Dissertations / Theses on the topic 'Cancer cells – Proliferation'
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Harnagea, Theophilus Eugenia. "Acetaminophen stimulates proliferation of breast cancer cells." Morgantown, W. Va. : [West Virginia University Libraries], 1999. http://etd.wvu.edu/templates/showETD.cfm?recnum=773.
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Thesis (Ph. D.)--West Virginia University, 1999.Title from document title page. Document formatted into pages; contains ix, 137 p. : ill. Vita. Includes abstract. Includes bibliographical references (p. 115-134).
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Liu, Po-shiu Jackie. "Effects of flavonoids on proliferation of breast cancer cells and vascular smooth muscle cells /." View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B38480189.
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廖寶韶 and Po-shiu Jackie Liu. "Effects of flavonoids on proliferation of breast cancer cells and vascular smooth muscle cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B45011394.
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Pfeiffer, Thomas J. "Phytoestrogens may inhibit proliferation of MCF-7 cells, an estrogen-responsive breast adenocarcinoma cell line." Link to electronic thesis, 2004. http://www.wpi.edu/Pubs/ETD/Available/etd-0430104-132238.
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Ng, Wai Yee. "Ginsenosides on the growth and proliferation of glial tumor cells." HKBU Institutional Repository, 2008. http://repository.hkbu.edu.hk/etd_ra/998.
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Fancher, Karen. "Transcriptional Alterations during Mammary Tumor Progression in Mice and Humans." Fogler Library, University of Maine, 2008. http://www.library.umaine.edu/theses/pdf/FancherK2008.pdf.
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SIPES, NANCY JO. "GROWTH REGULATION OF HUMAN MELANOMA: FACTORS INVOLVED IN THE EXPRESSION OF THE TRANSFORMED PHENOTYPE (SOFT AGAR, GROWTH FACTORS, PLATELETS, ENDOTHELIAL CELLS, PARACRINE)." Diss., The University of Arizona, 1986. http://hdl.handle.net/10150/183788.
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Cellular transformation is accomplished in vitro through the concerted action of growth factors and oncogenes. This association has demonstrated that malignant growth results from aberrations in pathways that normally operate to control proliferation. Activation of genes that code for growth factors, their receptors, and/or molecules essential in the transduction of signals from the cell surface to the nucleus are all potential mechanisms by which tumor cells could establish a selective growth advantage over normal cells. This dissertation addresses the question of what oncogenic mechanisms are important in the development and progression of human melanoma. These studies show that melanoma growth is regulated by endogenous substances produced by the melanoma cells themselves (autocrine stimulation), as well as by exogenous substances supplied by neighboring cells and platelets (paracrine stimulation). These factors work to drive the expression of the transformed phenotype for melanoma as evidenced by induction of serum-free soft agar growth. Human platelets were found to the the richest source of paracrine growth promoters. The factor from human platelets was characterized and partially purified. Melanoma cells respond to this 60,000 molecular weight, disulfide-bond-containing protein in colony formation assays. In addition, the protein has endothelial cell growth factor activity. Purified fractions which promoted optimal colony formation for human melanoma cells also maximally stimulated monolayer growth of bovine aortic endothelial cells, while melanocytes were nonresponsive. This implies that melanoma cells are expressing receptors for a protein which plays no known or apparent role in the normal growth of melanocytes. Melanoma cells are sensitive to growth regulatory molecules of autocrine and paracrine nature. This dissertation provides clues to the genetic lesions which have occurred in these melanoma cells to influence their proliferation. The aberrations appear to reside in those genes important in growth factor pathways at the level of endogenous production and misguided response to exogenous factors through receptor expression. We can not hope to fully inhibit the proliferation of tumor cells until we identify and understand those forces which drive their growth. These studies have increased our knowledge of those signals which stimulate melanoma cellular proliferation, and thus provide insight into important therapeutic targets.
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Fettig, Amy E. "Identification of cellular targets influenced by ectopic expression of TAL1 and LMO1 genes." Virtual Press, 2001. http://liblink.bsu.edu/uhtbin/catkey/1222830.
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Cancer has been a disease, which has generated intense research interest for many years. Misexpression of two oncoproteins, TAL 1 and LMO 1, has been found to help induce a particular type of leukemia, called T-cell acute lymphoblastic leukemia (T-ALL). Presently, it is not completely understood how these proteins induce leukemogenesis or what other cellular proteins they interact with to drive this progression. In this study, a series of experiments were conducted to identify downstream targets of TALI and LMO1. Using retroviral gene transfer, both genes were introduced, either singly or in combination, into a murine T-cell line called AKR-DP-603. Empty vectors were introduced as controls. In order to assay the effects of TALI and LMO I expression on expression of other proteins, a series of Western blots were completed on all populations of engineered cells. It was determined that there were differences in expression of Bcl-2 and p16 as indicated by differences in band intensities on the blots. This is important because it implies an effect on protein levels by TAL 1 and LMO 1. However, there were no differences in protein expression levels for Bax or cyclin D1. This suggests that TAL1 and LMOI do not have any regulatory effects on these proteins. In addition, apoptotic assays were completed on all populations of cells. The results of both a TUNEL assay and ethidium bromide/acridine orange staining protocol showed TAL1- and LMO1expressing cells to have an increase in cell survival under starvation conditions and a lower frequency of apoptosis. Statistical analysis verified significant difference in the apoptosis assays. The data suggests an up-regulation of anti-apoptotic proteins. The finding of this research allow a clearer understanding of the process of leukemogenesis and may lead to a development of better cancer treatments.Department of Biology
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Wang, Haizhen. "The C-Phycocyanin/Beta Protein Inhibits Cancer Cell Proliferation." unrestricted, 2008. http://etd.gsu.edu/theses/available/etd-04212008-155113/.
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Thesis (M.S.)--Georgia State University, 2008.Title from file title page. Zhi-Ren Liu, committee chair; Delon W. Barfuss, Jenny J. Yang, committee members. Electronic text (69 p. : ill. (some col.)) : digital, PDF file. Description based on contents viewed June 11, 2008. Includes bibliographical references (p. 61-67).
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Hui, Cheuk-man, and 許卓文. "Role of Id-1 in proliferation and survival of esophageal carcinoma cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B29947492.
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鄭珊 and Shan Amy Cheng. "Structure-function studies of secreted PDZ domain-containing protein 2(sPDZD2)." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39558101.
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Miller, Jason. "The Effects of Lipophilicity of Propofol Derivatives on Lung Cancer Cells." Marietta College Honors Theses / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=marhonors1525433134267396.
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Perkins, Denise Mary. "Isolation of and interaction of nutrients with the linoleoyl-coa desaturase complex." Thesis, Rhodes University, 1990. http://hdl.handle.net/10962/d1018264.
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The termina1 enzyme in the linoleoyl-CoA desaturase enzyme complex, delta-6-desaturase was implied in the control of cell proliferation in cancer cells. One of the aims of this study was to isolate the terminal enzyme. It was decided that in order to isolate this enzyme it was first necessary to isolate the entire complex and then to enzymatically solubilise the first two components of the complex i e cytochrome b5 reductase and cytochrome b5 from the complex resulting in a pure delta-6-desaturase . The first two components were isolated and purified using simplified and easily reproducible methodologies which could be utilised in the final purification of delta-6- desaturase. The entire enzyme complex, linoleoyl-CoA desaturase was also isolated in a pure form and this pure complex was used to attempt to isolate delta-6-desaturase. The terminal enzyme was isolated with some cytochrome b5 still bound to it. The methods used had proven to be successful and with some modifications should yield a pure enzyme. Zinc and GLA were known to play a role in the inhibition of cancer cell proliferation and zinc was hypothesised to inhibit cell growth by stimulating the activity of the linoleoyl-CoA desaturase enzyme complex which is involved in the regulation of cell proliferation. GLA is the product of the reaction that this enzyme complex catalyses and GLA has been shown to inhibit cancer ce ll growth. The effect of GLA on cell growth and linoleoyl-CoA desaturase activity was thus investigated. Results showed that both zinc and GLA inhibited cell growth and that the combined addition of zinc and GLA generally resulted in the inhibition of cell growth and the activation of linoleoyl-CoA desaturase activity in the BL-6 cells while having a less pronounced effect on the LLCMK cells. The results of this study support the hypothesis that zinc may be a cofactor of linoleoyl-CoA desaturase.
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Amunjela, Johanna Ndamwena. "The roles of POPDC proteins in the migration and proliferation of breast cancer cells." Thesis, University of Aberdeen, 2017. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=235948.
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Despite advances breast cancer management, it remains a leading cause of death in women globally. Breast cancer is molecularly heterogeneous with some subtypes that are challenging to therapeutically target. This necessitates identification and validation of novel targets for breast cancer therapy. This study hypothesised that Popeye domain-containing (POPDC) proteins are dysregulated to promote breast malignancy. The study aimed to determine the potential of POPDC proteins as novel targets for inhibiting breast cancer cell migration and proliferation. Western blot and immunofluorescence assays demonstrated that POPDC1 and POPDC2 were significantly suppressed in malignant breast cells relative to non-malignant breast cells. In ductal carcinoma tissues, POPDC1 was significantly suppressed without correlation to clinical progression. In contrast, POPDC2 and POPDC3 were overexpressed in ductal carcinoma tissues and significantly correlated to HER2+ status and high tumour grade. Secondly, cell membrane expression of POPDC1 and POPDC2 were significantly reduced in malignant cells instead shifted to endosomal trafficking vesicles. Thirdly, suppression and gain of function studies showed that POPDC suppression significantly promoted cell migration and proliferation, while gain of POPDC function significantly inhibited cell migration and proliferation. The study also demonstrated that cAMP interacted with POPDC1, regulates POPDC1 expression levels and potentially controls POPDC1-mediated inhibition of cell migration and proliferation in breast cancer. Finally, this study showed for the first time that EGFR negatively regulates POPDC1 expression in breast cancer cells and the overexpression of POPDC1 can reduce EGFR-mediated cell migration and proliferation in breast cancer cells. In conclusion, POPDC protein expression, localisation and functions change in breast cancer. POPDC1 was also identified as a novel therapeutic target for inhibiting breast cancer cell migration and proliferation that could potentially be targeted to inhibit EGFR-driven breast malignancy. The study also demonstrated POPDC2 and POPDC3 are dysregulated in breast cancer, but in a less consistent and more complex manner.
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Ojo, Evelyn. "Approaches to Improve the Proliferation and Activity of Natural Killer Cells for Adoptive Cell Therapy." Case Western Reserve University School of Graduate Studies / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=case1536760957918928.
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Ward, Stephen. "Small Interfering RNA Decreases VEGF mRNA Expression and Proliferation of Colorectal Cancer Cells." Yale University, 2006. http://ymtdl.med.yale.edu/theses/available/etd-06282006-151558/.
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Vascular endothelial growth factor (VEGF-A) was first described in 1989 for its angiogenic and mitogenic properties. Early studies indicated that VEGF-A acts primarily in a paracrine pathway which is limited to vascular endothelium. Further investigation showed that VEGF-A and VEGF receptor-2 (VEGFR-2) are expressed by many solid tumors and improve cell growth and survival. Therefore, VEGF-A may act via an autocrine pathway that effects tumor cellular proliferation by binding VEGFR-2 at the cell surface. This study utilizes small interfering RNA (siRNA) technology to investigate the presence of an autocrine loop in human RKO colorectal cancer cells. RT-PCR demonstrated the expression of VEGF-A, VEGF-B, VEGF-D, placental growth factor (PlGF), VEGFR-2, neuropilin-1 (NP-1) and neuropilin-2 (NP-2) in vitro by RKO cells. Transfection with siRNA against VEGF-A resulted in a 94% knockdown of VEGF-A expression by ELISA. Northern blot, quantitative real time PCR and semiquantitative RT-PCR confirmed the knockdown data. In addition, transfected RKO cells showed a 67% decrease in cellular proliferation by WST-1 assay. This data correlated to the ELISA results. In summary, the presence of VEGF-A and VEGFR-2 argues in favor of an autocrine loop in human colorectal cancer cells. siRNA targeting of VEGF-A remains a promising anti-tumor therapeutic strategy.
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Willmer, Tarryn. "The role of Hsp90/Hsp70 organising protein (Hop) in the Proliferation, Survival and Migration of Breast Cancer Cells." Thesis, Rhodes University, 2012. http://hdl.handle.net/10962/d1015720.
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Hop (the Hsp90/Hsp70 organising protein) is a co-chaperone that acts as an adapter between the major molecular chaperones Hsp90 and Hsp70 during the cellular assembly of the Hsp90 complex. The Hsp90 complex regulates the stability and conformational maturation of a range of important cellular proteins, many of which are deregulated in cancer. In this study, we hypothesised that Hop knockdown inhibits proliferation and migration of cancer cells. We characterised the expression of Hop in cell models of different cancerous status, and provided evidence that Hop was upregulated in tumour cells compared to normal cell counterparts. Using an RNA interference approach, a 60-90% knockdown of Hop was achieved for up to 144 hours in the MDA-MB-231 and Hs578T breast cancer cell lines. Hop knockdown resulted in downregulation of the Hsp90 client proteins, Akt and Stat3, as well as a change in the expression of other Hsp90 co-chaperones, p23, Cdc37 and Aha1, while no change in the levels of Hsp90 or Hsp70 was observed. Silencing of Hop impaired cell proliferation in Hs578T cells but an increase in proliferation in MDA-MB-231, suggesting that the role of Hop in cancer cell proliferation was dependent on type of cancer cell. Hop knockdown in Hs578T and MDA-MB- 231 cells did not lead to any significant changes in the half maximal inhibitory concentrations (IC50) of selected small molecule inhibitors (paclitaxel, geldanamycin and novobiocin) in these cell lines after 72 hours. Hop knockdown cells were however, more sensitive than control cells to the Hsp90 inhibitors geldanamycin and novobiocin at earlier time points and in the presence of the drug transporter inhibitor, verapamil. Hop knockdown caused a decrease in cell migration as measured by the wound healing assay in both Hs578T and MDA-MB-231 cells. Hop was present in purified pseudopodia fractions of migrating cells, and immunofluorescence analysis showed that Hop colocalised with actin at the leading edges of pseudopodia, points of adhesion and at intercellular junctions of cells that have been stimulated to migrate with the chemokine stromal derived factor-1. Hop was able to bind to actin in vitro using actin cosedimentation assays, and silencing of Hop dramatically reduced the capacity of Hs578T cells to form pseudopodia. These results establish a correlation between Hop and actin dynamics, pseudopodia formation and migration in the context of Hop silencing, and collectively suggest that Hop plays a role in cancer cell migration. This study presents experimental evidence for a promising alternative to targeting Hsp90 and Hsp70 chaperones, a novel drug target in cancer therapy.
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Hernandez, Sarah. "Characterization of arginine methyltransferase PRMT8 in cells with increased plasticity." Digital WPI, 2016. https://digitalcommons.wpi.edu/etd-dissertations/533.
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Identification of therapeutically relevant molecules is necessary for the advancement of non-viral reprogramming of human cells for regenerative medicine. We have developed a novel non-viral model system that transforms primary human dermal fibroblasts into cells with induced regeneration competence (iRC). Low oxygen-mediated effects of fibroblast growth factor FGF2 lead to an increased cellular lifespan with a two fold increase in population doublings before senescence, remaining non-tumorigenic when injected into SCID mice while maintaining regeneration competence. This system allows us to study molecules that participate in increased cellular lifespan in a non-tumorigenic system. Analysis of chromatin modification enzymes by hybridization array, RT-PCR, and Western blots revealed upregulation of the arginine methyltransferase PRMT8 in iRC cells, challenging the paradigm that PRMT8 is solely expressed in brain tissue at the plasma membrane. Possibly leading to the erroneous conclusions that PRMT8 is brain specific at the plasma membrane is the fact that PRMT8 has several mRNA variants and protein isoforms. Here, I report expression of a novel PRMT8 variant in human dermal fibroblasts. Essential participation of PRMT8 in cellular proliferation was identified as a novel function for this enzyme through siRNA-mediated knockdown in both non-tumorigenic and tumorigenic cell lines. While other members of the PRMT family have known roles in cell cycle progression, I show for the first time that PRMT8 expression is reduced in both natural senescence and by premature induction of replicative senescence using sub-cytotoxic levels of hydrogen peroxide, implicating a correlation between PRMT8 expression and cell cycle progression. However, PRMT8 overexpression causes no significant change in the number of population doublings or the amount of time spent in culture prior to senescence, and does not alter the expression of key cell cycle regulatory genes. These results suggest that maintenance of PRMT8 expression is critical for cellular proliferation, but overexpression of PRMT8 alone is not sufficient to increase cellular lifespan. I determined that oxygen is the primary mediator of PRMT8 upregulation in the iRC system and therefore investigate histone occupancy of the PRMT8 promoter at hypoxia response elements. Through this analysis, I found bivalent occupancy regardless of culture conditions, indicating that PRMT8 maintains a state of poised readiness for transcriptional accessibility. The mechanism by which PRMT8 participates in cellular proliferation was investigated through binding partner identification. A binding partner of endogenous PRMT8 is identified here for the first time as FGF2 using co-IP and mass spectrometry. As iRC cells demonstrate a unique phenotype that uncouples the mechanisms of increased lifespan from tumorigenesis, I investigated the feasibility of PRMT8 as a cancer biomarker by mining publically available data in light of our own. I showed that PRMT8 is not only expressed in a variety of cancers, but that its expression is amplified. Moreover, PRMT8 expression significantly correlates to patient survival in specific cancers, strengthening the feasibility of this molecule as a biomarker. Aberrant expression of most PRMT family members has been described in various cancers, and specific PRMT variants are currently being used as prognostic markers. As such, I analyzed variant-specific PRMT8 expression in primary cancer cell lines and show that tumorigenic glioblastomas express PRMT8 mRNA variant 2. These data suggest that PRMT8 is a viable candidate for further study as a prognostic cancer biomarker, specifically for brain cancer.
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Johnson, Jodee Lee. "Effect of Black Raspberry Extracts on Colon Cancer Cell Proliferation." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1244025041.
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Boyle-Walsh, Elizabeth Ann. "Investigations into the roles of female hormones and cytokines on meningioma cell proliferation in vitro." Thesis, University of Liverpool, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284221.
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Falcone, Emilia Liana. "Ovarian cancer cells exhibit aberrations in the Wnt signaling pathway, which affect cell proliferation and cadherin expression." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=101121.
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Ovarian cancer is the leading cause of death from a gynecological malignancy in North America. It is an incomplete understanding of the early molecular events in ovarian carcinogenesis which limit our ability to diagnose and effectively treat this disease at a stage when it is still curable. The Wnt/beta-catenin canonical signaling pathway is involved in development, wound repair, and tumorigenesis. Studies examining the involvement of Wnt/canonical signaling in ovarian carcinogenesis, however, have only recently begun to emerge. In this study, we hypothesize that ovarian cancer cells exhibit aberrations in Wnt/canonical signaling, which may cause and/or effect ovarian tumorigenesis. Our objectives were therefore to (1) determine whether ovarian cancer cells exhibit alterations in the expression patterns of Wnt signaling pathway components, (2) determine whether ovarian cancer cells exhibit functional aberrations in response to Wnt/canonical stimulation and (3) determine whether these aberrations affect cell proliferation and cadherin expression. Our study shows that ovarian cancer cells exhibit alterations in the expression profiles of Wnt signaling pathway components and that these cells display aberrations at different levels of the Wnt/canonical signaling pathway, which in turn, modulate cell proliferation, and cadherin expression. These results suggest that Wnt/canonical signaling may be involved in ovarian tumorigenesis and that further study of this involvement may contribute to a better understanding of early molecular events in ovarian cancer.
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Chen, Ru. "Promoter-level transcriptome identifies stemness associated with relatively high proliferation in pancreatic cancer cells." Kyoto University, 2020. http://hdl.handle.net/2433/259015.
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付記する学位プログラム名: 充実した健康長寿社会を築く総合医療開発リーダー育成プログラムKyoto University (京都大学)
0048
新制・課程博士
博士(医科学)
甲第22747号
医科博第116号
新制||医科||8(附属図書館)
京都大学大学院医学研究科医科学専攻
(主査)教授 長船 健二, 教授 武藤 学, 教授 小川 誠司
学位規則第4条第1項該当
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Tam, Chun-wai, and 談振偉. "Combating prostate diseases with ethnobotanical drugs: inhibition of prostate cancer cell proliferation by SawPalmetto (Serenoa repens) extracts." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29188969.
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Hui, Chun-fai Ivan, and 許振輝. "Study of mammalian target of rapamycin (mTOR) signaling and the effects of its specific inhibitors in hepatocellular carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39558459.
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Sancho, Medina Mònica. "Role of linker Histone H1 variants in cell proliferation, Chromatin Structure and Gene expression in breast cancer cells." Doctoral thesis, Universitat Pompeu Fabra, 2008. http://hdl.handle.net/10803/7118.
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At least eleven histone H1 variants exist in mammalian somatic cells that bind to the linker DNA and stabilize the nucleosome particle contributing to higher order chromatin compaction. In addition of playing a structural role, H1 seems to be involved in the activation and repression of gene expression. It is not well known whether the different variants have specific roles or regulate specific promoters. We have explored this by inducible shRNA-mediated knock-down of each of the H1 variants in a human breast cancer cell line. Rapid inhibition of each H1 variant was not compensated by changes of expression of other variants. A different, reduced subset of genes is altered in each H1 knock-down. Interestingly, H1.2 depletion represses expression of a number of cell cycle genes. This is concomitant with a G1 arrest phenotype observed in this cell line. In addition, H1.2 depletion caused decreased global nucleosome spacing. These effects are specific of H1.2 depletion as they are not complemented by overexpression of other variants and they do not occur in knock-downs for the other variants. Moreover, H1.4 depletion caused cell death in T47D, being the first report of the essentiality of an H1 variant for survival in a human cell type. In addition to this, we have also investigated specificities of H1 subtypes location in particular promoters of interest in our laboratory, as well as specific interactions with other factors by generating HA-tagged H1 variant expressing cell lines.Al menos once variantes de la histona H1 han sido identificadas en mamíferos, todas ellas se unen al ADN entre nucleosomas contribuyendo así, a la estabilización de la partícula nucleosómica y a la compactación de la cromatina en estructuras de alto orden. Además de jugar un papel estructural, H1 parece estar implicada en la activación y represión de la expresión génica. Se desconoce si las diferentes variantes de H1 tienen funciones específicas o regulan promotores específicos. Con el objetivo de investigar esta hipótesis se han generado líneas celulares que inhiben de forma inducible, mediante la tecnología de ARN interferente, la expresión de cada una de las variantes de forma específica. La inhibición de cada una de las variantes no es compensada por cambios en la expresión del resto de subtipos. Distintos grupos de genes resultan alterados con la depleción de cada una de las variantes de H1. La inhibición de H1.2 reprime la expresión de una serie de genes de ciclo celular, correlacionando con un fenotipo de arresto celular en fase G1 observado en esta línea. Además, la inhibición de H1.2 causa una disminución global del espaciamiento entre nucleosomas. Todos estos efectos parecen ser específicos para la falta de H1.2 ya que no son complementados por la sobreexpresión de otras variantes. Por otro lado, la inhibición de H1.4 causa muerte celular en T47D. Ésta es la primera vez que se describe que una variante de H1 es esencial para la supervivencia de una línea celular humana.
En un segundo plano, se han construido líneas celulares con expresión de las variantes de H1 fusionadas al péptido HA, con el objetivo de estudiar la especificidad de su localización en promotores de interés para el grupo, así como interacciones específicas con otros factores celulares.
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Rieger, Megan Elizabeth. "Transcription Cofactor LBH is a Direct Target of the Oncogenic WNT Pathway with an Important Role in Breast Cancer." Scholarly Repository, 2010. http://scholarlyrepository.miami.edu/oa_dissertations/659.
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Limb-Bud and Heart (LBH) is a novel key transcriptional regulator of vertebrate development. However, the molecular mechanisms upstream of LBH and its role in adult development are unknown. Here we show that in epithelial development, LBH expression is tightly controlled by Wnt signaling. LBH is transcriptionally induced by the canonical Wnt pathway, as evident by the presence of functional TCF/LEF binding sites in the LBH locus and rapid beta-catenin-dependent upregulation of endogenous LBH by Wnt3a. In contrast, LBH induction by Wnt/beta-catenin signaling is inhibited by Wnt7a, which in limb development signals through a non-canonical pathway involving Lmx1b. Furthermore, we show that Lbh is aberrantly overexpressed in mammary tumors of MMTV-Wnt1 transgenic mice and in aggressive basal-subtype human breast cancers that display Wnt/beta-catenin hyperactivation. Deregulation of LBH in human breast cancer appears to be Wnt/beta-catenin dependent as DKK1 and Wnt7a inhibit LBH expression in breast tumor cells. RNAi mediated knockdown of LBH in basal breast cancer cell lines resulted in loss of CD44high/CD24low tumor cells, luminal differentiation, reduced cell growth, reduced colony forming ability, and increased apoptosis, suggesting a novel pro-survival and stem cell maintenance function of LBH in breast cancer. Reciprocal overexpression studies in the basal breast carcinoma line BT549 resulted in increased tumorigenicity in vitro, suggesting that LBH overexpression is indeed oncogenic. Finally, we further characterized LBH protein expression patterns and post-transcriptional regulation. Collectively, this thesis demonstrates that LBH is a direct Wnt target gene in both development and basal breast cancer that promotes the undifferentiated phenotype and survival of basal breast tumor cells.
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Di, Kaijun, and 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.
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Liao, Ximan, and 廖喜漫. "A study of proteoglycan production during suppressed cell proliferation of a human colon carcinoma cell line." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B3123897X.
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McEwan, David George. "Cyclic AMP modulation and its effects on chemo-resistant colon cancer cell proliferation and survival." Connect to e-thesis, 2007. http://theses.gla.ac.uk/81/.
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Thesis (Ph.D.) - University of Glasgow, 2007.Thesis submitted in part fulfilment of the Ph.D. to The Beatson Institute for Cancer Research, Faculty of Medicine, University of Glasgow, 2007. Includes bibliographical references. Print version also available.
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阮曉峰 and Hiu-fung Yuen. "Roles of twist in prostate cancer progression." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39558319.
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Palmer, Jodie. "The IL-6 type cytokine family in prostate cancer." Monash University, Centre for Functional Genomics and Human Disease, 2003. http://arrow.monash.edu.au/hdl/1959.1/9441.
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Latham, Peter. "Effects of N-3 polyunsaturated fatty acids on proliferation and apoptosis of colonic epithelial cells." Thesis, University of Bristol, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302105.
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Clubbs, Elizabeth Ann. "INFLUENCE OF SOY ISOFLAVONES ON THE PROLIFERATION AND DIFFERENTIATION OF PROSTATE EPITHELIAL CELLS." The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1208956436.
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Willig, Jennifer Anne. "The Effect of Anthocyanin Acylation on the Inhibition of HT-29 Colon Cancer Cell Proliferation." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1237842900.
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Vázquez, Ferrer Eric 1990. "The Role of adult stem cells in tumor formation : mutations in Sox2+ cells induce lineage-specific proliferation." Doctoral thesis, Universitat Pompeu Fabra, 2017. http://hdl.handle.net/10803/664240.
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It has been well-established that progressive accumulation of genetic mutations in proto-oncogenes and tumor suppressors induces cancer. However, the early molecular mechanisms leading to tumor initiation remain elusive. Recent studies have shown that there are tissue- and cell-type-specific vulnerabilities to oncogenic stimuli. Mutations in adult stem/progenitor cells (ASCs/PCs) have been suggested to underlie the formation of tumor initiating cell populations. Here, we sought to identify proliferative ASCs/PCs that are the most susceptible to oncogenic mutations. Expression of different oncogenic stimuli (oncogenic KrasG12D, knockout of p53, overexpression of Myc) in Sox2-positive ASCs, led to a hyperplasic phenotype. Interestingly, this was confined to the stomach and esophagus, despite there being Sox2+ cells in many other organs. These observations point to Sox2+ foregut epithelial cells as the most vulnerable to oncogenic insults. Our observations also revealed distinct roles for each of the oncogenic stimuli in cancer progression. Kras expression, but not p53 deletion, suffices for tumor formation while p53 is involved in the acquisition of an invasive potential. Finally, Myc activation not only induced hyperplasia in the esophagus and forestomach, but also drove metastatic transplantable adenocarcinomas in the glandular stomach, suggesting that Sox2+ cells could be the Cancer Cells of Origin (CCOs) for gastric cancer. Together, our results may open new paths for a better understanding of tumor initiation and promotion.És ben sabut que l’acumulació progressiva de mutacions genètiques en proto-oncogens i en gens supressors de tumors indueix càncer. Ara bé, els mecanismes moleculars que condueixen a la iniciació dels tumors són encara incerts. Estudis recents mostren que hi ha vulnerabilitats específiques cel·lulars i de teixits quant als estímuls oncogènics. Mutacions en cèl·lules mare adultes o en cèl·lules progenitores s’han proposat com a mecanismes de formació de cèl·lules tumorals iniciadores de tumors. En aquest estudi, hem volgut identificar cèl·lules mare adultes o cèl·lules progenitores que són més susceptibles a mutacions oncogèniques. L’expressió de diferents estímuls oncogènics (l’oncogen KrasG12D, l’eliminació de p53, la sobreexpressió de Myc) en cèl·lules mare adultes Sox2 positives promou un fenotip hiperplàsic. Aquest fenomen només l’observem en l’estómac i en l’esòfag, tot i havent cèl·lules mare adultes Sox2 positives en molts altres òrgans. Aquestes observacions senyalen que les cèl·lules més vulnerables als estímuls oncogènics són les cèl·lules epitelials del tracte digestiu més superior. A més, també observem rols diferents per cadascun dels estímuls oncogènics en la progressió del càncer. L’oncogen KrasG12D, però no l’eliminació de p53, és suficient per a la iniciació del tumor, mentre que p53 es troba involucrat en la invasió. També, la sobreexpressió de Myc no només indueix hiperplàsia en l’estómac i en l’esòfag sinó que també forma en l’estómac glandular adenocarcinomes metastàtics amb capacitat de transplantament, suggerint que les cèl·lules Sox2 positives podrien ésser les cèl·lules iniciadores de tumors en els càncers gàstrics. En resum, els nostres resultats obren noves vies per a una millor comprensió de la iniciació i progressió dels tumors.
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Liu, Wing-yee, and 廖穎宜. "Effects of bioactive constituents of Astragalus membranaceus on the proliferation of colon cancer and endothelial cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/206745.
Full textAbstract:
Uncontrolled cell growth may lead to pathological conditions such as cancer. During the progression of cancer, cancer cells stimulate endothelial cells for angiogenesis to support their growth and migration. Previous studies suggest that Astragalus membranaceus, of which the dried root [Astragali Radix] is used as a traditional Chinese medicine, and its bioactive components, astragalus saponins (AST), astragaloside IV (AS IV) and isoflavonoid calycosin, inhibit cancer growth. The present study aimed to examine whether or not these components inhibit the growth and/or metastasis of colon cancer cells and/or angiogenesis of endothelial cells, and to determine the possible mechanisms involved.
The growth of HCT 116 colon cancer cells and human umbilical vein endothelial cells (HUVEC) after 72 hours incubation with AST (1 to 25 μg/ml), AS IV (0.5 to 100 μM) or calycosin (10 to 200 μM) were detected with thiazolyl blue tetrazolium bromide assay. Wound healing migration and tube formation assays were used to examine the metastatic and angiogenic potential of HCT 116 cells and HUVEC. Moreover, the expressions of apoptotic [B-cell lymphoma 2 and procaspase-3] and metastasis/angiogenesis-related proteins [matrix metalloproteinase (MMP)-2, MMP-9 and vascular endothelial growth factor (VEGF)] were measured with Western immunoblotting. To investigate the potential mechanism(s) through which astragalus components affect the proliferation and/or migration of HCT 116 cells and HUVEC, the activities of mitogen-activated protein (MAP) kinases [extracellular signal-regulated kinase 1 and 2 (ERK1/2), p38 MAP kinase (p38) and c-Jun amino-terminal kinases] were studied by measuring the expressions of their phosphorylated and total proteins with Western immunoblotting.
Calycosin (200 μM) inhibited the growth of HCT 116 cells without affecting that of HUVEC. While it inhibited the migration of both cell types, it stimulated tube formation only in HUVEC. In HCT 116 cells, calycosin downregulated the expressions of procaspase-3, VEGF, MMP-2 and MMP-9 proteins, inhibited ERK1/2 but activated p38. These effects of calycosin were not observed in HUVEC. Neither AST nor AS IV had any significant effects on the parameters studied in HCT 116 cells. AST also showed no effect in HUVEC; AS IV, at 100 μM, appeared to increase the number of tube formation by HUVEC.
In conclusion, the present findings suggest that AST has no significant effect on both cancer and endothelial cells while AS IV may promote angiogenesis without any direct action in colon cancer cells. In colon cancer cells, calycosin induces apoptosis, possibly through activation of caspase-3 and p38, and inhibits metastasis, possibly by downregulating MMP-2 and MMP-9, and inhibiting ERK1/2. However, in endothelial cells, the effect of calycosin is not conclusive as it promotes tube formation but inhibits migration. These findings provide the pharmacological basis for the use of Astragali Radix in the treatment of colon cancer, and the scientific evidence for a therapeutic potential of calycosin in the management of this disorder. Further studies are needed to verify the effect of calycosin on endothelial cells. In order to better mimic the clinical situation, the interaction between cancer and endothelial cells [for example, tumor-induced angiogenesis] needs to be taken into consideration.published_or_final_version
Pharmacology and Pharmacy
Master
Master of Philosophy
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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.
Full textAbstract:
[Truncated abstract] For this thesis, the molecular biology of cancer was approached from two directions. Firstly, an investigation was conducted on the role of growth factor receptor-bound protein 7 (Grb7) in breast cancer. Grb7 is an adapter molecule that binds to a variety of proteins, including the growth factor receptor and proto-oncogene, ErbB2, and mediates signalling to downstream pathways. It has been linked to cell migration and an invasive phenotype, and is of interest as a therapeutic target. To investigate the role of Grb7 in breast cancer, preliminary experiments were performed that, firstly, determined the expression of wild-type Grb7 and a splice variant, Grb7V, in a range of cell lines, and secondly, aided the development of a protocol for treating cells with short interfering RNA (siRNA) against Grb7 and the ErbB ligand, heregulin (HRG), in a cell system appropriate for measuring the functional outcomes. Using this protocol in conjunction with CellTitre (CT) proliferation assays, it was demonstrated that Grb7 does not play a role in the proliferation of either unstimulated or HRG-stimulated SK-BR-3 breast cancer cells. Furthermore, using the protocol in conjunction with Boyden chamber migration assays, it was shown that inhibition of Grb7 expression has a slight stimulatory effect on HRG-stimulated SK-BR-3 cell migration. Thus, Grb7 was found to play only a minor role in the migration of SK-BR-3 cells, suggesting that it is not an ideal anti-cancer target for breast cancers modelled by this cell system. Concurrently, a second investigation was conducted, which similarly sought insight into the molecular biology of cancer, but adopted a more strategic approach. ... These results provide evidence for a biologically significant role for the miR-7-mediated regulation of EGFR expression. A microarray experiment was also performed to identify genes that were down-regulated following treatment with miR-7 compared to NS precursor. Of 248 down-regulated genes, including EGFR, 37 promising new miR-7 target candidates were identified. Functional clustering of down-regulated genes and promising target candidates suggested that miR-7 may have functionally-related targets involved in processes including cell motility and brain-associated functions. This investigation thus yielded a program capable of accurately predicting a miRNA target not predicted by any other target prediction program, verified a previously unknown miRNA:target interaction with functional consequences in cancer cells and provided the first steps towards investigating miR-7-mediated regulation in greater depth. Furthermore, EGFR was, to our knowledge, the first example of a verified miRNA target with target sites that are not conserved across mammals, an observation with important implications for computational target prediction and the evolution of miRNA regulatory systems. In addition, the demonstrated growth inhibitory and cytotoxic effects of miR-7 on lung cancer cells raise the possibility of a miR-7-based therapeutic for the treatment of EGFR-overexpressing tumours.
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Shih, Hung-Feng, and 施鴻鳳. "Participation of IRSp53 in cell proliferation of SW620 colon cancer cells." Thesis, 2007. http://ndltd.ncl.edu.tw/handle/84557400531641503239.
Full textAbstract:
碩士國立成功大學
藥理學研究所
95
Eps8 (EGF receptor pathway substrate NO.8) is a substrate of both EGFR and Src. It exists in two isoforms p97EPS8 and p68Eps8 in many cell lines. Our previous studies indicated that only the 97-kDa isoform was expressed and promoted cell proliferation of SW620 cells. To understand whether Eps8-interacting protein, IRSp53 is involved in Eps8-mediated cell proliferation of colon cancer cells, first, we observed that expression of IRSp53 is varied in several colon cancer cell lines including SW620. Then we confirmed the interaction between Eps8 and IRSp53 in SW620 and WiDr cells by co-immunoprecipitation. In addition, transient overexpression of myc-tagged IRSp53 and IRSp58 but not IRSp53-△363 (Eps8 binding region deletion) in NIH3T3 cells increased colony formation in soft agar. We also observed that co-transfection of Eps8 and IRSp53 into NIH3T3 cells could synergistically enhanced the number of colony formed in soft agar. These data indicated that the association between IRSp53 and Eps8 could be important for cell transforming ability. Moreover, we utilized small interference RNA (siRNA) technology to generate SW620 cell lines stably expressing IRSp53 siRNA or nonspecific control siRNA and observed that the expression of IRSp53, Akt Pi-Ser473, cyclin D1 and cyclin E is reduced in these cells. Furthermore, the growth rate and the ability of anchorage independent growth were reduced in IRSp53 siRNA expressing cells. Therefore, our results indicated that IRSp53 may participate in cell proliferation of human colon cancer cell SW620.
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楊所芳. "The Role of KDM8 in Breast Cancer Cells: Cell Proliferation and Migration." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/15474248973694324183.
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"Suppression of thromboxane synthase inhibits lung cancer cell proliferation." Thesis, 2008. http://library.cuhk.edu.hk/record=b6074592.
Full textAbstract:
Further studies were done to investigate the mechanism responsible for 1-BI-induced apoptosis in NCI-H460. It was found that 1-BI stimulated the expression of pro-apoptotic p53, Bax and cytosolic NF-kB p65 subunit but decreased pERK in NCI-H460 cells. The active forms of caspase 3 and caspase 9 were detected by Western blot, accompanied by an increase in caspase 3 activity. Reactive oxygen species (ROS) was highly generated at 24 hours after the treatment and the mitochondrial membrane potential was significantly decreased at 48 and 72 hours. The application of either N-acetyl cysteine (NAC) or glutathione (GSH) attenuated the cell growth inhibition caused by 1-BI. NCI-H460 cells pretreated with NAC showed a decrease in ROS production and p65 protein but an increase in pERK.Taken together, these findings suggest that the inhibition of THXS suppresses lung cancer cell growth by promoting either G1 cell cycle arrest or apoptosis. The status of p53 is critical for both cell cycle arrest and apoptosis in 1-BI-mediated growth inhibition, which is evident by enhanced apoptosis detected in p53-transfected NCI-H23 and DMS 114 cells and G1 cell cycle in lung cancer cells treated with PFT-alpha. The 1-BI-induced growth-inhibitory pathway is associated with the generation of ROS, alteration of mitochondrial membrane potential, down-regulation of pERK and p65.
The result showed that THXS expressed in all of the three lung cancer cell lines (NCI-H23, DMS 114 and NCI-H460). The activity of THXS was also reflected by the presence of THXS metabolite thromobxane B2 (TXB2) in the cells, which was detected by ELISA. 1-Benzylimidazole (1-BI), a specific THXS inhibitor, suppressed the lung cancer cell proliferation measured by MTT assay. 1-BI treatment caused G1 phase arrest and enhanced the level of cyclin dependent kinase inhibitor p27 in a time-dependent manner in NCI-H23 and DMS 114 cells. It markedly increased DNA fragmentation in NCI-H460 cells. The findings suggest that 1-BI inhibits cell growth by arresting cell cycle and inducing cell death. Annexin V/PI staining revealed that the cell death induced by I-BI was mainly in the format of apoptosis. Further experiments showed that the I-BI-induced apoptosis could be enhanced by the introduction of p53 into NCI-H23 and DMS 114 cells, and such enhancement was associated with a decrease in mitochondrial membrane potential. This result suggests that the p53 may play a positive role in apoptosis induced by 1-BI through changing of the mitochondrial membrane potential. The role of p53 in I-BI-mediated apoptosis was further confirmed by the experiment of the p53 inhibition. Pifithrin-alpha hydrobromide (PFT-alpha), a p53 specific inhibitor, suppressed the 1-BI-induced p53 protein expression and increased G1 cell cycle arrest.
Thromboxane A2 (TXA2) is a potent arachidonate metabolite in the cyclooxygenase-2 (COX-2) pathway, which is produced by a member of cytochrome P450 (CYP) superfamily called thromboxane synthase (THXS). Recent studies have showed that thromboxane and THXS are associated with cancer cell migration, angiogenesis, tumor metastasis and cancer proliferation but there is limited information on their role in lung cancer development. This thesis is to test the hypothesis that inhibition of THXS could alter lung cancer cell growth.
Leung, Kin Chung.
Adviser: George G. Chen.
Source: Dissertation Abstracts International, Volume: 70-06, Section: B, page: 3319.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2008.
Includes bibliographical references (leaves 130-144).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstracts in English and Chinese.
School code: 1307.
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Yu-HuaWang and 王毓華. "Establishing IRSp53S-inducible SW480 colorectal cancer cell lines and studying how IRSp53S affects cell proliferation in colon cancer cells." Thesis, 2019. http://ndltd.ncl.edu.tw/handle/ekmvtg.
Full textAbstract:
碩士國立成功大學
藥理學研究所
107
In addition to epidermal growth factor receptor (EGFR), overexpression of its downstream substrate EGFR pathway substrate number 8 (Eps8) occurs in human colorectal cancer (CRC). Eps8 overexpression promotes the kinase activity of Src and FAK, leading to the enhancement of cell proliferation and motility in cancer cells. Insulin Receptor tyrosine kinase Substrate Protein of 53 kDa (IRSp53) is an adaptor protein that links Rho-family small GTPases such as Rac and Cdc42 to the actin cytoskeleton reorganization. Previously, our study indicated that Eps8-IRSp53S complex participated in v-Src-mediated tumorigenesis. To substantiate the importance of Eps8-IRSp53 interaction in CRC, we generated cells expressing both Eps8 and IRSp53S in SW480 cells that exhibits much lower level of these proteins as compared to their metastasized counterpart SW620 cells. Unfortunately, we were unable to obtain cell lines constitutively expressing both Eps8 and IRSp53 in SW480 cells suggestting that Eps8-IRSp53 interaction might cause growth arrest and/or apoptosis in SW480 cells. To confirm this, we generate Tet-Off control and Tet-Off regulated IRSp53S-expressing SW480 cells first. Then, IRSp53S-inducible cells were transfected with EGFP-expressing or EGFP-Eps8 epressing plasmid DNA. In this way, we observed enhanced chromatin condensation only in IRSp53S/EGFP-Eps8-overexpressing cells, but not in IRSp53S/EGFP-expressing cells, nor in doxycycline-treated IRSp53S/EGFP-Eps8 overexpressing cells. In addition, MTT assay revealed that double-overexpressing Eps8 and IRSp53S reduced cell viability/proliferation in SW480 cells. Flow cytometry studies also showed that double-expressing Eps8 and IRSp53S retarded cell cycle progression as indicated by increased G1 phase and reduced S phase population. However, our prelimery study in animal xenografted tumor model revealed that due to low percentage (less than 10%) of cells really expressing both Eps8 and IRSp53S at the same time, tumors derived from this double overexpressing cell line were not statistically different from those derived from IRSp53S-expressing cells nor from vector control cells. Nevertheless, our data highlighted IRSp53S-Eps8 interaction might play a sophisticated role in regulating colon cancer progression, which deserves further study.
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I-HsiaLi and 李易遐. "Studying the role of IRSp53 in cell proliferation and motility in colorectal cancer cells." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/3dd6m2.
Full textAbstract:
碩士國立成功大學
藥理學研究所
102
Previous studies showed that IRSp53 (Insulin Receptor tyrosine kinase Substrate Protein of 53 kDa) was identified as one of the Eps8-binding partners. The interaction between Eps8 and IRSp53 contributed to Src-mediated transformation. There are at least four IRSp53 isoforms (IRSp53S, IRSp53T, IRSp58M, and IRSp53L) identified in human cells. However, the detailed functions of these isoforms remain largely unknown. Therefore, we wanted to address the importance of IRSp53 and these isoforms in cell proliferation and motility in colorectal cancer cells. First, we generated IRSp53 knockdown cells from SW620 colon cancer cells and observed both anchorage-dependent and -independent growth were reduced. In addition, IRSp53 attenuation resulted in reduced Src activity. In WST-1 cell viability assay, IRSp53 depletion might increase chemosensitivity in colon cancer cells under the treatment of anti-cancer drug oxaliplatin. In wound healing assay, there were no significant differences between IRSp53 knockdown cells and Ctrl cells. On the other hand, overexpression of myc-tagged human IRSp53S and IRSp53S-YA mutant (Eps8-binding detective mutant) but not IRSp58M in SW480 colon cancer cells resulted in elevated expression of Src，Pi-Y416 Src and Pi-Y861 FAK. However, IRSp53S, but not its YA mutant increased cell growth in SW480 cells. We also found decreased cell motility in both IRSp53S- and IRSp58M-overpressing cells. Overexpression of IRSp53S-YA mutant showed the slowest cell motility. In conclusion, IRSp53S may play a positive role in cell proliferation but not motility in colon cancer cells.
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Chiang, Chien-Chuan, and 江健銓. "Guava extracts inhibit cell proliferation and induce apoptosis in triple-negative breast cancer cells." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/4sxf66.
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TSAI, YA-RU, and 蔡雅如. "Microalgal Extract Decreases Cell Proliferation in Oral Cancer Cells by Downregulating Unfolded Protein Response." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/2zp7q4.
Full textAbstract:
碩士國立中正大學
生命科學系生物醫學研究所
106
Microalgae produce a large variety of bioactive compounds, including carotenoids, fatty acids, glycolipids, polysaccharides, proteins and peptides. Both microalgae and macroalgae have long been used in anti-cancer research based on the anti-tumor activities from either crude extracts or purified bioactive compounds of various algae have shown to have anti-tumor activities. In this thesis, we used the crude extract of Coelastrella sp. F50 (C. F50), a microalga identified in Taiwan, to investigate the anticancer effects on two domestically-established oral cancer cell lines, OC2 and OCSL. We found that C. F50 extract can decrease cell viability in a time- and dosage-dependent manner in OC2 and OCSL cells with IC50 around 500 μg/ml. C. F50 extract can also inhibit migration, epithelial-mesenchymal transition, and expression of cancer stem cell marker. C. F50 extract also showed to increase cellular reactive oxygen species (ROS) in both cells. Increased cellular ROS is often associated with increased ER stress and unfolded protein response (UPR). Surprisingly, we found out that C. F50 extract can downregulate the UPR response, but result in inhibiting cell proliferation. We speculate that the extract downregulate early UPR responses and make ROS accumulated beyond the threshold, which is prone to trigger late ER stress/UPR responses, leading to cell death.
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LIN, PING-CHENG, and 林平正. "Effects of osthole and klotho on cell proliferation in human esophageal squamous cancer cells." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/gmd9v8.
Full textAbstract:
碩士中華醫事科技大學
生物科技系暨生物醫學研究所
106
Esophageal cancer is rapidly increasing in incidence in the world and it is one of the ten most prevalent and deadly cancers in Taiwan. The most common histopathologic subtype of esophageal cancer is squamous cell carcinoma. Effective therapeutic strategies are required to solve the poor survival outcomes in esophageal cancer patients. Osthole is natural coumarin derived from mature fruit of Cnidium monnieri. It has been widely reported to have pharmacological activities such as anti-osteoporosis, anti-inflammation and anti-hyperlipidemic effects. Klotho was identified as an anti-senescence protein in a variety of tissues. Evidence suggested that loss of klotho has been associated with metabolic diseases. However, the effects and molecular events of osthole and klotho on the progression of esophageal squamous cell carcinoma remain unclear. In the present study, we undertook to study the effect of osthole on klotho protein synthesis in human esophageal squamous cell carcinoma CE81T/VGH and CE146T/VGH cells, and to investigate the molecular mechanisms of osthole and exogenous klotho against cell proliferation and migration. From the results of cell number analysis and MTT assay, we found that osthole and exogenous klotho markedly decreased cell growth in concentration- and time-dependent manners in CE81T/VGH and CE146T/VGH cells. Osthole and exogenous koltho had no significant effect on cytotoxicity as compared with control. In addition, osthole and exogenous klotho significantly decreased cell migration in CE81T/VGH cells. Interestingly, osthole caused increase in protein synthesis of klotho. Furthermore, osthole and exogenous klotho could suppress activation of the ERK/JNK/p38 MAPK and STAT1 pathways. These findings demonstrate that osthole and exogenous klotho are effective in attenuating cellular growth of human esophageal squamous cell carcinoma. Osthole suppresses cellular proliferation partly through inducing klotho protein synthesis and inhibiting the ERK/JNK/p38 MAPK or STAT1 activation.
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Tien, Yi-Li, and 田薏莉. "Effects of Osthole and Nitric Oxide on Cell Proliferation in Human Colon Cancer Cells." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/03636063354912356856.
Full textAbstract:
碩士中華醫事科技大學
生物科技系暨生物醫學研究所
102
Colorectal cancer is one of the most commonly diagnosed tumors worldwide and is known to be resistant to conventional chemotherapy. Osthole, a natural coumarin derivative, has been shown to have antitumor activity mediated by the modulation of oxidative stress. Nitric oxide (NO) is important mediator of the expression of many transcription factors and signaling cascades that affect tumor responses to therapy. However, the effects of osthole and NO on cell growth of colorectal cancer are not well understood. The aim of this study was to investigate the effects and mechanisms of osthole and NO on proliferation in colorectal cancer cells. We found that exposure of two human colorectal adenocarcinoma cell lines (HT-29 and SW-480) to osthole and NO donors S-nitroso-N-acetylpenicillamine (SNP) and sodium nitroprusside (SNAP) significantly inhibited the cell growth in concentration- and time-dependent manners. Osthole and NO donors had no significant effect on cytotoxicity as compared with control. Additionally, treatments of osthole and NO donors enhanced NO generation and iNOS (but not eNOS) protein synthesis. Furthermore, osthole and NO donors could suppress activation of the JAK2 and ERK/p38 MAPK pathway in these cells. The JAK2 inhibitor AG490, the ERK inhibitor PD98059 and the p38 MAPK inhibitor SB203580 may have the ability to decrease cellular proliferation. The results obtained in this study suggest the new mechanistic evidence that osthole and exogenous NO donors attenuate the cell growth by inhibiting the JAK2 and ERK/p38 MAPK activation and promoting the iNOS/NO pathway in HT-29 and SW-480 cells.
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Huang, Chih-Jou, and 黃芷柔. "The potential of inhibiting cancer cell proliferation in human gastric cancer cells treated with the non-chemo drug." Thesis, 2019. http://ndltd.ncl.edu.tw/cgi-bin/gs32/gsweb.cgi/login?o=dnclcdr&s=id=%22107NCHU5114006%22.&searchmode=basic.
Full textAbstract:
碩士國立中興大學
生物醫學研究所
107
Gastric cancer is one of the most common and deadly cancers. In the treatment of gastric cancer, chemotherapy drugs will cause a variety of side effects, which reduce patients'' quality of life and their willingness for treatment. Several non-chemotherapy drugs may inhibit the proliferation of gastric cancer cells, which were found in the drug repurposing program in our laboratory. This study focuses on exploration the effect of the combination treatment of non-chemo drugs and chemo drugs using gastric cancer cell lines AGS. Cell survival rate and cell cycle analysis showed that SMCL4 at a dose of 10M could significantly reduce cell proliferation and promote apoptosis in gastric cancer AGS cells line. Furthermore, observation on the ability of SMCL4 to induce apoptosis, it showed that SMCL4 inhibited the cell proliferation at 5M and induced apoptosis within 48 hours at 10M. In addition to promoting intracellular caspase 3 activation, SMCL4 also promotes autophagy. Later, we further studied whether SMCL4 could enhance the cytotoxicity of chemotherapy drugs. SMCL4 could enhance the cytotoxicity of Cisplatin, Docetaxel and Doxorubicin. In summary, SMCL4 has a significant inhibitory effect on the proliferation of gastric cancer. Although the mechanism is not clear, the possibility of its efficacy in the treatment of gastric cancer can be confirmed. In addition, SMCL4 can enhance the cytotoxicity of Cisplatin, Docetaxel and Doxorubicin, commonly used chemotherapy drugs for gastric cancer, which makes it possible to reduce the dose of chemotherapy drugs without reducing the drug''s inhibitory effect on cancer cells.
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Fu-Chi and 林富祺. "Inhibitory effects of diosgenin on the proliferation of breast cancer cells." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/16516846452231773272.
Full textAbstract:
碩士中山醫學大學
生化暨生物科技研究所
98
Diosgenin, a steroidal sapogenin, is similar to estrogen. It has been reported to have anti-inflammation and hypolipidemic effects, and it can inhibit proliferation and induce apoptosis in several human cancer cells. The mechanisms of anti-proliferation induced by diosgenin in breast cancer cell are not understood, we therefore treated breast cancer cell lines Hs578T and MCF7 with diosgenin. In our experiments, diosgenin caused DNA damages including double-strand break in breast cancer cell lines Hs578T and MCF7. We discovered that diosgenin reduced the expressions of cyclin D1 and Cdk4 protein, and induced G1 phase cell cycle arrest through activations of chk1, p53 and p21. We want to know whether diosgenin can affect non-homologous end-joining repair (NHEJ repair) when DNA double-strand break occurs. In outcome, diosgenin don’t influence the expressions of ku70 and ku80 in NHEJ enzymes. In addition, we add the protein kinase inhibitor (UCN-01) and diosgenin to treat breast cancer cell lines. This study suggests that breast cancer cells treated with diosgenin and UCN-01 reduced cell viability and induced G1 phase cell cycle arrest through the inhibition of cyclin D1 and cdk4. We infer that UCN-01 and diosgenin may have synergy to inhibit the proliferation of the breast cancer cells, but the detailed mechanisms are not understood. The addition of UCN-01 reduced the expression of ku80 in NHEJ enzyme in breast cancer cell Hs578T. That whether is related to synergy of UCN-01 and diosgenin still is needed to confirm.
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LU, JUI-HUA, and 呂瑞華. "Adipose-Derived Mesenchymal Stem Cells Facilitate Cancer Proliferation and Initiating Cells via IL-6 Pathway." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/66334176579764466314.
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Mannon, Sara. "Effects of endosulfan on human MCF-7 breast cancer cells." Thesis, 2011. http://hdl.handle.net/10155/193.
Full textAbstract:
Organochlorine pesticides (OCs) are environmental toxicants with important links to human health. They have been found to activate signalling pathways within cells and thereby affect cell survival and proliferation. Receptor Activator of Nuclear Factor kB (RANK) ligand and its receptor RANK are crucial for mammary epithelial proliferation in pregnancy and have recently been linked to hormone induced breast cancers. The objectives of this study were to confirm the proliferative effects of an OC (endosulfan) on human MCF-7 breast cancer cells, identify activated intracellular signaling pathways and investigate changes in RANK and RANKL gene expression. This study showed that endosulfan has a stimulatory effect on human MCF-7 cell proliferation, which may be invoked through activated intracellular signaling pathways (JNK, ERK1/2 and p38). In addition, there was a down regulation of RANK and upregulation of RANKL gene expression suggesting endosulfan is capable of modulating both cellular behavior and gene expression.UOIT