Dissertations / Theses on the topic 'Cancer cell metastasis'
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Park, Se Hyung. "Estrogen in ovarian cancer cell metastasis." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/1287.
Full textOosterhout, Anselmus Gerardus Maria van. "Small cell lung cancer and brain metastasis." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1995. http://arno.unimaas.nl/show.cgi?fid=6643.
Full textVillafañe, Johann Sebastian Bergholz. "Role of P63 in cell migration and cancer metastasis." Thesis, Boston University, 2012. https://hdl.handle.net/2144/12282.
Full textThe p53-related p63 protein is expressed as multiple isoforms involved in diverse biological functions, including cell proliferation, survival, apoptosis, differentiation, senescence, and aging. An inverse correlation between p63 expression and cancer progression in a variety of human cancers suggests that p63 functions as a metastasis suppressor. Here, we show that the predominant isoform of p63, ΔNp63α, plays a major role in inhibiting cell migration, invasion, and cancer metastasis by modulating Extracellular signal-regulated protein kinase 1 and 2 (Erk1/2) signaling. We profiled gene expression in human breast cancer Hs-578T cells stably expressing wild type ΔNp63α, or a mutant derivative defective in DNA binding or protein-protein interaction. We observed that wild type ΔNp63α, but not the mutant derivatives, up-regulated Mitogen-activated Protein (MAP) Kinase Phosphatase 3 (MKP3), a negative regulator of Erk1/2 signaling. Accordingly, exogenous ΔNp63α expression in breast cancer MDA-MB-231 cells up-regulated MKP3 expression, decreased nuclear levels of phosphorylated Erk1/2, and down-regulated Matrix Metalloprotease 1 and 9 (MMP1/9) expression. In addition, ΔNp63α inhibited cancer cell invasion, which was significantly rescued by disrupting MKP3 expression. Conversely, pan-p63 knockdown in mammary epithelial MCF-1OA and head and neck squamous cell carcinoma FaDu cells resulted in decreased MKP3 expression and concomitant higher levels of Erk1/2 phosphorylation, while Mek1/2 phosphorylation levels were not affected. Consistently, pan-p63 knockdown led to increased cell motility and invasion, which was reversed either by reintroduction of the ΔNp63α isoform alone, but not by other isoforms, or by expression of MKP3. Interestingly, p63 ablation-induced cell motility is dependent on Erk2, but not Erk1 expression. Moreover, we found that both p63 and MKP3 expression is usually decreased in invasive breast carcinoma, indicating a clinical correlation between p63 and MKP3 down-regulation and cancer progression. Finally, we found that reduced p63 expression in Her2/Neu-transformed MCF-1OA cells dramatically increased metastatic frequency to the lungs in a mouse model of breast cancer. Taken together, these results not only reveal a novel molecular pathway by which p63 plays an important pathological role in cancer metastasis, but also contribute to the design of therapeutic strategies in the treatment of cancer.
Chan, Pui-man Poemen. "Micrometastases of esophageal cancer /." View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36404652.
Full textShirure, Venktesh S. "Molecular Mechanisms of Circulating Tumor Cell Adhesion in Breast Cancer Metastasis." Ohio University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1357706517.
Full textXing, Fei. "ROLE OF NOTCH SIGNALING IN BREAST CANCER METASTASIS." OpenSIUC, 2012. https://opensiuc.lib.siu.edu/dissertations/514.
Full textLomax-Browne, Hannah Jane. "Interactions between cancer cell glycans and endothelial cells during adhesion events in metastasis." Thesis, Oxford Brookes University, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501906.
Full textMarshall, John Francis. "The role of integrins in melanoma progression and metastasis." Thesis, Open University, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295235.
Full textHarihar, Sitaram. "The Role of Phosphoinositide Signaling in Breast Cancer Metastasis Suppressor 1-Mediated Metastasis Suppression of Human Breast Carcinoma Cells." DigitalCommons@USU, 2011. https://digitalcommons.usu.edu/etd/870.
Full textZhang, Hanshuo. "Large-scale identification of functional genes regulating cancer cell migration and metastasis using the self-assembled cell microarray." Diss., Georgia Institute of Technology, 2013. http://hdl.handle.net/1853/49066.
Full textGronau, Julian Hendrik. "The role of Endo180 in prostate cancer cell migration and metastasis." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/27289.
Full textRud-Majani, Zahra Erami. "Investigation of E-cadherin dynamics in cancer cell adhesion and metastasis." Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/5619/.
Full textTang, Yuanyuan. "Nitric Oxide/Peroxynitrite Imbalance Induces Adhesion of Cancer Cells to Lymphatic Endothelium - Clinical Implications for Cancer Metastasis." Ohio University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1439563414.
Full textPardo, Pastor Carlos 1989. "Piezo ion channels in cancer cell mechanotransduction." Doctoral thesis, Universitat Pompeu Fabra, 2018. http://hdl.handle.net/10803/664209.
Full textLa dependència mecànica de la transformació i la metàstasi és un camp d’estudi / de recerca emergent, però el paper que hi juguen els canals iònics mecanosensibles s’ha omès fins ara. Aquesta tesi se centra en els rols dels canals Piezo1 i Piezo2 en la transducció d’estímuls mecànics per cèl·lules canceroses, com ara confinament, adhesió, rigidesa del substrat, concentració de lligands adhesius. En un primer capítol, mostrem que el confinament dispara l’entrada de calci per mitjà de Piezo1. Això activa la fosfodiesterasa 1, que redueix els nivells d’AMPc i, en conseqüència, l’activitat PKARac1, que deixen d’inhibir Miosina II. També trobem una activació paral·lela de Miosina II directament per confinament. Com a resultat final, les cèl·lules guanyen rigidesa i optimitzen el seu mode migratori independent d’adhesions, que és el preponderant in vivo durant la invasió metastàtica. Reduir els nivells de Piezo1 suprimeix l’entrada de calci induïda per confinament i desactiva el circuit subjacent en cèl·lules ovàriques epitelials (CHO) i de melanoma (A375). Això minva la capacitat migratòria de les cèl·lules siPiezo1. En un segon capítol, descobrim un rol essencial per a Piezo2 com a activador de RhoA en resposta a estímuls mecànics. Això modula les respostes mecanobiològiques de les cèl·lules MDA-MB-231-BrM2, de càncer de mama metastàtic a cervell. La reducció dels nivells de Piezo2 destorba la formació de fibres d’estrès, l’orientació de les adhesions, la transmissió de forces i l’acumulació nuclear del regulador transcripcional prometastàtic YAP. Suprimir el calci extracel·lular fenocòpia aquests resultats. Promoure la polimerització d’Actina amb jasplaquinolida o mer mitjà de la sobreexpressió de formes constitutivament actives de RhoA o mDia1 restableix les fibres d’estrès i l’acumulació nuclear de YAP. A més, la reducció de Piezo2 suspèn diverses funcions prometastàtiques: proliferació cel·lular, migració, formació d’invadopodis, degradació de la matriu extracel·lular i secreció de SERPINB2, una proteïna necessària per protegir les cèl·lules invasores dels mecanismes de defensa del parènquima cerebral. Els treballs presentats en aquesta tesi desvelen rols importants pels canals Piezo com a una primera línia de detectors d’estímuls mecànics en diferents tipus cel·lulars. Aquests descobriments són rellevants per a diversos àmbits, com ara la recerca en càncer, i remarquen la importància dels canals iònics com a transductors d’estímuls ambientals.
Douglas, Temple Anne. "Development of a Dielectrophoresis-Based Cancer-Cell Analysis Tool." Diss., Virginia Tech, 2018. http://hdl.handle.net/10919/85239.
Full textPh. D.
Dielectrophoresis is a method by which cells are polarized in response to an electric field gradient. This work optimizes this technique so that it can be used to separate highly similar subpopulations of cancer cells in a microfluidic device. Computer code is also developed to automate data processing. A technique for analyzing these cell subpopulations is also proposed and some feasibility testing performed.
Chan, Pui-man Poemen, and 陳培文. "Micrometastases of esophageal cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B45012842.
Full textGEHLSEN, KURT RONALD. "IN VITRO AND IN VIVO STUDY OF MELANOMA TUMOR CELL INVASION AND METASTASIS." Diss., The University of Arizona, 1986. http://hdl.handle.net/10150/188148.
Full textLakins, Matthew. "The role of stroma microenvironments in prostate cancer cell migration and metastasis." Thesis, University of York, 2012. http://etheses.whiterose.ac.uk/3106/.
Full textDye, Danielle E. "The role of MCAM in melanoma and metastasis." University of Western Australia. School of Biomedical, Biomolecular and Chemical Sciences, 2007. http://theses.library.uwa.edu.au/adt-WU2007.0207.
Full textMillarte, Valentina [Verfasser]. "Signaling at the Golgi Apparatus During Cell Migration and Implication for Cancer Cell Metastasis / Valentina Millarte." Konstanz : Bibliothek der Universität Konstanz, 2015. http://d-nb.info/1080908919/34.
Full textHarper, Kelly. "Autotaxin promotes cancer cell invasion via the lysophosphatidic acid receptor 4." Mémoire, Université de Sherbrooke, 2010. http://savoirs.usherbrooke.ca/handle/11143/4035.
Full textMaeda, Ryo. "Circulating CD14+CD204+ Cells Predict Postoperative Recurrence in Non-Small-Cell Lung Cancer Patients." Kyoto University, 2016. http://hdl.handle.net/2433/215213.
Full textHsu, Rich. "The role of toll-like receptor 4 (TLR4) in lipopolysaccaride (LPS) induced gastrointestinal cancer metastasis." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=92293.
Full textDes données récentes suggèrent que le développement de complications infectieuses à la suite d'une résection curative chez les patients atteints d'un cancer gastro-intestinal peut être associé à une récidive du cancer, cependant le mécanisme exact n'est pas bien compris. Toll-like receptor 4 (TLR4) est le seul récepteur connu pour le lipopolysaccharide (LPS), un antigène provenant des bactéries à Gram négatif impliquées dans de telles complications infectieuses. Précédemment, l'expression de TLR4 a été détectée pour plusieurs types de cancers incluant la prostate et le poumon. Dans le cadre de cette étude, nous avons caractérisé l'expression de TLR4 pour de multiples lignées cellulaires sophagiennes et colorectales, ainsi qu'évalué l'effet du LPS sur la prolifération tumorale, la production de cytokine tumorale, et l'adhésion tumorale. Malgré le fait que le LPS n'ait aucun effet sur la prolifération cellulaire tumorale, la stimulation par LPS augmente la production de IL-6 chez les cellules cancéreuses HKESC-2 provenant de l'sophage. Le signalement intracellulaire LPS-TLR4 par p38 MAP Kinase est nécessaire pour l'attachement à la fibronectin des cellules cancéreuses traitées avec LPS, une composante importante de la matrice extracellulaire hépatique. Les cellules provenant du colon traitées avec LPS ont démontrées une augmentation de leur adhésion aux sinusoïdes hépatiques. Cette étude a fournie quelques-uns des mécanismes responsables de la récurrence cancéreuse associée à l'inflammation chez les patients subissant une résection chirurgicale curative. Ces résultats suggèrent que la signalisation par LPS-TLR4 dans les cancers gastro-intestinaux augmente leur potentiel métastatique et que le blocage de TLR4 ait possiblement un effet thérapeutique dans la prévention des métastases cancéreuses.
Wright, 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.
Full textLiu, Tiffany. "The role of macrophage chemoattractant signaling in cancer cell migration, metastasis and neovascularization." Diss., [La Jolla] : University of California, San Diego, 2010. http://wwwlib.umi.com/cr/ucsd/fullcit?p1476514.
Full textHeidemann, Franziska Verfasser], and Udo [Akademischer Betreuer] [Schumacher. "Selectins Mediate Small Cell Lung Cancer Systemic Metastasis / Franziska Heidemann. Betreuer: Udo Schumacher." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2015. http://d-nb.info/1074642244/34.
Full textGraham, Alastair Noel John. "An investigation into the factors promoting metastasis in non-small cell lung cancer." Thesis, Queen's University Belfast, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326409.
Full textAlkishi, Ahmed. "Investigating the mechanisms of oral cancer cell binding to the endothelium during metastasis." Thesis, University of Sheffield, 2015. http://etheses.whiterose.ac.uk/9642/.
Full textBarnes, James Matthew. "Influence of matrix and fluid microenvironments on cancer cell migration, survival, and metastasis." Diss., University of Iowa, 2011. https://ir.uiowa.edu/etd/2818.
Full textAkunuru, Shailaja. "Regulation of cancer stem cell activity and epithelial mesenchymal transition by Rac1 in Human lung adenocarcinoma cells." University of Cincinnati / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1314301864.
Full textOh, Jaeho. "Cell adhesion chromatography system for biophysical to biochemical analysis of human colon cancer metastasis through the vasculature." Thesis, Georgia Institute of Technology, 2014. http://hdl.handle.net/1853/52307.
Full textCampbell, Thomas. "The role of voltage-gated sodium channels in non-small cell lung cancer." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-voltagegated-sodium-channels-in-nonsmall-cell-lung-cancer(a65f4c5e-b217-483b-91d3-bb669965eb03).html.
Full textTabassum, Doris Priscilla. "Exploring Intra-tumor Cooperation in Metastasis and Drug Resistance using Heterogeneous Xenograft Models of Breast Cancer." Thesis, Harvard University, 2016. http://nrs.harvard.edu/urn-3:HUL.InstRepos:33493472.
Full textMedical Sciences
Huisken-Hill, Alyse Lynn. "Influencing Pathways that Cause Metastasis and Stemness in Epithelial Ovarian Cancer." CSUSB ScholarWorks, 2016. https://scholarworks.lib.csusb.edu/etd/355.
Full textLimestoll, Scott R. "Discrete Modeling of Cell Island Migration." Case Western Reserve University School of Graduate Studies / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1228413862.
Full textVolakis, Leonithas I. "Evaluating Dynamic Changes in Cancer Cell Mechanics during Epithelial to Mesenchymal Transition." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1492739871307445.
Full textMolina, Delgado Angie. "Role of the microtubule-associated protein ATIP3 in cell migration and breast cancer metastasis." Phd thesis, Université René Descartes - Paris V, 2014. http://tel.archives-ouvertes.fr/tel-01068663.
Full textMunro, 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.
Full textTavares, Nuno Tiago Fidalgo. "Radium-223 in metastatic prostate cancer: effects on metastasis microenvironment." Master's thesis, 2019. http://hdl.handle.net/10773/26898.
Full textO cancro da próstata é a segunda neoplasia mais frequente em homens e a quinta causa de morte relacionada com cancro em todo o mundo. A terapia de privação de andrógenos tem sido o gold standard para o tratamento do cancro da próstata avançado, mas apesar desta terapia ser associada com a remissão do tumor, é também associada com a recorrência do cancro na próstata, que pode levar a um estádio mais avançado da doença designado cancro da próstata resistente à castração. Apesar deste ser ainda um estádio mortal da doença, hoje em dia existem algumas opções terapêuticas para aumentar a sobrevida e providenciar maior qualidade de vida aos doentes. Uma destas opções é o Rádio-223, um radiofármaco emissor de partículas alfa que tem um efeito positivo na taxa de sobrevivência dos doentes, e também na diminuição de eventos sintomáticos relacionados com o esqueleto. Sendo assim, os principais objetivos deste trabalho experimental foram a otimização e caracterização de um modelo celular em três dimensões de duas linhas celulares de cancro da próstata, e a avaliação dos efeitos do Rádio-223 no modelo tridimensional utilizando diversas técnicas de biologia molecular e celular. Na primeira fase do trabalho, utilizou-se o método de levitação magnética para a formação de esferóides tridimensionais de PC3 e LnCap, utilizando-se posteriormente o ensaio MTT para verificar a influência do modelo no metabolismo celular, microscopia de fluorescência e colorações histoquímicas para estudar a estrutura e viabilidade dos esferóides, imunocitoquímica para a expressão proteica e citometria de fluxo para avaliar a viabilidade e as vias de morte celular. Os efeitos do Rádio-223 foram estudados posteriormente pelo ensaio SRB, para avaliar o conteúdo proteico total, por Alamar Blue, para estudar a proliferação celular, e pela coloração May-Grünwald-Giemsa, para avaliação da morfologia celular pós-irradiação. As duas linhas celulares demonstraram formar diferentes tipos de estruturas tridimensionais em cultura, e por formarem estruturas mais compactas, decidiu-se estudar a linha celular PC3. As estruturas das células PC3 demonstraram ter uma conformação esférica e apresentaram extensas zonas necróticas e apoptóticas, visto que os esferóides possuíam dimensões na ordem dos mm2. Além disso, os esferóides exibiram diferenças na expressão de algumas proteínas chave quando comparadas com células controlo em monocamada, facto que deve também ser tido em conta no estudo de terapêuticas para o cancro com este tipo de modelos. Após a irradiação dos esferóides com Rádio-223, todas as doses testadas apresentaram uma diminuição comparadas com o controlo, quer em conteúdo proteico total ou proliferação celular. Os resultados mostraram também que o tratamento com Rádio-223 exibiu menor eficácia nos esferóides quando comparados com células em monocamada, o que se pode dever ao facto das estruturas tridimensionais serem modelos mais próximos do cenário in vivo, e, portanto, a citotoxicidade do Rádio-223 poderá ser diminuída. Além disso, como as partículas alfa têm baixo alcance de penetração e o esferóide tem um tamanho consideravelmente grande, o radiofármaco pode não penetrar com eficácia na estrutura tridimensional. Assim, com este estudo foi possível concluir que, como expectável, o Rádio-223 atua de forma diferente quando testado em monocamada e em culturas tridimensionais, e que é de grande importância avaliar este, e no futuro outros fármacos, com culturas em três dimensões, pois estas podem funcionar como uma “ponte” entre os estudos in vitro em monocamada e os estudos in vivo, melhor mimetizando o microambiente tumoral.
Mestrado em Biologia Molecular e Celular
(11200086), Odalys Torres Luquis. "The Lymphatic System in Breast Cancer Metastasis." Thesis, 2021.
Find full textLin, Hsin-Hsien, and 林信賢. "PLAU Promotes Cancer Cell Metastasis By Activating CDCP1." Thesis, 2019. http://ndltd.ncl.edu.tw/handle/a7f9m9.
Full textLin, Chia-Liang, and 林佳良. "Molecular mechanisms of the metastasis associated protein 2 in cell metastasis of human cervical cancer cells." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/ubjswy.
Full text中山醫學大學
生化微生物免疫研究所
106
Metastasis Associated 1 Family Member 2 (MTA2) is a central components of the Mi-2/NuRD complex, which possesses both nucleosome remodeling and histone deacetylase activities. Recent studies have indicated that MTA2 was associated with cells proliferation and metastasis in many cancer cells. The present study investigated the effect of MTA2 knockdown in cell proliferation and metastasis of human cervical cancer cells and the specific mechanism. Herein, we showed that MTA2 expression was correlated significantly with tumor differentiation and Gleason''s grade in cervical cancer tissue. Lentivirus mediated short hairpin RNA (shRNA) was used to knockdown MTA2 expression in cervical cancer cell lines. In vitro migration and invasion assay demonstrated MTA2 depletion inhibited cells metastasis ability, but not affect of the cells proliferation. In addition, MTA2 knockdown decreased MMP-12 protein levels and increased KLK10 in cervical cancer cells, as determined by proteinase microarray analysis. Furthermore, western blot analysis indicated ASK1, MEK3/6, and p38 signaling pathways were activated, then induced p-YB1 (phosphorylated of Y box-binding protein 1) nuclear translocation, significantly inhibited AP-1 activity binding to the MMP-12 promoter, and trans-suppressed the expression of MMP-12. In vivo studies using tail intravenous injection in mice models indicated that MTA2 knockdown significantly inhibited metastasis to lung. In addtion, MTA2 depletion increased mirR-7 expression, which targets Sp1, by MicroRNA Sequencing analysis. Mechanistic investigations suggested that MTA2 knockdown inhibited Sp1 expression and interaction with the KLK10 5’-flank region via regulating miR-7 expression. Moreover, the protein levels of Sp1 were up-regulated and down-regulated of KLK10 after transfection with miR-7 inhibitor that reversed cell metastasis and invasion in cervical cancer cells. In conclusion, our findings suggest that MTA2 is important for tumor metastasis through knockdown of MTA2 will regulate p38/YB1/MMP-12 signaling pathway and induce miR-7 expression by targeting Sp1 mediated KLK10 expression.
Zhang, Chentian. "Microfabricated systems for studying cancer metastasis." Thesis, 2016. https://hdl.handle.net/2144/14637.
Full text2017-02-17T00:00:00Z
Luga, Valbona. "Tumour-stroma Signalling in Cancer Cell Motility and Metastasis." Thesis, 2013. http://hdl.handle.net/1807/43634.
Full textChang, Jeng-Shou, and 張正守. "The Role of GIT1 in lung cancer cell metastasis." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/uu9epu.
Full text國立陽明大學
生化暨分子生物研究所
105
Lung cancer is the leading cause of cancer-related deaths worldwide and the prognosis of non-small-cell lung cancer (NSCLC) remains poor. Identification of novel prognostic markers and therapeutic targets are urgently needed. Here we identified G-protein-coupled receptor-kinase interacting protein 1 (GIT1) gene from 5,000 High-throughput antibodies library screening using tissue microarray (TMA) after comparing protein expression differences of five major human cancer primary tumors and normal adjacent tissues. The results were further confirmed by online microarray database analysis to show GIT1 as a prognosis predictor in NSCLC. GIT1 is participated in cell movement activation, which is a fundamental process during tissue development and cancer progression. GIT1/(PAK interacting exchange factor, PIX) forming a functional protein complex that contributes to (Ras-related C3 botulinum toxin suxstrate 1, Rac1)/(Cell division cycle 42, Cdc42) activation, resulting in increasing cell mobility. Although the importance of Rac1/Cdc42 activation is well documented in cancer aggressiveness, the clinical importance of GIT1 remains largely unknown. Here, we investigated the clinical significance of GIT1 expression in NSCLC and also verified the importance of GIT1-Rac1/Cdc42 axis in stimulating NSCLC cell mobility. The result indicated higher GIT1 expression patients had significantly poorer prognoses in disease-free survival (DFS) and overall survival (OS) compared with lower GIT1 expression patients. Higher GIT1 expression was an independent prognostic factor by multivariate analysis and associated with migration/invasion of NSCLC cells in transwell assay. In vivo studies indicated that GIT1 promotes metastasis of NSCLC cells. Finally, GIT1 was found to stimulate migration/invasion by altering the activity of Rac1/Cdc42 in NSCLC cells. Together, the GIT1 expression is associated with poor prognosis in patients with NSCLC. GIT1 is critical for the invasiveness of NSCLC cells through stimulating the activity of Rac1/Cdc42.
Tan, Izza Maria Doreen A. "ADAMTS1 is a promoter of metastatic cell behaviour in mammary cancer cells." Thesis, 2014. http://hdl.handle.net/2440/87148.
Full textThesis (Ph.D.) -- University of Adelaide, School of Paediatrics and Reproductive Health, 2014
Chen, Min-Wei, and 陳民瑋. "H3K9 Histone Methyltransferase G9a Promotes Cancer Cell Invasion and Metastasis." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/23603814540857504865.
Full text國立臺灣大學
毒理學研究所
99
G9a is a mammalian histone methyltransferase that contributes to the epigenetic silencing of tumor suppressor genes. Emerging evidence suggests that G9a is required to maintain the malignant phenotype, but the role of G9a function in mediating tumor metastasis has not been explored. Here, we show that G9a is expressed in aggressive lung cancer cells, and its elevated expression correlates with poor prognosis. RNAi-mediated knockdown of G9a in highly invasive lung cancer cells inhibited cell migration and invasion in vitro and metastasis in vivo. Conversely, ectopic G9a expression in weakly invasive lung cancer cells increased motility and metastasis. Mechanistic investigations suggested that repression of the cell adhesion molecule Ep-CAM mediated the effects of G9a. First, RNAi-mediated knockdown of Ep-CAM partially relieved metastasis suppression imposed by G9a suppression. Second, an inverse correlation between G9a and Ep-CAM expression existed in primary lung cancer. Third, Ep-CAM repression was associated with promoter methylation and an enrichment for dimethylated histone H3K9. G9a knockdown reduced the levels of H3K9 dimethylation and decreased the recruitment of the transcriptional cofactors HP1, DNMT1, and HDAC1 to the Ep-CAM promoter. Our findings establish a functional contribution of G9a overexpression with concomitant dysregulation of epigenetic pathways in lung cancer progression. In addition, G9a may also have functions in cancer cell motility, survival and angiogenic activity. Our results underscore the utility of developing G9a inhibitors as a potentially powerful therapeutic target. We also established the HTS platform for inhibitors against the G9a.
Kung, Chang-I., and 龔倉義. "The Effects of Tanshinone IIA on Breast Cancer Cell Metastasis." Thesis, 2006. http://ndltd.ncl.edu.tw/handle/19403025722012435911.
Full text國立陽明大學
解剖暨細胞生物學研究所
94
Recent studies have shown that Tanshinone IIA, a kind of lipid-soluble extract isolated from a traditional herb medicine, salvia miltiorrhiza BUNGE, exhibits a potent cytotoxicity and growth inhibition on various human carcinomas and ability to inhibit the growth of human carcinomas. NQO1 in normal cell contributes a function preventing from hurt of reactive quinone and maintain the antioxidant in normal cell, but in human cancer cell, it is over-expressed and contributes drug-resistant function. There are not many studies about the effect of Tanshinone IIA on human breast cancer. In this study, we investigate the cytotoxicity of Tanshinone IIA on human breast cancer cell line, the ability in inhibiting metastasis, and the decrease the expression of NQO1. The result shows that treatment of MDA-MB-435s cells with 25μM Tanshinone IIA increase the sub G0-G1 phase. After 48hour treatment of MDA-MB-435s cells with 25μM Tanshinone IIA, expression of the CD44 cleavage product decreases. After 48 hour treatment of MDA-MB-435s cells with 25μM Tanshinone IIA, expression of NQO1 decreases. The data also shows that the expression of standard form CD44 increases after treating MDA-MB-435S with 25μM Tanshinone IIA for 48 hour. According to this data, Tanshinone IIA has cytotoxicity to MDA-MB-435S cells, and Tanshinone IIA could decrease the cleavage of CD44 and the expression of NQO1. According to this study, we suggest that Tanshinone IIA has potential to treat human breast tumor, decrease the migration of breast cancer cell by inhibiting CD44 cleavage.
Jiang, Zhe-Yu, and 江哲佑. "Identification of the factors that promote ovarian cancer cell metastasis." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/89939179597039925212.
Full text國立陽明大學
生命科學系暨基因體科學研究所
104
Ovarian cancer is the most lethal gynecologic malignancy. It not only is hard to be diagnosed at the early stages, but also comes along with a high recurrent rate as well as chemoresistance at the advanced stages even after surgical treatment. In order to improve the current treatment of ovarian cancer, I attempted to identify the important factors potentially involved in the progressions of metastasis and angiogenesis. Firstly, I designed an in vivo selection scheme using nude mice to select ovarian cancer cells tending to metastasis and recurrence. A2780 and SKOV3 were subjected by intraperitoneal injection to selection for three cycles and the corresponding A2780M3 and SKOV3M3 were obtained. In the cell-based experiments, A2780M3 exhibited the ability of proliferation under high cell density, whereas SKOV3M3 evolved the ability of anchorage-independent growth. The mRNA expression of EMT markers and the ability of migration were also altered in both cell lines. Furthermore, both A2780M3 and SKOV3M3 showed higher tumoral formation ability than their parental cells in boh intraperitoneal and subcutaneous xenografts in nude mice. In addition, immunohistochemical staining indicated that the tumors formed by A2780M3 have less apoptotic signal than those formed by A2780. These results concluded that A2780M3 is more malignant. Therefore, cDNA microarray was further used to differentiate the gene expression profile between A2780 and A2780M3. I then obtained three candidates, CYP1B1, LOX and SALL1, after genomic analysis of the microarray data. In the preliminary experiment, I found that higher CYP1B1 expression is correlated with TMS-mediated suppression of cell proliferation. Secondly, I also established a hypoxia model mimicked by DFO supplement, trying to identify the crucial factors involved in the angiogenesis process of ovarian cancer. I applied angiogenesis array to detect the changes of angiogenic factors in the conditioned media harvested from A2780, SKOV3 and OVCAR3 with or without DFO treatment. Following this, three angiogenic factors upregulated by HIF-1were selected, including VEGF, IL-6 and IL-8. Taken together, the results in my thesis allow me to find three candidate genes involved in ovarian cancer metastasis and three candidate genes involved in ovarian cancer angiogenesis. These candidate genes might play important roles in ovarian cancer progression.
Wang, Chung Chiang, and 王重強. "The mechanism of penta-acetyl geniposide inhibits cancer cell metastasis." Thesis, 2002. http://ndltd.ncl.edu.tw/handle/64032358168912194288.
Full text中山醫學大學
生物化學研究所
90
Penta-acetyl geniposide【(Ac)5GP】was a acetylated product from geniposide, a glycoside existing in Gardenia Fructus. Our previous studies have shown that (Ac)5GP is involved in the chemoprevention and induction of apoptosis of C6 glioma cells. In this study, we demonstrate that (Ac)5GP may inhibits the invasion of C6 glioma cells. Cancer cell invasion requires coordinated processes, such as changes in cell-matrix adhesion, degradation of the extracellular matrix, and cell migration. We found that (Ac)5GP inhibited motility and cell-matrix adhesion of C6 glioma significantly via Boyden chamber migration assay and cell-matrix attachment assay. Moreover, (Ac)5GP reduced expression of matrix metalloproteinase-2 and -9 via semi-RT-PCR and gelatin zymography. On the other hand, We found (Ac)5GP inhibited C6 glioma cells PI-3K protein expression and ERK1.2 phosphorylation. Furthermore, PI-3K and MEK phosphorylation inhibitors: Wortmannin and PD98059 inhibited MMP-2 and MMP-9 activity respectively. So, we suggested that (Ac)5GP may inhibits C6 glioma cells MMP-2 amd -9 activity by inhibiting PI-3K protein level and ERK1.2 phosphorylation.