS: LN patients showed higher serum levels of DKK-1 (2802.04 ± 1380.06 x 696.3 ± 421.22pg/ml, p < 0.001), OPG (560.12 ± 333.56 x 340.24 ± 102.08pg/ml, p=0.0212), TNF-alfa (9.63 ± 14.49 x 1.27 ± 0.35pg/ml, p=0.0337), IL-6 (15.58±39.08 x 8.02±3.49, 0.0053) and IL-2 (3.36 ± 3.06 x 1.54 ± 0.9pg/ml, p=0.0353) than HCs. After exposure to medium enriched with LN serum, osteoblasts expressed higher RANKL mRNA (fold change 1.573, p=0.045) and lower OPG protein (178.81 ± 66.40 x 298.76 ± 114.94pg/mg, p=0.0016). 1,25(OH)2D3 supplementation increased the difference between LN and HC expression of DKK-1 (673.03 ± 171.93 x 456.69 ± 234.53pg/mg, p=0.0215), IL-6 (0.80 ± 0.25pg/mg x 0.66 ± 0.18, p=0.0417) and IL-2 (4.97 ± 2.2 x 3.90 ± 1,66pg/mg, p=0.042) proteins and diminished Beta-catenin mRNA in LN cells. DISCUSSION: Within the limitations of this study, the results suggest that the higher serum levels of proinflammatory cytokines, such as TNF-alfa, IL-6 and perhaps IL-2, detected in LN patients would possibly have induced RANKL genes, as demonstrated by an enhanced RANKL mRNA expression in LN osteoblasts, and suppressed OPG protein in cell lysates, which would have contributed to the increased osteoclastogenesis detected in bone biopsies of women with new onset of LN. 1,25(OH)2D3 addition to osteoblast cultures did not prevent the effects of inflammatory LN serum in vitro
Buchteile zum Thema "Wnt/b-Catenin pathway"
Thakkar, Roshni D., Ruimin Wang, Gangadhara R. Sareddy, Ratna K. Vadlamudi und Darrell W. Brann. „Estrogen Neuroprotection and Anti-Inflammation Actions in the Hippocampus“. In Estrogens and Memory, 401–15. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780190645908.003.0024.
Der volle Inhalt der QuelleNazir, Aqsa, Muhammad Aqib und Muhammad Usman. „Liver Cancer-Genesis, Progression and Metastasis“. In Liver Cancer - Genesis, Progression and Metastasis [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.106020.
Der volle Inhalt der QuelleKonferenzberichte zum Thema "Wnt/b-Catenin pathway"
Vaira, Sergio, R. Ellen Friday, Keith Scott, Steven Conrad, Glenn Mills und Francesco Turturro. „Abstract 3141: Hyperglycemia modulates the Wnt /b-catenin signaling pathway in breast cancer“. In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3141.
Der volle Inhalt der QuelleKanwar, Shailender S., Yingjie Yu, Jyoti Nautiyal, Bhaumik Patel und Adhip P. N. Majumdar. „Abstract 4254: The Wnt/ B-catenin pathway regulates colon cancer stem cells proliferation“. In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4254.
Der volle Inhalt der QuelleShomali, Maysoun, Patrick McGlynn, Dmitri Wiederchain, Paul August, Francisco Adrian, Carlos Garcia-Echeverria, Joachim Theilhaber und Monsif Bouaboula. „Abstract B158: Transcriptional profile of NAMPTi unveils modulation of Tankyrase and Wnt/B-catenin pathway.“ In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-b158.
Der volle Inhalt der QuelleKhan, Shahanshah, und Hasan Zaki. „Abstract 2732: NLRP12 suppresses colorectal cancer progression and invasion via downregulation of the Wnt/b-catenin pathway“. In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2732.
Der volle Inhalt der QuelleBarrueco, R. Rodriguez, EA Nekritz, J. Yu, D. Llobet Navas und JM Silva. „PO-085 MiR-424(322)/503 regulates Wnt/b-catenin pathway and resistance to treatment in breast cancer“. In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.128.
Der volle Inhalt der QuelleRo, Eun Ji, Jeong-Ha Hwang, Yong-Hee Cho und Kang-Yell Choi. „Abstract 4181: Simultaneous inhibition of the Wnt/B-catenin and Ras pathways by KY1022 effectively suppresses tumor initiation and progression of colorectal cancer“. In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4181.
Der volle Inhalt der QuelleRadhakrishnan, Sridhar, Lavanya Reddivari und Jairam Vanamala. „Abstract 1882: Resveratrol and grape seed extract synergistically elevate human colon cancer cell apoptosis and suppress cell proliferation via upregulation of p53 and suppression of Wnt/b-catenin signaling pathways“. In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1882.
Der volle Inhalt der QuelleBerichte der Organisationen zum Thema "Wnt/b-Catenin pathway"
Williams, Bart O. Analysis of the Role of the Wnt/B-Catenin Pathway in Prostate Development and Tumorigenesis. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada437150.
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