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Regulation of apoptosis in human cancer cells

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dc.contributor.advisor Steven Robert Tannenbaum. en_US
dc.contributor.author Lloyd, S. Julie-Ann (Simone Julie-Ann) en_US
dc.contributor.other Massachusetts Institute of Technology. Biological Engineering Division. en_US
dc.date.accessioned 2006-08-25T18:52:55Z
dc.date.available 2006-08-25T18:52:55Z
dc.date.copyright 2005 en_US
dc.date.issued 2005 en_US
dc.identifier.uri http://hdl.handle.net/1721.1/33873
dc.description Thesis (S.M.)--Massachusetts Institute of Technology, Biological Engineering Division, 2005. en_US
dc.description Includes bibliographical references (leaves 38-44). en_US
dc.description.abstract Nitric oxide is postulated to protect cancer cells from the death-inducing effects of tumour necrosis factor alpha by S-nitrosating the active site cysteines, inhibiting cleavage of caspase-9. We aimed to test this hypothesis and to determine its validity across cancer cell types. In addition, we hoped to explain the involvement of certain kinases in nitric oxide-induced apoptosis. The experimental setup involved stimulating human colorectal cancer cells, HT-29 and HCT- 116, and human prostate cancer cells, LNCaP, with cytokines in order to induce cell death. Then, we observed the effects of NO inhibitors, kinase inhibitors, and activation of Akt, a kinase up-stream of the caspase cascade, following transfection of a DNA sequence that was proven to protect cells against apoptosis induction. In our series of experiments, inhibition of the nitric oxide synthases removes nitric oxide protection from apoptosis, but inhibition of only the inducible synthase has opposite effects with prostate and colon cancer cells that are considered insignificant, and its effects on the two types of colon cancer cells are in discord. Transformation and transfection of ARK5 into the colorectal cancer cell line, HT-29 did not prove beneficial. Similarly, glucosamine showed no clear pattern of reducing apoptosis in the cells. Therefore, we propose further exploration of the inhibition of constitutive nitric oxide synthases as a potential therapy. en_US
dc.description.statementofresponsibility by S. Julie-Ann Lloyd. en_US
dc.format.extent 74 leaves en_US
dc.format.extent 4452399 bytes
dc.format.extent 4455428 bytes
dc.format.mimetype application/pdf
dc.format.mimetype application/pdf
dc.language.iso eng en_US
dc.publisher Massachusetts Institute of Technology en_US
dc.rights M.I.T. theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission. See provided URL for inquiries about permission. en_US
dc.rights.uri http://dspace.mit.edu/handle/1721.1/7582
dc.subject Biological Engineering Division. en_US
dc.title Regulation of apoptosis in human cancer cells en_US
dc.type Thesis en_US
dc.description.degree S.M. en_US
dc.contributor.department Massachusetts Institute of Technology. Biological Engineering Division. en_US
dc.identifier.oclc 66464462 en_US


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