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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.
Pełny tekst źródłaTitle from document title page. Document formatted into pages; contains ix, 137 p. : ill. Vita. Includes abstract. Includes bibliographical references (p. 115-134).
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.
Pełny tekst źródła廖寶韶 i 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.
Pełny tekst źródłaPfeiffer, 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.
Pełny tekst źródłaNg, Wai Yee. "Ginsenosides on the growth and proliferation of glial tumor cells". HKBU Institutional Repository, 2008. http://repository.hkbu.edu.hk/etd_ra/998.
Pełny tekst źródłaFancher, 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.
Pełny tekst źródłaSIPES, 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.
Pełny tekst źródłaFettig, 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.
Pełny tekst źródłaDepartment of Biology
Wang, Haizhen. "The C-Phycocyanin/Beta Protein Inhibits Cancer Cell Proliferation". unrestricted, 2008. http://etd.gsu.edu/theses/available/etd-04212008-155113/.
Pełny tekst źródłaTitle 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).
Hui, Cheuk-man, i 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.
Pełny tekst źródła鄭珊 i 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.
Pełny tekst źródłaMiller, 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.
Pełny tekst źródłaPerkins, Denise Mary. "Isolation of and interaction of nutrients with the linoleoyl-coa desaturase complex". Thesis, Rhodes University, 1990. http://hdl.handle.net/10962/d1018264.
Pełny tekst źródłaAmunjela, 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.
Pełny tekst źródłaOjo, 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.
Pełny tekst źródłaWard, 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/.
Pełny tekst źródłaWillmer, 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.
Pełny tekst źródłaHernandez, Sarah. "Characterization of arginine methyltransferase PRMT8 in cells with increased plasticity". Digital WPI, 2016. https://digitalcommons.wpi.edu/etd-dissertations/533.
Pełny tekst źródłaJohnson, 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.
Pełny tekst źródłaBoyle-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.
Pełny tekst źródłaFalcone, 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.
Pełny tekst źródłaChen, Ru. "Promoter-level transcriptome identifies stemness associated with relatively high proliferation in pancreatic cancer cells". Kyoto University, 2020. http://hdl.handle.net/2433/259015.
Pełny tekst źródłaKyoto 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
Tam, Chun-wai, i 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.
Pełny tekst źródłaHui, Chun-fai Ivan, i 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.
Pełny tekst źródłaSancho, 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.
Pełny tekst źródłaAl 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.
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.
Pełny tekst źródłaDi, Kaijun, i 狄凱軍. "The role of Id-1 on the proliferation, motility and mitotic regulationof prostate epithelial cells". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B38944704.
Pełny tekst źródłaLiao, Ximan, i 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.
Pełny tekst źródłaMcEwan, 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/.
Pełny tekst źródłaThesis 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.
阮曉峰 i 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.
Pełny tekst źródłaPalmer, 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.
Pełny tekst źródłaLatham, 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.
Pełny tekst źródłaClubbs, 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.
Pełny tekst źródłaWillig, 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.
Pełny tekst źródłaVázquez, 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.
Pełny tekst źródłaÉs 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.
Liu, Wing-yee, i 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.
Pełny tekst źródłapublished_or_final_version
Pharmacology and Pharmacy
Master
Master of Philosophy
Webster, Rebecca. "Complementary investigations of the molecular biology of cancer : assessment of the role of Grb7 in the proliferation and migration of breast cancer cells; and prediction and validation of microRNA targets involved in cancer". University of Western Australia. School of Medicine and Pharmacology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0179.
Pełny tekst źródłaShih, Hung-Feng, i 施鴻鳳. "Participation of IRSp53 in cell proliferation of SW620 colon cancer cells". Thesis, 2007. http://ndltd.ncl.edu.tw/handle/84557400531641503239.
Pełny tekst źródła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.
楊所芳. "The Role of KDM8 in Breast Cancer Cells: Cell Proliferation and Migration". Thesis, 2012. http://ndltd.ncl.edu.tw/handle/15474248973694324183.
Pełny tekst źródła"Suppression of thromboxane synthase inhibits lung cancer cell proliferation". Thesis, 2008. http://library.cuhk.edu.hk/record=b6074592.
Pełny tekst źródłaTaken 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.
Yu-HuaWang i 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.
Pełny tekst źródła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.
I-HsiaLi i 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.
Pełny tekst źródła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.
Chiang, Chien-Chuan, i 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.
Pełny tekst źródłaTSAI, YA-RU, i 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.
Pełny tekst źródła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.
LIN, PING-CHENG, i 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.
Pełny tekst źródła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.
Tien, Yi-Li, i 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.
Pełny tekst źródła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.
Huang, Chih-Jou, i 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.
Pełny tekst źródła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.
Fu-Chi i 林富祺. "Inhibitory effects of diosgenin on the proliferation of breast cancer cells". Thesis, 2010. http://ndltd.ncl.edu.tw/handle/16516846452231773272.
Pełny tekst źródła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.
LU, JUI-HUA, i 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.
Pełny tekst źródłaMannon, Sara. "Effects of endosulfan on human MCF-7 breast cancer cells". Thesis, 2011. http://hdl.handle.net/10155/193.
Pełny tekst źródłaUOIT