Дисертації з теми "Cancer and invasion"
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Smith, Neil Jonathan. "Extramural vascular invasion in colorectal cancer." Thesis, Institute of Cancer Research (University Of London), 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.510379.
Повний текст джерелаÜnlü, Ali. "Mechanism of invasion by prostate cancer." Thesis, University of Glasgow, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244438.
Повний текст джерелаPeng, Lu. "Multiscale mathematical modelling of cancer invasion." Thesis, University of Dundee, 2015. https://discovery.dundee.ac.uk/en/studentTheses/c0aec459-7953-4172-b1f9-5ad029aae9df.
Повний текст джерелаSafuan, Sabreena. "Lymphovascular invasion in melanoma and breast cancer." Thesis, University of Nottingham, 2012. http://eprints.nottingham.ac.uk/12771/.
Повний текст джерелаStarobinska, Ella. "Matrix Degradation and Invasion in Breast Cancer." Thesis, The University of Arizona, 2012. http://hdl.handle.net/10150/244788.
Повний текст джерелаPlanchon, Damien. "Etude du rôle de la surexpression des flotillines dans l'invasion cellulaire." Thesis, Montpellier, 2017. http://www.theses.fr/2017MONTT056.
Повний текст джерелаTumor cell invasion and consecutive metastasis formation are the main cause of death in cancer patients. Invading tumor cells are surrounded by stroma and extracellular matrix (ECM) that is remodeled or degraded during the metastatic process. ECM degradation is mediated by specialized organelles called invadosomes. Their function strongly depends on matrix metalloproteinases (MMPs) that degrade ECM. Among all the MMPs, MT1-MMP plays a major role the invasive behavior of metastatic cells.Flotillin 1 and 2 are two ubiquitous and highly conserved membrane proteins that can assemble in large oligomers, known to participate in membrane proteins clustering and endocytosis. Flotillins are overexpressed in many invasive cancers and considered as markers of poor prognosis, results we confirmed using several sarcoma and carcinoma models. During my project we identified Flotillins as regulators of MT1-MMP trafficking and cell invasion.We used a dual reciprocal approach consisting of the overexpression of Flotillins in non tumoral cells and of down-regulation of Flotillins in metastatic cells. We showed that flotillins downregulation in invasive cancer cells dramatically inhibit their invasive properties as monitored in vitro using a 3D-collagen invasion assay and in vivo using zebrafish xenografts. Reciprocally, ectopic overexpression of Flotillins in non-tumoral cells is sufficient to induce their invasive behavior in vitro and in vivo. This increase of invasion is mainly due to a higher ability to degrade the matrix in a MT1-MMP-dependent manner. Finally, we showed that Flotillins are critical regulators of the trafficking and the release of MT1-MMP at the degradation site
Woodward, Julia Keren Lynda. "Adhesion and invasion studies of uveal melanoma." Thesis, University of Sheffield, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251213.
Повний текст джерелаGarcía, de Albéniz Xabier. "Mechanisms of invasion and metastasis in colorectal cancer." Doctoral thesis, Universitat de Barcelona, 2015. http://hdl.handle.net/10803/300900.
Повний текст джерелаParte de esta investigación consiste en explorar los mecanismos involucrados en el patrón metastático de CCR. Asimismo usamos datos epidemiológicos donde evaluamos la asociación entre el polimorfismo intrónico de SMAD7 (rs4939827, 18q21) con el genotipo y características tumorales. En el primer proyecto usamos un modelo murino de metástasis hepáticas para crear un derivado celular con alto tropismo metastático a hígado y pulmón. Mediante análisis de expresión de genes usando chips de transcripción identificamos 194 genes diferencialmente expresados El análisis de muestras clínicas mostró que aquellos pacientes cuyo tumor presentaba bajos niveles de p38 sufrían una mayor frecuencia de metástasis al pulmón, pero no a otros órganos. Al tratar ratones que habían desarrollado metástasis hepáticas derivadas de la línea celular parental con un inhibidor específico de p38, vimos que se incrementaba la afinidad metastática al pulmón. Evidenciamos que p38, a través del silenciamiento de PTHLH, en el derivado celular altamente metastático disminuía su capacidad de colonizar el pulmón. Demostramos que PTHLH induce la apoptosis de células humanas de endotelio pulmonar a través del factor AIFM1, facilitando que las células metastáticas puedan extravasarse al pulmón. En el segundo proyecto evaluamos la asociación de un polimorfismo intrónico del gen SMAD7 con el fenotipo y varias características moleculares del tumor. Para ello empleamos 1509 casos de cáncer de colon y recto y 2307 controles emparejados anidados en las cohortes Nurses Health Study y Health Professionals Follow-up Study. Encontramos que el alelo de menor frecuencia de rs4939827 (G) se asociaba con un menor riesgo de desarrollar un CCR con un estadio pT1 o pT2 [razón de odds (OR) ajustada, 0.73; intervalo de confianza al 95\% (CI) 0.62-0.87] pero no con tumores con estadio pT3 o pT4 (OR ajustada, 1.07; 95\% CI 0.93-1.23, valor p de heterogeneidad = 1.2 x 10-4). La asociación entre el polimorfismo de rs4939827 y CCR también difería significativamente según la metilación de RUNX3 (valor p de heterogeneidad = 0.005). Entre aquellos pacientes diagnosticados con CCR, el alelo de menor frecuencia de rs4939827 (G) estaba significativamente asociado con peor supervivencia (hazards ratio, 1.20; 95\% CI, 1.02-1.42).
Koo, V. S. W. "Bioimaging and quantitative analysis of bladder cancer invasion." Thesis, Queen's University Belfast, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.484961.
Повний текст джерелаMarchesin, Valentina. "Role of ARF6 in breast cancer cell invasion." Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066297/document.
Повний текст джерелаThe ability of cancer cells to traffic through the extracellular matrix relies on the action of the membrane-anchored matrix metalloprotease MT1-MMP. MT1-MMP is exocytosed to invadopodia, the actin-based membrane protrusions responsible for matrix degradation. The small GTP-binding protein ARF6 is known to coordinate post-endocytic recycling and actin cytoskeletal organization at the plasma membrane and was shown to be up-regulated in breast cancer cells. In my PhD work I showed that ARF6 and two of its effectors JIP3 and JIP4 are required for MT1-MMP endosomes intracellular positioning and exocytosis at invadopodia and consequently for tumor cells ability to remodel the matrix and invade through a three-dimensional matrix environment. ARF6, through the interaction with JIP3/4, negatively controls the activity of the minus-end-directed microtubule motor dynactin/dynein, thus negatively regulating the clearance and inward movement of MT1-MMP endosomes from the cell periphery. In human samples ARF6 is accumulated at the plasma membrane, together with MT1-MMP, in a subset of highly aggressive breast carcinomas, thus corroborating the ARF6-JIP3/JIP4-MT1-MMP axis in breast cancer invasion. In a second study I addressed the contribution of ARF6 activation on actin cytoskeleton remodeling in breast cancer cells. ARF6 links epidermal growth factor receptor signaling to Rac1 activation and targeting to the leading edge where it activates the SCAR/WAVE complex and regulates ventral actin polymerization during lamellipodia extension. Collectively my work identifies novel molecular mechanisms through which ARF6 contributes to the invasive program of breast tumor cells
Behmoaram, Emy. "Biological studies of fascin function in cancer cell invasion and cancer progression." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111596.
Повний текст джерелаSin, Sai-lung Steven, and 冼世隆. "Chloride channel in glioma cell invasion." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41508555.
Повний текст джерелаSin, Sai-lung Steven. "Chloride channel in glioma cell invasion." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41508555.
Повний текст джерела周穎嫻 and Wing-han Vivian Chow. "Genes associated with invasion and metastasis of head and neck cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31222468.
Повний текст джерелаTurner, Stephen. "Mathematical modelling of cancer invasion and biological cell movement." Thesis, Heriot-Watt University, 2002. http://hdl.handle.net/10399/438.
Повний текст джерелаNeisen, Jessica. "Chemokine regulation of microenvironment-enhanced invasion in prostate cancer." Thesis, Queen's University Belfast, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.677956.
Повний текст джерелаTod, Jo. "The role of Eps8 in regulating pancreatic cancer invasion." Thesis, University of Southampton, 2013. https://eprints.soton.ac.uk/375024/.
Повний текст джерелаPaterson, Chay Giles Blair. "Minimal models of invasion and clonal selection in cancer." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/28986.
Повний текст джерелаEsmaeili, Pourfarhangi Kamyar. "Effect of Extrinsic and Intrinsic Factors on Cancer Invasion." Diss., Temple University Libraries, 2019. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/585155.
Повний текст джерелаPh.D.;
Metastasis is the leading cause of death among cancer patients. The metastatic cascade, during which cancer cells from the primary tumor reach a distant organ and form multiple secondary tumors, consists of a series of events starting with cancer cells invasion through the surrounding tissue of the primary tumor. Invading cells may perform proteolytic degradation of the surrounding extracellular matrix (ECM) and directed migration in order to disseminate through the tissue. Both of the mentioned processes are profoundly affected by several parameters originating from the tumor microenvironment (extrinsic) and tumor cells themselves (intrinsic). However, due to the complexity of the invasion process and heterogeneity of the tumor tissue, the exact effect of many of these parameters are yet to be elucidated. ECM proteolysis is widely performed by cancer cells to facilitate the invasion process through the dense and highly cross-linked tumor tissue. It has been shown in vivo that the proteolytic activity of the cancer cells correlates with the cross-linking level of their surrounding ECM. Therefore, the first part of this thesis seeks to understand how ECM cross-linking regulates cancer cells proteolytic activity. This chapter first quantitatively characterizes the correlation between ECM cross-linking and the dynamics of cancer cells proteolytic activity and then identifies ß1-integrin subunit as a master regulator of this process. Once cancer cells degrade their immediate ECM, they directionally migrate through it. Bundles of aligned collagen fibers and gradients of soluble growth factors are two well-known cues of directed migration that are abundantly present in tumor tissues stimulating contact guidance and chemotaxis, respectively. While such cues direct the cells towards a specific direction, they are also known to stimulate cell cycle progression. Moreover, due to the complexity of the tumor tissue, cells may be exposed to both cues simultaneously, and this co-stimulation may happen in the same or different directions. Hence, in the next two chapters of this thesis, the effect of cell cycle progression and contact guidance-chemotaxis dual-cue environments on directional migration of invading cells are assessed. First, we show that cell cycle progression affects contact guidance and not random motility of the cells. Next, we show how exposure of cancer cells to contact guidance-chemotaxis dual-cue environments can improve distinctive aspects of cancer invasion depending on the spatial conformation of the two cues. In this dissertation, we strive to achieve the defined milestones by developing novel mathematical and experimental models of cancer invasion as well as utilizing fluorescent time-lapse microscopy and automated image and signal processing techniques. The results of this study improve our knowledge about the role of the studied extrinsic and intrinsic cues in cancer invasion.
Temple University--Theses
Atieh, Youmna Marie Lyne. "Interplay between cancer cells and cancer-associated fibroblasts in tumor invasion and metastasis formation." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066140/document.
Повний текст джерелаCancer-associated fibroblasts (CAFs) are the most abundant cells of the tumor stroma. Their capacity to contract the matrix and induce invasion of cancer cells has been well-documented. However, it is not clear if CAFs remodel the matrix by other means (degradation, matrix deposition or stiffening). This project demonstrates that CAFs induce cancer cell invasion through assembly of FN into the matrix. CAFs assembled fibronectin (FN) mainly via integrin α5 but integrin αvβ3 was necessary for initial mechanosensing and fibrillar adhesion formation. In the absence of FN, contractility of the matrix by CAFs is preserved. When degradation is impaired, CAFs retain the capacity to induce invasion in a FN-dependent manner. In all cases, the levels of expression of integrin β3 and the amount of assembled FN was directly proportional to the invasion induced by fibroblast populations. Our results highlight FN assembly and integrin β3 as new hallmarks of CAFs. We also noticed that cancer cells migrate towards CAFs suggesting a possible chemotactic response. Using Dunn’s chemotaxis chamber, we found that cancer cells migrate along a gradient of CAF-conditioned media and a gradient of fibronectin. Finally, orthotopic injections of cancer cells and CAFs in the colon wall of mice revealed that CAFs stimulate metastasis of cancer cells to the liver. In conclusion, our data show that CAFs promote cancer cell invasion by depositing fibronectin that can guide cancer cells favoring metastasis formation
Allen, Victoria. "Uncovering Pathways Regulating ILC Metastasis Through miRNA Expression Analysis and Generation of Novel Invasive ILC Models." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/39616.
Повний текст джерелаMonteiro, Pedro. "Rôle des complexes WASH et exocyste dans l’invasion tumorale." Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066291/document.
Повний текст джерелаCancer cell invasion is a prerequisite to tumor progression and metastasis. In order to disseminate, tumor cells must degrade and remodel the extracellular matrix (ECM) in a process that requires the trans-membrane matrix metalloproteinase MT1-MMP, which is a key component of the ECM remodeling apparatus of cancer cells. MT1-MMP overexpression in cancers is associated with increased invasion and metastasis. Many cellular proteins are involved in the transport and delivery of MT1-MMP-containing vesicles to the PM. Previous work from the laboratory identified the exocyst complex (EC) as a key component required for matrix proteolysis and invasion of cancer cells. This multiprotein complex (Sec3, Sec5, Sec6, Sec8, Sec10, Sec15, Exo70 and Exo84) plays essential roles in docking secretory vesicles at the PM for exocytosis. To better characterize this complex, a yeast two-hybrid screen was performed, identifying the protein WASH as a potential partner of Exo84 and Sec3. WASH is a Nucleation Promoting Factor (NPF) able to activate the actin nucleating Arp2/3 complex. Results of the present study showed that WASH and the exocyst complexes interact and localize on MT1-MMP-positive endosomes in MDA-MB-231 breast cancer cells. This study highlight a direct implication of WASH and exocyst complex in ECM degradation by cancer cells through the docking and exocytosis of MT1-MMP-containing endosomes at the PM through connections between these compartments and the extracellular medium. This WASH- and exocyst-dependent MT1-MMP exocytosis mechanism is required for degradation of adjacent tissue by cancer cells during tumour cell invasion
Hamyeh, Mohamed. "Régulation de l'agressivité tumorale mammaire par la protéine tyrosine phosphatase PTPL1/PTPN13." Thesis, Montpellier, 2016. http://www.theses.fr/2016MONTT015/document.
Повний текст джерелаThe regulation of breast tumor aggressiveness by Protein Tyrosine Phosphatase PTPL1/ PTPN13Breast cancer is a major problem for public health of which the incidence continues to increase. Its mortality is often linked to metastasis formation. Studies on PTPL1, the largest protein tyrosine phosphatase, have shown that it presents the characteristics of a tumor suppressor gene. PTPL1 is mutated in several types of cancers and its expression is associated with good prognostic in prostate and breast cancers. My team has shown that PTPL1 mediates the pro apoptotic effect of anti-estrogen in hormone-sensitive tumor cells by dephosphorylating IRS1, Insulin growth factor-1 receptor substrate, thus blocking PI3K/Akt pathway. In addition, PTPL1 regulates the growth, the invasion, and the adhesion of low aggressive breast tumor cells MCF-7.Our team established an isogenic cellular model capable of expressing PTPL1 or its mutants (phosphatase-dead and substrate-trapping mutants) in an inducible fashion in invasive cells. We showed that functional PTPL1 expression has a negative impact on cell aggressive phenotypes. Interestingly, the phosphatase-dead mutant exhibits the same behavior as the transfection control. This evidences that PTPL1 activity is crucial for the inhibition of aggressiveness. We are currently testing the clones tumorigenicity in athyemic mice.Furthermore, we conducted a comparative proteomic (SILAC) in order to study the global tyrosine phosphatome in MCF-7 and MDA-MB-231 cells with or without PTPL1. Our findings suggest that PTPL1 regulates the phosphorylation of proteins involved in different signaling pathways already described in the literature to be impacted by PTPL1. Remarkably, the quarter of proteins identified belong to cell junction structure or regulation. We then studied the impact of this phosphatase on cell junctions and showed that PTPL1 overexpression enhances cell aggregate formation in 3D culture, increases cell contact stability, relocates desmoglein to the cell junctions, and induces E-cadherin re-expression at the level of cell-cell contacts in MDA-MB-231 cells.Cell junctions and polarity are very important in oncology and particularly in the invasive process which is the first step in the metastatic dissemination. Our ongoing work focuses on identifying direct substrates for PTPL1 in order to elucidate the underlying PTPL1 signal leading to cell junctions and consequently propose a novel therapeutic targets
Hatzikirou, Haralambos. "Lattice-gas cellular automata for the analysis of cancer invasion." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2009. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-21387.
Повний текст джерелаKrebszellen zeigen charakteristische Merkmale, die sie in einem schrittweisen Vorgang während der Karzinogenese erworben haben. Einige dieser Merkmale sind autonomes Wachstum, die Induktion von Angiogenese, Invasion und Metastasis. Der Schwerpunkt dieser Arbeit liegt auf der Tumorinvasion, einer der letzten Phasen der Tumorprogression. Die Tumorinvasion ensteht aus der kombinierten Wirkung von den Wechselwirkungen Tumorzelle-Zelle und Zelle-Mikroumgebung, die mit die Hilfe von mathematischer Analyse untersucht werden können. Zelluläre Automaten (CA) können als einfache Modelle von selbst-organisierenden komplexen Systemen betrachtet werden, in denen kollektives Verhalten aus einer Kombination von vielen interagierenden "einfachen" Komponenten entstehen kann. Insbesondere konzentrieren wir uns auf eine wichtige CA-Klasse, die sogenannten Zelluläre Gitter-Gas Automaten (LGCA). Im Gegensatz zu traditionellen CA bieten LGCA eine einfache und intuitive Umsetzung der Teilchen und Wechselwirkungen. Zusätzlich erleichtert die Struktur der LGCA die mathematische Analyse ihres Verhaltens. Die wichtigsten Werkzeuge der mathematischen Analyse der LGCA sind hier die Mean-field Approximation und die entsprechende Lattice - Boltzmann - Gleichung. Das wichtigste Ziel dieser Arbeit ist es, wichtige Aspekte der Tumorinvasion unter dem Mikroskop der mathematischen Modellierung und Analyse zu erforschen: Auswirkungen der Tumorumgebung: Wir stellen einen LGCA als mikroskopisches Modell der Tumorzellen-Migration in Verbindung mit einer mathematischen Beschreibung der verschiedenen Tumorumgebungen vor. Wir untersuchen die Auswirkungen der verschiedenen Tumorumgebungen (z. B. extrazellulären Matrix) auf die Migration von Tumorzellen dürch Schätzung der Tumorzellen-Dispersionsgeschwindigkeit in einem gegebenen Umfeld. Wirkung von Tumor-Zellenproliferation und Migration: Wir untersuchen die Wirkung von Tumorzellenproliferation und Migration auf das invasive Verhalten der Tumorzellen durch die Entwicklung eines vereinfachten LGCA Tumorwachstumsmodells. Wir leiten die entsprechende makroskopische Dynamik und berechnen die Tumorinvasionsgeschwindigkeit im Hinblick auf die Tumorzellenproliferation- und Migrationswerte. Darüber hinaus berechnen wir die Breite der invasiven Zone, wo die Mehrheit der mitotischer Aktivität konzentriert ist, und es wird festgestellt, dass diese proportional zu den Invasionsgeschwindigkeit ist. Mechanismen der Tumorinvasion Entstehung: Wir untersuchen Mechanismen, die für die Entstehung von Tumorinvasion im Verlauf des Krebs zuständig sind. Wir kommen zu dem Schluss, dass die Reaktion eines mikroskopischen intrazellulären Mechanismus (Migration/Proliferation Dichotomie) zu Sauerstoffmangel, d.h. Hypoxie, möglicheweise für den Übergang von einem gutartigen (proliferative) zu einer bösartigen (invasive) Tumor verantwortlich ist. Berechnung der in-vivo Tumorinvasion: Schließlich schlagen wir einen evolutionären Algorithmus vor, der die Parameter eines LGCA Modells von Tumorwachstum auf der Grundlage von medizinischen Daten des Patienten für mehrere Zeitpunkte (insbesondere die Magnet-Resonanz-und Diffusion Tensor Imaging Daten) ermöglicht. Diese Parameter erlauben Szenarien für einen klinisch relevanten Tumorwachstum für einen bestimmten Patienten zu reproduzieren, die eine Vorhersage des Tumorwachstums zu einem späteren Zeitpunkt möglich machen
Adoki, Samson. "Involvement of scribble protein in breast cancer invasion and metastasis." Thesis, University of Essex, 2016. http://repository.essex.ac.uk/17655/.
Повний текст джерелаZeelenberg, Ingrid Saskia. "Chemokine receptor signals: role in migration, invasion and cancer metastasis." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2004. http://dare.uva.nl/document/72874.
Повний текст джерелаTang, Haoran. "Scar/WAVE complex suppresses cell invasion and cancer cell transformation." Thesis, University of Glasgow, 2012. http://theses.gla.ac.uk/3633/.
Повний текст джерелаThomas, Dustin G. "ROLE OF NON-MUSCLE MYOSIN IIB IN BREAST CANCER INVASION." Case Western Reserve University School of Graduate Studies / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=case1449156792.
Повний текст джерелаBair, Elisabeth Laurine. "Cell-cell and cell-matrix interactions involved in cancer invasion." Diss., The University of Arizona, 2004. http://hdl.handle.net/10150/280673.
Повний текст джерелаChinigò, Giorgia. "TRP channels functional role in prostate cancer angiogenesis and invasion." Electronic Thesis or Diss., Université de Lille (2022-....), 2022. http://www.theses.fr/2022ULILS103.
Повний текст джерелаProstate cancer (PCa) is the second most lethal tumor among men and its mortality is mainly due to metastasis. Thus, it is critical to understand the mechanisms by which tumors grow and how metastases can diffuse throughout the body. Cell migration of both epithelial and endothelial cells (EC) is required for cancer cell invasion of neighboring tissues as well as for the formation of tumor vasculature. Several Transient Receptor Potential (TRP) channels are deregulated in cancer cells and have been suggested as valuable markers in predicting cancer progression as well as potential targets for pharmaceutical therapy. In the present Ph.D. thesis, I established the role of TRP channels regulating Ca2+ signature in PCa cells and vasculature focusing, in particular, on the channels that affect migration, a common key step in tumor vascularization and invasion.The role of TRP channels in prostatic angiogenesis was studied in prostate tumor-derived EC (PTEC): we fully profiled the expression of all TRPs in normal ECs and TECs derived from PCa, breast, and renal tumors. We identified three ‘prostate-associated’ genes whose expression appears selectively upregulated in PTECs: TRPV2, TRPC3, and TRPA1. Among them, TRPA1 seems to play a critical role in regulating PCa angiogenesis, promoting PTEC migration, vascular network formation, and angiogenic sprouting both in vitro and in vivo.As regards, instead, epithelial PCa cells' motility, emerging evidence indicates that TRPM8 may exert a protective role in metastatic PCa by impairing the motility of these cancer cells. Investigating the molecular mechanism underlying this biological effect, we found that, as previously described for ECs, TRPM8 inhibits PCa cell migration and adhesion independently from its channel function by intracellularly trapping the small GTPase Rap1A in its inactive form and thus avoiding its translocation and activation on the plasma membrane. Moreover, we identified and validated the residues involved in the interaction between TRPM8 and Rap1A: residues E207 and Y240 in the sequence of TRPM8 and Y32 in that of Rap1A.Our data shed new light on the roles played by TRPA1 and TRPM8 in prostate cancer angiogenesis and invasion by affecting cell migration of endothelial and epithelial cells, respectively.In the fight against metastasis, the development of efficient nanodelivery systems can be as crucial as the identification of new molecular targets in cancer therapy to fill the gap between “drug discovery” and “drug delivery” which is one of the most challenges in clinical perspectives. In this context, the second part of this Ph.D. project focused on the study of lipid nanoparticles as suitable drug delivery systems. In particular, the use of solid lipid nanoparticles (SLN) and quatsomes (QS) for the incorporation of polymethine dyes (PMD) suitable for both diagnostic and therapeutic purposes was investigated. We demonstrated that lipid nanocarriers not only increase the solubility of PMD in physiological conditions but even enhance their spectroscopic performances, making PMD-loaded nanocarriers potential and appealing candidates for in vivo imaging and/or PDT applications.Overall, the present Ph.D. thesis deepens our knowledge of the role of TRP channels in PCa progression, providing new insight into their possible use as new therapeutic targets in PCa treatment and, at the same time, proposes new therapeutic tools to improve drug delivery in cancer therapy
Scott, Rebecca Wilson. "LIM kinase regulation of cell motility and invasion." Thesis, University of Glasgow, 2010. http://theses.gla.ac.uk/2247/.
Повний текст джерелаMacArthur, Benjamin Daniel. "Mathematical modelling of malignant growth and invasion." Thesis, University of Southampton, 2002. https://eprints.soton.ac.uk/50611/.
Повний текст джерелаZangari, Joséphine. "Contribution du transfert du miR-223-3p des neutrophiles aux cellules tumorales dans la progression du cancer du poumon." Thesis, Nice, 2016. http://www.theses.fr/2016NICE4040.
Повний текст джерелаLung cancer is the leading cause of cancer mortality in France and worldwide. Today in France, the overall five-year survival rate after diagnosis is only 14%, making it one of the most challenging cancers to treat. Personalized medicine is now the preferred approach for lung cancer for metastatic stage, including so-called immunotherapy. Within a tumor, cancer cells are surrounded by an inflammatory microenvironment rich in polymorphonuclear neutrophils (PMN). While it is established that the presence of PMN is associated with the development of carcinomas, the contribution of intratumoral PMN and their interaction with cancer cells in tumor progression is unclear. To explore these hypotheses, objectives of our study were: 1) to decrypt the communication between neutrophils and tumor cells (miRNAs and microvesicles) and 2) the regulation of these actors in the recipient cells, 3) to demonstrate their role in tumor progression and dissemination. Tumor plasticity and invasion are part of the most important features of cancer progression. This work has allowed us to identify a new mechanism of transient acquisition of phenotype by transfer of extracellular miRNA (ex-miRNA) into cancer cells with and, importantly, by letting the ex-miRNA decay. We observed that the ex-miR-223-3p is transferred from PMN to lung tumor cells via exosomes. This transfer is functional, as demonstrated by the occurrence of epithelial to mesenchymal transition (EMT) associated with an invasive phenotype and inhibition of one of its targets, FOXO1 transcription factor
Perumpanani, Abbey John. "Malignant and morphogenetic waves." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318866.
Повний текст джерелаMacDonald, Patricia. "Defining functional domains within GPNMB important for breast cancer cell invasion." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=96829.
Повний текст джерелаGlycoprotein non-metastatic melanoma protein B (GPNMB), aussi connu sous le nom de Ostéoactivine (OA), est une protéine transmembranaire fréquemment exprimée dans les tumeurs mammaires appartement au sous-type triple négatif. Notre groupe a mis en évidence que l'expression de GPNMB/OA est suffisante pour accroître, in vitro, les capacités migratoires et invasives associées aux cellules murines de cancer du sein faiblement métastatiques. In vivo, l'expression de GPNMB/OA est caractérisée par une augmentation de la formation des métastases osseuses et pulmonaires. Dans cette étude, nous avons cherché à caractériser le rôle pro-invasif associé à l'expression de GPNMB/OA dans les cellules humaines de cancer du sein en identifiant les domaines ou motifs de GPNMB/OA impliqués dans le phénotype invasif des cellules de cancer du sein. D'une part, nous avons entrepris l'identification de protéines interagissant avec GPNMB/OA et qui pourraient participer aux phénotypes associés à l'expression de GPNMB/OA. Pour ce faire, nous avons généré une série de mutants pour la protéine GPNMB et nous les avons exprimées dans les lignées cellulaires BT-549 et MDA-MB-453, qui n'exprime normalement pas GPNMB/OA, que nous avons par la suite soumis à des essais d'invasion in vitro. D'autre part, une étude de la littérature scientifique, associée à une analyse par spectrométrie de masse, ont été utilisées pour identifier les protéines partenaires potentielles de GPNMB/OA. Finalement, nous avons généré une lignée de souris transgénique qui exprime la forme humaine de GPNMB/OA sous le contrôle du promoteur Mouse Mammary Tumor Virus (MMTV). Ce modèle murin a été utilisé pour étudier le rôle de GPNMB/OA sur le développement de la glande mammaire et sur la tumorigenèse in vivo. Ainsi, ces travaux ont démontré que la forme humaine de GPNMB/OA est suffisante pour induire une augmentation des propriétés invasives des cellules BT549 et que ce phénotype requiert à la fois la région cytoplasmique et le motif RGD de la protéine GPNMB/OA. La caractérisation, des souris transgéniques MMTV-GPNMB/OA a révélé, pour sa part, que GPNMB/OA n'interfère pas avec le développement normal des glandes mammaires chez les femelles vierges et aucune tumeur n'a été détectée à ce jour. L'ensemble de nos données démontre que GPNMB/OA est capable d'induire les propriétés invasives associées aux cellules de cancer du sein, et que ce phénotype requiert l'interaction du motif RGD de la protéine GPNMB avec les intégrines et/ou des résidus ou motifs présents dans la partie cytoplasmique de GPNMB/OA et qui pourraient induire le recrutement de molécule de signalisation dans cette région de GPNMB/OA.
Qazi, Romena. "The role of the urokinase family in invasion by breast cancer." Thesis, University of Glasgow, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266538.
Повний текст джерелаOrd, Jonathan J. "Microarray analysis of pathways involved in bladder cancer invasion and metastasis." Thesis, Queen Mary, University of London, 2008. http://qmro.qmul.ac.uk/xmlui/handle/123456789/1571.
Повний текст джерелаHarper, Kelly. "Autotaxin promotes cancer cell invasion via the lysophosphatidic acid receptor 4." Mémoire, Université de Sherbrooke, 2010. http://savoirs.usherbrooke.ca/handle/11143/4035.
Повний текст джерелаSells, Earlphia. "Role of Tissue Kallikrein-Related Peptidase 6 in Colon Cancer Invasion." Diss., The University of Arizona, 2015. http://hdl.handle.net/10150/605219.
Повний текст джерелаZheng, Yun, Jinjun Guo, Jin Zhou, Jinjian Lu, Qi Chen, Cui Zhang, Chen Qing, H. Philip Koeffler, and Yunguang Tong. "FoxM1 transactivates PTTG1 and promotes colorectal cancer cell migration and invasion." BioMed Central Ltd, 2015. http://hdl.handle.net/10150/610293.
Повний текст джерелаAdams, Matthew. "The expression and distribution of Tenascin C in breast cancer invasion." Thesis, University of Leicester, 2002. http://hdl.handle.net/2381/29410.
Повний текст джерелаTruong, Danh, Julieann Puleo, Alison Llave, Ghassan Mouneimne, Roger D. Kamm, and Mehdi Nikkhah. "Breast Cancer Cell Invasion into a Three Dimensional Tumor-Stroma Microenvironment." NATURE PUBLISHING GROUP, 2016. http://hdl.handle.net/10150/621806.
Повний текст джерелаShimizu, Yosuke. "SPA-1 controls the invasion and metastasis of human prostate cancer." Kyoto University, 2011. http://hdl.handle.net/2433/147332.
Повний текст джерелаFite, Kristen. "Dysregulation of Phospholipase D (PLD) isoforms increases breast cancer cell invasion." Wright State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=wright149557402792618.
Повний текст джерелаChow, Wing-han Vivian. "Genes associated with invasion and metastasis of head and neck cancer /." Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B22142526.
Повний текст джерелаHoque, Apu E. (Ehsanul). "Migration and invasion pattern analysis of oral cancer cells in vitro." Doctoral thesis, Oulun yliopisto, 2018. http://urn.fi/urn:isbn:9789526220239.
Повний текст джерелаTiivistelmä Desmogleiini 3 (Dsg3) on desmosomien adheesioreseptori, jonka merkityksestä syövässä tiedetään vähän. Koska Dsg3 on tärkeä epiteelisolujen välisissä liitoksissa, oletimme sillä olevan vaikutusta myös suun karsinoomasolujen tarttumisessa ja niiden liikkuvuudessa. Testasimme hypoteesiamme muuttamalla Dsg3:n toimintaa ihmisen posken karsinoomasolulinjassa SqCC/Y1, josta oli aiemmin valmistettu neljä erilaista muunnosta: tyhjän vektorin sisältävä kontrollisolulinja (Ct), kokopitkää Dsg3 tuottava solulinja (FL), sekä kaksi Dsg3 C-päästä lyhennettyä mutanttisolulinjaa (Δ238 ja Δ560). Immunofluoresenssi-menetelmää käyttäen analysoimme solulinjoissamme solujen välisiä liitoksia. Lisäksi mittasimme solujen liikkeitä 2D-migraatio- ja 3D-sandwich-kokeissa. Testasimme myös Dsg3:n solunulkoista osaa tunnistavan monoklonaalisen vasta-aineen (AK23) vaikutusta solujen invaasioon. Osoitimme, että Dsg3:n rakenteen muuttaminen ja toiminnan estyminen häiritsi solujen tarttumista. 2D-kokeissa sekä FL että mutanttilinjat (Δ238 ja Δ560) migroivat kontrollisoluja nopeammin ja pidemmälle, mutta 3D-kokeissa vain mutanttilinjat invasoituivat kontrollisoluja tehokkaammin. AK23-vasta-aine esti vain FL-solujen invaasiota. Syöpäsolujen 3D-invaasiota mittaavissa kokeissa käytetään yleensä hiiren kasvaimesta valmistettua kaupallista Matrigeeliä® tai rotan kudoksista eristettyä tyypin I kollageenia. Tutkimusryhmämme on jo aiemmin kehittänyt organotyyppisen myoomamallin, jossa valmistamme myoomakudosnapit ihmisen kohdun leiomyoomakasvaimista. Tässä työssä valmistimme leiomyoomasta Myogeelia, vertasimme sitä Matrigeeliin®, sekä tutkimme tarkemmin Myogeeli-valmisteen soveltuvuutta 3D-tutkimuksiin. Totesimme, että kielen (HSC-3) ja posken (SqCC/Y1) karsinoomasolut invasoituivat tehokkaimmin Myogeeli-pitoisissa matrikseissa kuin Matrigeeliä® tai kollageeniä sisältävissä kasvatusalustoissa. Tutkimustulostemme perusteella Myogeeli-pohjaiset 3D-mallit soveltuvat hyvin sekä syöpäsolulinjojen invaasiotutkimuksiin että yhteisviljelmiin, joissa syöpäsoluja viljellään yhdessä syöpäkasvaimen ympärillä olevien solujen, kuten fibroblastien, kanssa
Lam, Hoyin. "3D co-culture spheroid drug screening platform for pancreatic cancer invasion." Thesis, King's College London (University of London), 2018. https://kclpure.kcl.ac.uk/portal/en/theses/3d-coculture-spheroid-drug-screening-platform-for-pancreatic-cancer-invasion(5fb01f64-2526-46c7-b171-933a4ec066d2).html.
Повний текст джерелаGillespie, H. C. "The role of the adhesion molecule CD44 in tumour invasion." Thesis, Queen's University Belfast, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390886.
Повний текст джерелаGibson, D. S. "The role of the cysteine proteinase cathepsins in astrocytoma invasion." Thesis, Queen's University Belfast, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368776.
Повний текст джерелаZhou, Chun, and 周純. "Effect of FTY720 on the growth and invasion ability of androgenindependent prostate cancer cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B31685742.
Повний текст джерела