Dissertations / Theses on the topic 'Fibrosarcoma cells'
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1
Rai, Anuradha. "Activated natural killer cell mediated cyto toxicity of fibrosarcoma cells in mouse." Thesis, University of North Bengal, 1998. http://hdl.handle.net/123456789/926.
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Devlin, Selina Jane. "Induction of fibronectin matrix and growth effects on fibrosarcoma cells." Thesis, University of Oxford, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334326.
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Alkarrawi, Mohammed. "2-Hydroxybenzoate analogue mediated apoptosis in human HT-1080 fibrosarcoma cells." Thesis, Cardiff University, 2005. http://orca.cf.ac.uk/56105/.
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The antitumour activities of 18 benzoic acid and 2-hydroxybenzoic acid analogues were investigated in HT-1080 fibrosarcoma cell line. Several approaches were used to identify the most effective apoptotic agents capable of inhibiting cell population expansion of HT-1080 cells mostly at a concentration of 0.4mM. Techniques used in this study included: cell viability assays (MTT, direct count and time-lapse tracking images), morphology (DAPI, haematoxylin-eosin, methyl green-pyronin y, and SEM), immunocytochemistry (Annexin V, caspase-3) and pharmacology (2-hydroxybenzoate uptake). The results indicated that most of these compounds showed antiproliferative activities at specific concentrations (range 0.025-8mM), with an incubation time of 2-180 hours. It is evident that zinc 2-hydroxybenzoate was the most effective antiproliferative agent at 0.3 and 0.4mM. Other analogues, mainly calcium, also showed antiproliferative activities but at higher concentrations (up to 8mM). The growth inhibitory effect on HT-1080 cells population after treatment with either calcium or zinc 2-hydroxybenzoates was identified as the occurrence of apoptosis. This was confirmed by the morphological techniques as well as by immunoassay including annexin V and caspase- 3, measured by flow cytometry. Although strong evidence has been presented here for apoptosis, the genetic mechanism remains uncertain. Neither the expression of the six proteins p53, p21, Bax, Bcl-2, histones and TNF-a, nor the cell cycle analysis was able to fully elucidate the mechanism of action of calcium and zinc 2-hydroxybenzoate on HT-1080 cells. Nonetheless, calcium and zinc 2-hydroxybenzoate-induced apoptosis clearly involved caspase-3 through Bax and p53/p21, respectively, and displayed the properties of potentially therapeutic compounds.
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Aabed, Tariq Ahmad. "Radiation effects on mesenchymal stem cells in a model of fibrosarcoma." Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/22347/.
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Background: Radiotherapy is a mainstay of sarcoma treatment, but can cause fibrosis, characterized by production of extra-cellular matrix proteins such as collagen by cancer-associated fibroblasts (CAFs) in the cancer stroma and surrounding normal tissues, which makes tumours more aggressive and resistant to further treatment. Mesenchymal stem cells (MSCs) can be recruited to irradiated tumours and can differentiate into CAF-like cells but the mechanisms of these effects remain unclear. Aim: Determine the mechanisms of radiation effects on the recruitment of MSCs to tumours and their differentiation into CAF-like cells. Methods: Mouse MSCs were irradiated directly or exposed to irradiated mouse fibrosarcoma cells (FS120 or FS188) or their conditioned media (CM) and/or irradiated endothelial cells. Expression of CAF/fibrosis markers (collagen, fibronectin, PDGF receptor-β and α-SMA) by MSCs was assessed 3-4 days’ post radiation. Trans-well migration assays were also performed. Candidate proteins were investigated for their ability to stimulate migration and maturation of MSCs to CAF-like cells and for the ability of radiation to stimulate their production in fibrosarcoma cells. Irradiated FS120 and FS188 solid tumours were analysed for collagen, using Masson’s trichrome staining, and α-SMA using IHC and immunofluorescence. Results: Direct irradiation of MSCs had limited effects on their expression of CAF markers and migration, but exposure to irradiated tumour cells or CM and/or endothelial cells increased these effects. Candidate proteins TGF-β1, MCP-1, and SDF-1α all significantly enhanced the migration of MSCs, and radiation increased their production in fibrosarcoma cells. FS188 cells produced more MCP-1 than FS120 cells and FS188 and FS120 cells and their CM increased MSC migration in a radiation-dependent manner. Migration could be at least partially blocked by an MCP-1 blocking antibody. MSC expression of the MCP-1 receptor, CCR2, was increased after exposure to irradiated FS188 cells or their CM. In vivo, irradiated fibrosarcomas showed significant increases in collagen content, with more collagen in FS188 than in FS120 tumours. Conclusion: Results support the notion that MSCs play an important role in radiation-induced CAF activity and fibrosis in sarcoma. MCP-1 was identified as an important mediator of these effects. Moreover, endothelial cells were shown to play an important role in the recruitment of MSCs in response to radiation. In vitro results identifying FS188 cells as being more pro-fibrotic than FS120 cells were consistent with in vivo results. Further work to understand these processes should help to develop novel treatment strategies for combination with radiotherapy.
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Gillingham, Helen. "Role and regulation of aminopeptidase N (CD13) in HT1080 fibrosarcoma cells." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610322.
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Zong, Fang. "Studies on syndecan-1 in mesenchymal tumors." Stockholm : Department of Laboratory Medicine, Karolinska Institutet, 2010. http://diss.kib.ki.se/2010/978-91-7409-749-8/.
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Alfaro, Alejandro. "In situ hybridization of the feline major satellite DNA FA-SAT in feline fibrosarcoma cell lines and feline fibrosarcoma tissue sections." Giessen DVG Service, 2009. http://geb.uni-giessen.de/geb/volltexte/2009/7271/index.html.
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Alfaro, Alejandro [Verfasser]. "In situ hybridization of the feline major satellite DNA FA-SAT in feline fibrosarcoma cell lines and feline fibrosarcoma tissue sections / by Alfaro, Alejandro." Gießen : DVG-Service, 2009. http://d-nb.info/1000186083/34.
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McConnell, Michael James. "Cell-surface Tumoricidal Molecules and NF-kB in the Tumor-burdened Host." Thesis, Virginia Tech, 2002. http://hdl.handle.net/10919/9609.
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Tumor-distal immune suppression promotes tumor growth by preventing the recruitment of leukocytes to the tumor-proximal microenvironment. Tumor necrosis factor (TNF)-a is both secreted by and expressed on the cell-surface (mTNF-a) of macrophages. When stimulated with LPS, tumor-burdened host (TBH) macrophages secrete more TNF-a than normal host (NH) macrophages. In this study, I showed that mTNF-a is elevated both in freshly isolated and stimulated TBH macrophages. Additionally, I analyzed the expression of Fas and FasL on freshly isolated and LPS-stimulated macrophages and found no differences between TBH and NH macrophages. Fas and Fas ligand (FasL) cell-surface expression was analyzed on NH and TBH T-cells. While no difference was observed in freshly isolated cells, cell-surface expression of both proteins remained higher in TBH T-cells than NH T-cells after mitogenic stimulation. Fas and FasL analysis was also extended to the MethKDE fibrosarcoma and I found that these tumor cells express high levels of FasL. Because past observations show increased TNF-a mRNA expression in TBH macrophages relative to NH macrophages, I hypothesized that NF-kB activation may be increased as well. NF-kB is a transcription factor whose activation is required for TNF-a transcription. I observed increased NF-kB activation in both splenic and peritoneal TBH macrophages. Interestingly, electrophoretic mobility shift analysis (EMSA) suggests that different species of NF-kB were found in each distinct population of macrophages. Together, these data demonstrate that cell-surface tumoricidal molecules and NF-kB are dysregulated in the tumor-burdened host.Master of Science
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Pecoraro, Matteo 1984. "The Role of p63 and the chromatin remodeler Lsh in senescence, tumor development and lymphangiogenesis." Doctoral thesis, Universitat Pompeu Fabra, 2014. http://hdl.handle.net/10803/326749.
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La senescencia celular es una detención irreversible del ciclo celular que tiene lugar en respuesta a diversos estímulos de estrés, actuando como un mecanismo supresor de tumores para impedir la proliferación de células con riesgo de transformación maligna. Así, mutaciones que interfieren con el proceso de la senescencia pueden favorecer la formación tumoral. De todas formas, cada vez hay más pruebas que sugieren que las células senescentes también pueden ejercer efectos pro-tumorigénicos en el tejido circundante mediante el fenotipo secretor asociado a senescencia (SASP). Así, descifrar los mediadores moleculares de la senescencia y el SASP es crítico para entender los estadios tempranos de la formación y progresión tumoral. Aquí mostramos que la isoforma ΔNα de p63, un factor de transcripción relacionado con p53, es un oncogén que promueve la iniciación tumoral en colaboración con Ras mediante la inhibición de la senescencia inducida por oncogenes (OIS). Efectivamente, el incremento en la expresión de ΔNp63α en queratinocitos primarios de ratón bloquea la OIS y directamente conduce a la formación de un carcinoma de células escamosas (SCC). También identificamos la Helicasa Específica Linfoide (Lsh), un miembro de la familia SNF2 de remodeladores de la cromatina, como nueva diana de p63 necesaria para la inhibición de la senescencia. Posteriormente, demostramos que Lsh es suficiente para iniciar la formación tumoral independientemente de p63, y que el aumento en su expresión conduce a un desarrollo tumoral más agresivo. Sorprendentemente, mostramos que Lsh tiene un papel en la inducción de la linfangiogénesis, un proceso característico de la progresión maligna y la metástasis. Es interesante notar que las pruebas apuntan hacia Lsh actuando sobre el SASP para dirigir la formación y la progresión tumoral. En conjunto, en este trabajo se identifican nuevos mediadores críticos de la senescencia y funciones de la desregulación de la senescencia durante la formación y la progresión tumoral.Cellular senescence is an irreversible cell cycle arrest that occurs in response to various stresses, acting as a tumor-suppressive mechanism to impede the proliferation of cells at risk for malignant transformation. As such, mutations that interfere with the senescence process can favor tumor formation. However, increasing evidence suggests that senescent cells can also exert pro-tumorigenic effects on the surrounding tissue, through the senescence-associated secretory phenotype (SASP). As such, understanding the molecular mediators of senescence and the SASP is critical to unravel the early stages of tumor formation and progression. Here we show that the ΔNα isoform of p63, a p53-related transcription factor, is an oncogene that promotes tumor initiation in cooperation with Ras, through the inhibition of oncogene-induced senescence (OIS). Indeed, increased expression of Np63 in primary mouse keratinocytes blocks OIS and directly leads to the formation of squamous cell carcinoma (SCC). We also identify Lymphoid Specific Helicase (Lsh), a member of the SNF2 family of chromatin remodelers, as a novel target of p63, required for senescence bypass. Subsequently, we demonstrate that Lsh is sufficient to initiate tumor formation independently of p63, and that its increased expression leads to aggressive tumor development. Surprisingly, we show a role for Lsh in the induction of lymphangiogenesis, a hallmark of malignant progression and metastasis. Interestingly, the evidence points towards Lsh acting on the SASP to instruct tumor formation and progression. Together, this work identifies critical new mediators of senescence, and functional roles for senescence deregulation during tumor formation and progression.
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Nievergelt, Alexandra. "Regulation of HT1080 fibrosarcoma cell migration : role of signalling pathways and extracellular matrix proteins /." [S.l.] : [s.n.], 2004. http://www.zb.unibe.ch/download/eldiss/04nievergelt_a.pdf.
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Mori, Akira. "Vascular endothelial growth factor-induced tumor angiogenesis and tumorigenicity in relation to metastasis in a HT1080 human fibrosarcoma cell model." Kyoto University, 1999. http://hdl.handle.net/2433/181717.
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Partridge, Juneth Ann Joaquin. "The role of MMPs in the intravasation of a highly disseminating HT-1080 fibrosarcoma cell variant a protective role for tumor-derived MMP-9 /." Diss., [La Jolla] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p3378523.
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Thesis (Ph. D.)--University of California, San Diego, 2009.Title from first page of PDF file (viewed October 22, 2009). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 119-134).
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Siqueira, Adriane Sousa de. "Peptídeo C16, derivado da laminina, regula invasão, dinâmica de formação e atividade de invadopódios em linhagens celulares de carcinoma epidermóide e fibrossarcoma." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/42/42134/tde-24092014-154312/.
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A laminina contém peptídeos que podem ser liberados por proteólise. Nosso laboratório estuda os efeitos de peptídeos da laminina em biologia tumoral. Neste trabalho, verificamos se C16 (cadeia g1) estimularia invasão e atividade de invadopódios em células de carcinoma epidermóide (CAL27) e fibrossarcoma (HT1080). C16 promoveu aumento na taxa de invasão e atividade de invadopódios em ambas às linhagens celulares, comparado ao peptídeo controle C16SX. Microscopia em time-lapse demonstrou que C16 induz aumento na atividade de invadopódios em função do tempo. C16 estimula fosforilação de Src e ERK 1/2, e inibição da via ERK reduz invasão e atividade de invadopódios relacionados ao peptídeo. C16 conjugado à rodamina foi encontrando decorando a membrana de células CAL27, sugerindo possível interação com receptores. Diminuição dos níveis de integrina b1 reduzem atividade de invadopódios em amostras tratadas com C16. Nossos dados sugerem que C16 regula invasão e atividade de invadopódios em células CAL27 e HT1080, provavelmente por meio de Src, ERK e integrina b1.Laminin harbors bioactive peptides released upon tumor-induced proteolysis. Our Laboratory has been studying laminin peptides effects in tumor biology. Here we addressed whether C16 (g1 chain) would regulate invasion and invadopodia activity in cell lines from squamous cell carcinoma (CAL27) and fibrosarcoma (HT1080). C16 increased invasion rate and invadopodia activity compared to control peptide (C16SX). Through time-lapse microscopy, we observed that C16 stimulated invadopodia activity overtime. We searched for signaling pathways related to peptide effects. C16 stimulated Src and ERK 1/2 phosphorylation, and ERK signaling cascade inhibition decreased C16-induced invasion and invadopodia. Next, we addressed how C16 would interact with tumor cells. Rhodamine-conjugated C16 was found decorating CAL27 cell membrane, suggesting an interaction with receptors. Knockdown of b1 integrin reduced invadopodia activity of C16-treated cells. We propose that C16 regulates invasion and invadopodia activity of CAL27 and HT1080 cells through Src, ERK and b1 integrin.
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Andeol, Yannick. "Contribution a l'etude des oncogenes cellulaires de la famille ras : caracterisation dans trois lignees tumorales humaines." Paris 6, 1987. http://www.theses.fr/1987PA066065.
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Liu, Yi Ching, and 劉怡青. "Human MOB2 Participates in Migration of Fibrosarcoma Cells." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/37257482382491250855.
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碩士東海大學
生命科學系
102
Mps One Binder proteins (MOB) are important components to control cellular processes, such as cell proliferation, cell migration, morphogenesis, and apoptosis. MOB family proteins can be found from yeast, Drosophila and mammals. In Drosophila, Mob1 protein acted as tumor suppressor to control the Hippo pathway and photoreceptor morphogenesis. In mammals, the human MOB protein family has six distinct members. Human (hMOB2) is known to bind with NDR1/2 and participates in regulating cell apoptosis and centrosome duplication. In mouse neuron cell, over-expression of MOB2 increases neurite formation. Cell migration is an important cellular process that occurs during embryo development, wound healing, inflammation and cancer metastasis. Cell migration involves cell protrusion at the leading edge and cell retraction at the rear end of cells. Although the mechanisms of cell migration have been widely studied, the regulation of cell migration remained unclear. To study whether hMOB2 participates in cell migration, we used human fibrosarcoma cell (HT1080) as a model system to study how hMOB2 participates in cell migration. Immunocytochemistry revealed that hMOB2 protein was mainly localized at the cytoplasm and at the leading edge of HT1080 cells. The localization of hMOB2 detected at the leading edge was colocalized with actin cytoskeleton at the lamellipodia. In wound healing and cell invasion assay, we found that the rate of cell invasion was reduced to 50% after knockdown of hMOB2. The invasion rate was restored as hMOB2 proetin was re-expressed in the hMOB2 knockdown cells. We also found that the rate of cell migration was slower in the hMOB2-knockdown cells. In addition, the expression of A107G, Y110A point mutation of hMOB2 in the hMOB2 knockdown cells showed no significant difference between hMOB2 knockdown cells in the rate of cell invasion and cell migration. These results suggest that hMOB2 plays an important function in cell invasion and cell migration.
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Choo, Lai Mun, and 朱麗雯. "The function of human MOB2 in cell spreading in fibrosarcoma cells." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/40238958167824388773.
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碩士東海大學
生命科學系
99
Cell spreading is an initial mechanism for cell migration which plays a vital role in cancer development. Cell spreading has been shown to act as one of the key regulating steps between static and metastatic transition of a cancer cell. Hence, by identifying regulatory networks controlling cell spreading, it may provide valuable information and therapeutic strategies for preventing tumor metastasis. Both cell spreading and cell migration involve actin polymerization at the leading edge of plasma membrane follow by cell retraction at the rear end of cells. The molecular mechanisms in regulating cell spreading and cell migration have been extensively studied but remain unclear. Studies from yeast, Drosophila to mammalian cells have shown that MOB2 protein plays an important role in controlling the cell morphology changes by affecting cell polarity and rearrangement of actin cytoskeleton. Currently there is no research done to study the function of Mob2 in cell spreading and cell migration. In this study, we identified hMOB2 protein which plays a significant role in promoting cell spreading in HT1080 human fibrosarcoma cells. Our results showed that hMOB2 was detected at the leading edge of migrating HT1080 human fibrosarcoma cell. To study whether hMOB2 was involved in cell motility, we downregulated hMOB2 expression using RNA interference and found that cell spreading was delayed in HT1080 cells. In addition, we observed that overexpression of hMOB2 enhanced cell spreading in HT1080 cells and enhanced its accumulation at the leading edge. Furthermore, to determine the possible functional domain in cell motility, we successfully generated A107G, Y110A point mutated hMOB2 stable cell lines. Over-expressed point mutated hMOB2 expression delayed cell spreading and suppressed its accumulation at the leading edge. These observations suggested that hMOB2 affects cell spreading by regulating its expression at leading edge. No significant difference was observed in the migration rate between the different HT1080 cell populations when the percentage of gap closure was determined. However, over-expressed wild type hMOB2 induced broad lamellipodial structures and moved as a coherent group when compared with parent cells. These studies provided additional information on the molecular mechanisms which control cell spreading.
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Deng, Edward F. "Molecular cloning of a gene from metastatic fibrosarcoma cells converted by viral insertional mutagenesis." 1996. http://hdl.handle.net/1993/19087.
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Li, Cho-Han, and 李卓涵. "Studies on Curcumin and its analogs on anti-metastatic activities of human fibrosarcoma cells (HT-1080)." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/00651349802485252607.
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碩士臺北醫學大學
生藥學研究所
97
Curcumin, a yellowish pigment existed in turmeric plant has been shown to exhibit numerous biological properties, such as anti-inflammation, antioxidation, anti-invasion, and antimetastatic activity. Chemical modifications of curcumin have been studied intensively in an attempt to find an analog with similar but enhanced biological activities of curcumin. In literatures, matrix metalloproteinases (MMPs) and urokinase plasminogen activator (uPA) played important roles in cancer cell invasion by hydrolysing extracellular matrix (ECM). In this study, curcumin and 23 novel analogs were used to screen for inhibition of matrix metalloproteinase-9 (MMP-9) activities, protein and gene expression of highly metastatic HT-1080 human fibrosarcoma cells to explore the mechanisms of action. All tested compounds, except analog 24 and analog 31 at concentration of 2.5 μM showed no cytotoxic activities at 5 μM. The analog 2 (six methoxy substitutes in phenyl groups) and analog 7 (three hydroxyl and one methoxyl substitutes in phenyl groups) showed higher MMP-9 inhibitory activities than curcumin did at 5 μM in gelatin zymography analysis. We comparatively examined the influence of analog 2, 7, 24 (three hydroxyl substitutes in phenyl groups), and 31(two hydroxyl and two methoxyl substitutes in phenyl groups) on the expression of MMP-9 of HT-1080 cells at concentration of 2.5 μM. Analog 2, 7, 24 and 31 suppressed the gene expression of MMP-9 as the results of RT-PCR assay and Western blot assay, and decreased their corresponding activities in HT-1080 cells revealed by gelatin zymography assay, MMP-9 activity ELISA and fibrin zymography assay which resulted in inhibition of HT-1080 cell invasion and migration differentially. All in all, analog 2 and 7 showed higher anti-metastatic activities than analog 24 and analog 31 did. Heme oxygenase 1(HO-1), a stress-responsive enzyme, which was found to correlate with production of reactive oxygen species (ROS), suggesting a causative relationship on MMP inhibition. Therefore, the effect of curcumin and analog 2, 7, 24 and 31 on HO-1 protein expression were also studied. Interestingly, exposure to curcumin, analog 2 and 31 treatment maximally induce HO-1 protein expression in HT-1080 cells, however, analog 7 and 24 were less apparently. These data suggested that the inhibitory effects of curcumin and analog 2, 7, 24 and 31 on MMP-9 gene expression and uPA activity was closely related to tumor invasion and migration in vitro. Furthermore, analog 2 showed highly MMP-9 inhibitory activity which possibly involved mechanisms related to its ability to induce HO-1 to suppress PMA-induced ROS, which can activate MMP-9 gene expression. In summary, these data demonstrated that analog 2, 7, 24 and 31 show higher anti-metastasis potency than curcumin by the differentially down-regulation of MMP-9 and uPA.
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Chen, Chia-Jung, and 陳珈融. "Construction of the solution-phase derived nucleoside library and screening of its cytotoxicity against HSV1-tk transfected murine fibrosarcoma cells." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/08706433629818907754.
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Chen, Sheng-Han, and 陳聖翰. "Study on the structure of electrospun chitosan/ poly(DL-lactide) composite fibrous scaffold for human fibrosarcoma cells (HT1080) attachment and proliferation." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/29700187425549394987.
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碩士中原大學
化學工程研究所
98
In this study, the effect of morphology design of chitosan/ poly(DL-lactide) electrospun composite fibrous scaffold on the attachment and proliferation of human fibrosarcoma cells (HT1080)were investigated. The bead-free and the most uniformity of PDLLA fibers could be fabricate through adjusting spinning parameters, e.g. under the condition of polymer concentration: 15wt%, working distance: 30 cm and needle diameter: 0.16 mm. Otherwise, the degradation test of chitosan spunning solution were also investigated. The result showed that the viscosity of chitosan solution decrease with increasing the degradation time. After 10 days of degradation, the spinnability and morphology of chitosan fibers were dramatically improved. The better alignment of chitosan fibers were collected successfully at 1000 rpm of rotating-drum collector. MTT assay results indicated the 3D structure of chitosan/ PDLLA composite fibrous scaffold could promote the ability of human fibrosarcoma cells proliferation compare with the 2D structure of PDLLA film and cover slip. When the collecting amount of chitosan aligned fibers increased to 12.66 g/cm2, the growth of cells were guided and elongated by the aligned chitosan fibers. And the 3D conforcal images showed that the cell growth could infiltration to the inside of fibrous scaffold, it’s consistent with the structure design of chitosan/PDLLA composite fibrous scaffold. According to the principle of tissue engineering, chitosan/PDLLA composite fibrous scaffold could have excellent potential for tissue regeneration and wound healing applications in the future.
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Chang, Meng-Lun, and 張孟倫. "Studies on the Regulation of MMP-2, -9 in HT-080 Human Fibrosarcoma cells by Chemical Constituents of the Leaves of Chamaecyparis formosensis." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/72912755133685454956.
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En-Shing, Hong, and 洪恩馨. "Mob2 Regulates Rab11 Recycling in fibrosarcoma Cell Migration." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/91020872957597153679.
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碩士東海大學
生命科學系
103
Cell migration is an important process which is involved in many biological functions. Focal adhesion, an integrin containing protein complex connected with extracellular matrix and cytoskeleton, plays the major role during cell migration. It has been reported that integrin is transported to cell membrane through vesicular trafficking and been regulated by Rab11, the endosome traffic protein. But how Rab11 been regulated is still unknown. Mob2, which has been first found in Saccharomyces cerevisiae, conserved from yeast, drosophila and mammals to human and is reported to regulate vesicular trafficking through Rab GTPase. Therefore, in this study, we investigated whether Mob2 could regulate sarcoma cell migration through Rab11 mediated integrin recycling. Results showed that Mob2 knockdown inhibited fibrosarcoma cell (HT1080) migration, and Mob2 regulated integrin recycling during the cell polarization. We further demonstrated Rab11 knockdown in Mob2 overexpressed cells inhibited cell migration; however, Rab11 overexpression in Mob2 knockdown cells has no effect on cell migration. This study also showed that miR758 overexpression induced Rab11 and Mob2 expression. Taken together, Mob2 may regulate Rab11-mediated integrin recycling for fibrosarcoma cell migration, and miR758 might play as a upstream regulator of Mob2, however, their causal relationship needs to be further investigated.
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Coons, William J. "Involvement of T suppressor lymphocytes in the progression of UV-induced fibrosarcomas." 1985. http://hdl.handle.net/2097/27421.
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Sahoo, P. P. "Study of expression of p15PAF and interaction with miR-429 in fibrosarcoma cell line HT-1080." Thesis, 2014. http://ethesis.nitrkl.ac.in/5923/1/e-92.pdf.
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MicroRNAs are a family of small, non-coding RNAs which regulate gene expression at post-transcriptional level. These ncRNAs influence cellular physiology by directly interacting with target gene transcripts. miRNA expression pattern can be correlated with cancer types, stages and other clinical variables. Therefore miRNA profiling can be used as a tool for cancer diagnosis and prognosis in almost all aspects of cancer biology such as proliferation, apoptosis, invasion and angiogenesis. Our study aims at identification of novel miRNA-mRNA target pairs that are hypothesized to play role in fibrosarcoma through an interaction map analysis from microarray data followed by experimental validation of selected pair of mRNA and miRNA by qRT-PCR. The target interaction map analysis revealed one novel target pair i.e. hsa-miR-429- p15PAF which can be potential therapeutic target in fibrosarcoma.
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Huang, Hwa-Chen, and 黃譁宸. "The study of cytotoxicity and mechanism of Co60 and beta-lapachone in mouse fibrosarcoma cell line and human umbilical vein endothelial cell." Thesis, 2005. http://ndltd.ncl.edu.tw/handle/35298189242687544741.
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碩士國立陽明大學
醫學生物技術研究所
93
β-lapachone is a natural plant derivative from the lapacho tree. It was reported that β-lapachone induced cell death of several cancer cell lines, and β-lapachone was then suggested to be a potential anti-cancer drug. Based on its severe toxicity on HUVEC cells, we are interested to know whether β-lapachone is an anti-angiogenic compound. The goal of this thesis is to find out the cytotoxicity and mechanism of Co60 and β-lapachone in mouse fibrosarcoma cell line and human umbilical vein endothelial cell. Final, we used animal model to study its tumor therapy effect. Single treatment with Co60 or β-lapachone has its effective result for different cancer cell. We used KHT and HUVEC cell as the way of this study. First, we used MTS assay to study the cytotoxicity of Co60 and β-lapachone. The results indicate that KHT is more sensitive to Co60 and HUVEC is more sensitive to β-lapachone. Additive effects were found in the combination of pre- or post- treatment of β-lapachone and Co60 in KHT cells, and also in post-treatment of β-lapachone and Co60 in HUVECs. In other hand, synergistic effect was found in the combination of pre-treatment β-lapachone and Co60 in HUVECs. Next, we utility flow cytometry to understand the cell cycle distribution, PI and LDH to study the cell death model. The results found that treatment with Co60 causes cell cycle delay in G2/M phase of KHT cells, and in G0/G1 phase of HUVECs; treatment with β-lapachone causes cell cycle delay in G0/G1 phase of KHT cells, but not in HUVECs. Both cells treated with both drugs were delayed at multiple checkpoints before committing to necrosis. To understand the mechanism of Co60 and/or β-lapachone on the cells, the alteration of several gene expressions were analyzed. Co60 was found to be able to turn on VEGF gene and protein expression, and only slight influence on other genes; β-lapachone was found to be able to turn on HIF gene expression, but no significant influence was found on other genes. In migration assay, β-lapachone significant effect neither. In animal model, we used β-lapachone pre-treatment plus Co60 for tumor therapy. The combined therapeutic effect is greater than single therapy. In conclusion, β-lapachone enhanced the killing effect of Co60 in vitro and in vivo.