Rozprawy doktorskie na temat „Cancer cells – Motility”
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Choi, Mi-Yon. "P53 mediated cell motility in H1299 lung cancer cells". VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/109.
Pełny tekst źródłaGarg, Ayush A. "Electromagnetic Fields Alter the Motility of Metastatic Breast Cancer Cells". The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1563816767104018.
Pełny tekst źródłaAdla, Shalini. "Characterization of the neural cell recognition molecule L1 in breast cancer cells and its role in breast cancer cell motility". Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 125 p, 2008. http://proquest.umi.com/pqdweb?did=1459905751&sid=5&Fmt=2&clientId=8331&RQT=309&VName=PQD.
Pełny tekst źródłaSeller, Zerrin. "Role of #alpha#4#beta#1-mediated signalling in malignant melanoma adhesion and motility". Thesis, King's College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266520.
Pełny tekst źródłaTian, Jing. "Inhibition of melanoma cell motility by the snake venom disintegrin eristostatin". Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 61 p, 2007. http://proquest.umi.com/pqdweb?did=1397900451&sid=10&Fmt=2&clientId=8331&RQT=309&VName=PQD.
Pełny tekst źródłaAhmad, Omaima Farid. "The Role of Filamin A in Cell Motility, Adhesion and Invasion in Ovarian Cancer Cells". University of Toledo Honors Theses / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=uthonors1503407822068426.
Pełny tekst źródłaWright, Adele Hart. "The role of integrins in the differential upregulation of tumor cell motility by endothelial extracellular matrix proteins". Diss., Georgia Institute of Technology, 1999. http://hdl.handle.net/1853/17352.
Pełny tekst źródłaHoppe, Andreas. "Adaptive spline method for the assessment of cell motility and its application to lesions". Thesis, University of South Wales, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341937.
Pełny tekst źródłaDi, Kaijun, i 狄凱軍. "The role of Id-1 on the proliferation, motility and mitotic regulationof prostate epithelial cells". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B38944704.
Pełny tekst źródłaPatel, Sabina. "The Development of Tetracycline Dependent Pancreatic Cancer Cells and the Evaluation of CapG and Gelsolin Expression on Pancreatic Cancer Cell Motility In Vitro". Thesis, University of Liverpool, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.491370.
Pełny tekst źródłaPaiwand, Frouz Frozan. "RHAMM, CD44 expression and erk activation are linked in malignant human breast cancer cells and are associated with cell motility". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ46047.pdf.
Pełny tekst źródłaPeng, Zhengang, Jennifer Weber, Zhaosheng Han, Rulong Shen, Wenchao Zhou, James Scott, Michael Chan i Huey-Jen Lin. "Dichotomy effects of Akt signaling in breast cancer". BioMed Central, 2012. http://hdl.handle.net/10150/610205.
Pełny tekst źródłaBailey, Kelly M. "Focal adhesion kinase mediates caveolin-1 expression during epithelial to mesenchymal transition a novel pathway regulating aspects of cell motility in cancer /". Morgantown, W. Va. : [West Virginia University Libraries], 2008. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=5804.
Pełny tekst źródłaTitle from document title page. Document formatted into pages; contains x, 229 p. : ill. (some col.). Includes abstract. Includes bibliographical references.
Webster, Rebecca. "Complementary investigations of the molecular biology of cancer : assessment of the role of Grb7 in the proliferation and migration of breast cancer cells; and prediction and validation of microRNA targets involved in cancer". University of Western Australia. School of Medicine and Pharmacology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0179.
Pełny tekst źródłaZhao, Rathje Li-Sophie. "Tropomyosin in Normal and Malignant Cells and the Action of Picropodophyllin on the Microfilament and Microtubule Systems". Doctoral thesis, Stockholms universitet, Wenner-Grens institut, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-27767.
Pełny tekst źródłaAdanja, Ivan. "Automated tracking of unmarked cells migrating in three-dimensional matrices". Doctoral thesis, Universite Libre de Bruxelles, 2012. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209703.
Pełny tekst źródłaThe focus in this thesis lies in two specific aspects that are important in anti-migratory drug screening: tracking cells inside an in vitro 3D environment and doing so using unmarked cells.
Doctorat en Sciences de l'ingénieur
info:eu-repo/semantics/nonPublished
Wyse, Meghan M. "CXCL12 Mediated Regulation of the Cytoskeletal Regulator mDia2 Formin Induces Amoeboid Conversions and Cellular Plasticity in Migrating Human Breast Carcinoma Cells". University of Toledo / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1404042854.
Pełny tekst źródłaAlamer, Maha Mohammed. "Cellular and molecular mechanisms of action of UV sunscreens in the regulation of growth and motility of human breast cancer cells". Thesis, University of Reading, 2016. http://centaur.reading.ac.uk/72239/.
Pełny tekst źródłaSubisak, Angel Dharshini. "Role of Substrate Stiffness on Migratory Properties and Epithelial to Mesenchymal Transition in Human Lung Cancer Cells". The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1356943256.
Pełny tekst źródłaGirault, Alban. "Inhibition du canal SK3 et du développement de métastases par un ether-lipide synthétique". Thesis, Tours, 2011. http://www.theses.fr/2011TOUR3305/document.
Pełny tekst źródłaIt has been shown that SK3 channel was a mediator of breast cancer cells migration, a fundamental property for metastasis formation. In addition, edelfosine inhibits SK3 channel. This ether-lipid owns a high anti cancerous potential in vitro but its clinical use was hampered by some side effects, Firstly, we showed the structural parts of edelfosine required for SK3 channel inhibition and cell motility inhibition. Moreover, we selected Ohmline (1-O-Hexadécyl-2-O-Méthyl-sn-glycéro-lactose), an edlefosine’s analogue that preserves SK3 channel and motility inhibitory properties. Secondly, we evaluated this lipid on tumor development in nude mice model. We showed that this lipid reduces metastasis formation without effect on primary tumor. To conclude, we described Ohmline, the first lipid inhibitor of SK3. This compound should become the first member of a new family of metastasis lipid inhibitors
Sequin, Emily Katherine. "Effects of Induced Electric Fields on Tissues and Cells". The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1403869854.
Pełny tekst źródłaTozluoglu, M. "Multiscale modelling of cancer cell motility". Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1383588/.
Pełny tekst źródłaActon, S. E. "Mechanisms of cancer cell motility in vivo". Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1387309/.
Pełny tekst źródłaPinner, Sophie Elizabeth. "Mechanisms of cancer cell motility in vivo". Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1444471/.
Pełny tekst źródłaBochenek, Magdalena Ludmila. "Regulation of cell motility by ephrin-B2 signalling". Thesis, University of Bristol, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492474.
Pełny tekst źródłaRucka, Marta. "Metabolic regulation of tumour cell motility". Thesis, University of Southampton, 2013. https://eprints.soton.ac.uk/380962/.
Pełny tekst źródłaVolakis, Leonithas I. "Effect of Myoferlin Depletion on Breast Cancer Cell Motility". The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1316453651.
Pełny tekst źródłaScott, Rebecca Wilson. "LIM kinase regulation of cell motility and invasion". Thesis, University of Glasgow, 2010. http://theses.gla.ac.uk/2247/.
Pełny tekst źródłaAloliqi, Abdulaziz A. "The Role of Connexin 43 in Prostate Cancer Cell Motility". Kent State University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=kent1556029596055296.
Pełny tekst źródłaIdoux-Gillet, Ysia. "Implication des voies de différenciation épithéliale précoce dans la morphogenèse mammaire et la progression des cancers du sein". Thesis, Montpellier 1, 2013. http://www.theses.fr/2013MON1T008.
Pełny tekst źródłaMammary gland morphogenesis results from the coordination of different pathways, including apoptosis, proliferation, differentiation, and stem/progenitor cell dynamics. Epithelial-mesenchymal transition (EMT) appears to be involved in these signalling pathways. Thus, we focused on transcription factor Slug, a key gene regulating EMT, and its involvement in mammary gland morphogenesis. First, using a Slug–LacZ transgenic mice model, we located Slug in a subpopulation covering about 10–20% basal duct cells and cap cells of terminal end bud, coexpressed with basal markers P-cadherin, CK5 and CD49f. Then, we have shown by in vitro experiments of loss and gain of function that Slug regulated the differentiation and proliferation of mammary epithelial cells. Moreover, we found that Slug inhibited apoptosis, promoted cell motility, and allowed the emergence and growth of clonal mammospheres. This last point shows the involvement of Slug in stem cells, which is reinforced by the fact that primary cells deficient for Slug were unable to give secondary mammospheres. Furthermore, we observed in vivo that mice deficient for Slug showed delayed development of the mammary gland, with less proliferating cells, and overexpression of markers of luminal cells CK8/18, GATA3 and ER. Other genes regulating EMT are found overexpressed, suggesting a compensatory mechanism, which can explain the fact that the delayed development of the mammary gland is caught up in adulthood. The Slug-knockout mammary glands also showed overbranching, evoking an early differentiation, similar to the mammary glands of mice deficient in P-cadherin, expressed in the basal cells. Knowing this, we found that P-cadherin was decreased in Slug-knockout mammary glands, and in CommaDβ cells treated with siRNA targeting Slug. We then found that Slug binds directly to the promoter of the P-cadherin and activated it, and that P-cadherin was involved in some functional effects of Slug, such as mammospheres growth, differentiation and cell migration. Thus, we have shown the importance of a new signalling pathway Slug/P-cadherin in the capacity of mammary epithelial stem/progenitor cells, integrating differentiation and cell motility, and we now have a better understanding of its role in the aggressiveness of some breast cancers
Biondini, Marco. "RALlying through cell motility and invasion". Thesis, Paris 11, 2014. http://www.theses.fr/2014PA11T042.
Pełny tekst źródłaMetastasis is a multistep process by which cancer cells migrate away from the primary neoplastic mass to give rise to secondary tumors at distant sites. Thus, the acquisition of motility and invasive traits by tumor cells is a crucial step for metastasis to occur. Depending on the cell type and the environment, cells can move collectively keeping stable cell-cell contacts or as individual cells, which translocate by exploiting either mesenchymal or amoeboid motility programs.Different molecules and pathways have been linked to the regulation of cell motility. Rho small GTPases (Rac1, Cdc42 and RhoA) control cell migration through their actions on actin assembly, actomyosin contractility and microtubules. Rac1 drives mesenchymal-type motility by promoting lamellipodia formation via the Wave Regulator Complex (WRC). On the contrary, amoeboid motility is governed by RhoA which promotes cell movement via the generation of actomyosin contractile force. Another family of small GTPases, the Ral proteins, was recently involved in the regulation of cell migration. RalB, through the mobilization of its main effector the Exocyst complex, was shown to play an essential role in cell motility. In this work of thesis we investigated the molecular mechanisms through which RalB/Exocyst pathway controls cell motility and invasion.In the first part of this manuscript we show that Exocyst interacts with the RacGAP SH3BP1 (project 1). In mesenchymal moving cells Exocyst/SH3BP1 interaction is required to organize membrane protrusion formation by spatially regulating the activity of Rac1 at the cellular front. In addition, in project 2, we show that the Exocyst binds to the wave regulator complex (WRC), a key promoter of actin polymerization. We provide evidences for Exocyst to be involved in driving the WRC to the leading edge of motile cells, where it can stimulate actin polymerization and membrane protrusions. Reactivation of a developmental program termed epithelial-mesenchymal transition (EMT) was recently shown to promote motility, invasion and metastasis of neoplastic cells. Tumor cells undergoing EMT loose cell-cell contacts acquire a fibroblastoid phenotype and invade the surrounding tissues as individual cells. In project 3 we characterized the invasion plasticity of cancer cells after EMT and we investigated the molecular contribution of Ral to post-EMT invasion. We showed that upon EMT cells disseminate individually in a Rho-driven fashion exploiting the generation of actomyosin force to deform the extracellular matrix. We document that RalB silencing severely impairs actomyosin contractility and dissemination of post-EMT cells. We hypothesize that RalB regulates invasion by controlling the dynamics of the Rho pathway via the Exocyst-associated RhoGEF GEF-H1 in post-EMT cells. Finally, in the last part of this thesis manuscript, we present the PIV-based “AVeMap” software which has been developed to quantify in a fully automated way cell migration and its parameters (Project 4).Taken together the results presented in this thesis manuscript point out the Ral/Exocyst pathway as a key molecular organizer of the execution of both Rac1- and Rho-driven motility programs
Sengupta, Sameer. "The influence of BRCA1's ubiquitin ligase activity on cell motility". Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:b14af4ae-1f95-4d0c-85a8-faaf4fa950c4.
Pełny tekst źródłaZago, Giulia. "Lighting up Invasion with Optogenetics : RalB Mobilizes the WRC Complex Downstream Ras". Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS333.
Pełny tekst źródłaMetastasis is a multistep process by which cancer cells migrate awayfrom the primary neoplastic mass to give rise to secondary tumors at distantsites. Thus, the acquisition of motility and invasive traits by tumor cells is acrucial step for metastasis to occur. Mutational activation of Ras proteinspromotes oncogenesis by disturbing a multitude of molecules andpathways that participate to the regulation of several processes includingalso cell invasion and motility. Among them a central role is played by Rhosmall GTPases (Rac1, Cdc42 and RhoA) which control cell migrationthrough their actions on actin assembly, actomyosin contractility andmicrotubules. Rac1 drives mesenchymal-type motility by promotinglamellipodia formation via the Wave Regulator Complex (WRC), a keypromoter of actin polymerization. Another family of small GTPases that actdownstream Ras, the Ral proteins, has been recently involved in theregulation of cell migration. RalB, through the mobilization of its maineffector the Exocyst complex, was shown to play an essential role in cellmotility. In this work of thesis, we investigated the molecular mechanismsthrough which RalB/Exocyst pathway controls cell motility and invasiondownstream oncogenic Ras.In the first part of this manuscript we describe the identification andcharacterization of the WRC complex as a novel interactor of the Exocyst.Furthermore, we provide evidences for Exocyst to be involved in drivingthe WRC to the leading edge of motile cells. This hypothesis, was finallydemonstrated in the second part of the manuscript. We were able to definethe mechanisms underlying the function of RalB in invasion by exploitingan optogenetic approach. We found that RalB, activated by Ras via the2Rgl1 and Rgl2 exchange factors, mobilizes the Exocyst complex whichrecruits the Wave Regulatory Complex (WRC) at cell edge, promotingprotrusions, migration and invasion. Even more, we show that the Rac1GTPase, usually considered the master of cell protrusions, is not involvedin this process. Finally, we analyzed Ral proteins expression in a cohort ofbreast cancer samples, pointing out for the first time an accumulation ofRalB in the invasive and metastasis compartments, suggesting a role ofRalB in invasiveness and metastatic spread of human breast cancers. Takentogether our work contribute to light up the role of the underestimated Ralpathway in the context of cancer invasion
Zhang, Yang. "A dynamical systems modelling framework for breast cancer cell motility and morphology analysis". Thesis, University of Sheffield, 2017. http://etheses.whiterose.ac.uk/16014/.
Pełny tekst źródłaMunro, Catriona. "Novel target identification & characterisation of key cell motility regulators in lung cancer metastasis". Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/24741.
Pełny tekst źródłaMcCarty, Samantha Keiko. "A NOVEL BRAF SIGNALING CASCADE THROUGH p-21 ACTIVATED KINASES REGULATES THYROID CANCER CELL MOTILITY". The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1366201525.
Pełny tekst źródłaButtermore, Stephanie T. "The Role of Elevated Hyaluronan-Mediated Motility Receptor (RHAMM/HMMR) in Ovarian Cancer". Scholar Commons, 2017. http://scholarcommons.usf.edu/etd/6808.
Pełny tekst źródłaShah, Nirav. "A novel link between Akt1 and Twist1 in ovarian tumor cell motility and invasiveness". Master's thesis, University of Central Florida, 2012. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/5490.
Pełny tekst źródłaM.S.
Masters
Molecular Biology and Micro
Medicine
Biotechnology
Flate, Elizabeth L. "THE EFFECT OF EXTRACELLULAR MATRIX COMPONENTS ON MOTILITY AND CHEMOSENSITIVITY OF SELECT OVARIAN CANCER CELL LINES". Kent State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=kent1353954902.
Pełny tekst źródłaHammer, Alan D. "Prolactin-Induced Tyrosyl Phosphorylation of PAK1 in Breast Cancer Cell Motility, Adhesion, and Epithelial-to-Mesenchymal Transition". University of Toledo / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1461066955.
Pełny tekst źródłaFoster, Clare Ruth. "A proteomic and genomic investigation into the role of lamin A in colorectal cancer cell motility". Thesis, Durham University, 2012. http://etheses.dur.ac.uk/3434/.
Pełny tekst źródłaBrunel, Benjamin. "Mesure des déplacements cellulaires dans les tissus non transparents : une application de la diffusion dynamique de la lumière". Thesis, Université Grenoble Alpes (ComUE), 2018. http://www.theses.fr/2018GREAY047/document.
Pełny tekst źródłaAs a tumor grows, it exerts a mechanical pressure on its surrounding tissue and is compressed back as a reaction. Recent experiments on an in vitro tumor model, called spheroid, have shown that this pressure is crucial for the fate of the cancerous tissue. In particular, the pressure slows down its growth, but makes it more invasive. To further understand the latter effect, we decided to study the migration of cells inside spheroids under pressure. However, imaging the inside of a spheroid is technically challenging as usual microscopy methods do not work on thick tissues (> 100 μm). Standard imaging methods are limited in terms of depth penetration because of light scattering. For this reason, we decided to take advantage of this scattered light with a method called Dynamic Light Scattering (DLS). We developed its application to cell migration in order to measure the distribution of cells displacements over time. The measurement is label-free and works with spheroids as thick as 400 μm in diameter. By this means, we revealed a radial organization inside the spheroid in terms of mobility, with fast cells at the surface and slower cells in the core. We also showed that applying a pressure onto spheroids decreases the average cell speed by a factor up to two for pressure greater than 15 kPa. Another team reported an increase in the speed of cells located at the surface of a compressed spheroid, which implies that the radial organization is also true for the impact of pressure. We demonstrated that this sensitivity to an external pressure is a 3D emergent property, in which the extracellular matrix plays an essential role. Finally, we explored the potential of our technique by addressing another question: how do apoptotic cells signals affect the migration of macrophages? We found that early apoptotic cells increase the speed of macrophages whereas late apoptotic cells decrease it. In both cases, the persistence length of the motion is the same
Brown, Louise E. "Role of human Desmoglein 3 in the regulation of cell morphology and motility via AP-1 and PKC dependent Ezrin activation". Thesis, Queen Mary, University of London, 2014. http://qmro.qmul.ac.uk/xmlui/handle/123456789/26964.
Pełny tekst źródłaStevens, Payton D. "THE FUNCTION OF ERBIN, A SCAFFOLD PROTEIN, AS A TUMOR SUPPRESSOR IN COLON CANCER". UKnowledge, 2018. https://uknowledge.uky.edu/biochem_etds/36.
Pełny tekst źródłaTakahashi, Ryo. "AFAP1L1, a novel associating partner with vinculin, modulates cellular morphology and motility, and promotes the progression of colorectal cancers". Kyoto University, 2014. http://hdl.handle.net/2433/189659.
Pełny tekst źródłaNoll, Bettina [Verfasser], i Monilola [Akademischer Betreuer] Olayioye. "Isoform specific functions of protein kinase D3 (PKD3) in breast cancer cell proliferation and motility / Bettina Noll. Betreuer: Monilola Olayioye". Stuttgart : Universitätsbibliothek der Universität Stuttgart, 2014. http://d-nb.info/105253158X/34.
Pełny tekst źródłaWoo, Ho-Hyung, Csaba Laszlo, Stephen Greco i Setsuko Chambers. "Regulation of colony stimulating factor-1 expression and ovarian cancer cell behavior in vitro by miR-128 and miR-152". BioMed Central, 2012. http://hdl.handle.net/10150/610206.
Pełny tekst źródłaDayal, Shubham. "Novel Roles of RNase L in Prostate Cancer". University of Toledo / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1492793747213566.
Pełny tekst źródłaDeLigio, James T., i James Thomas DeLigio. "ALTERNATIVE SPLICING OF CYTOPLASMIC POLYADENYLATION ELEMENT BINDING PROTEIN 2 IS MODULATED VIA SERINE ARGININE SPLICING FACTOR 3 IN CANCER METASTASIS". VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5660.
Pełny tekst źródłaGueguinou, Maxime. "Complexe canalaires KCa/Ca sensibles aux éther-lipides : régulation de la signalisation calcique dans la migration de cellules cancéreuses". Thesis, Tours, 2015. http://www.theses.fr/2015TOUR4032.
Pełny tekst źródłaIn most cases of cancer, metastasis and not the primary tumor per se is the main cause of mortality. To establish secondary growth in distant organs cancer cells must develop an enhanced propensity to migrate. The key objective of this thesis proposes that some actors of Ca2+ signaling (Orai, and TRPC, STIM) coupled to SK3 channel would form complexes that play a critical role in cell migration of various cancers (breast, colon and prostate). Furthermore we showed that the localization of these channels complexes in lipid-rafts is essential to their regulation and function. Thus, the delocalization of these complexes of lipid-raft outside by alkyl-phospholipids could be a new way to modulate the SK3/Ca2+ dependent cell migration and metastasis development