Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/28135
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dc.titleArsenic trioxide in ovarian cancer
dc.contributor.authorONG PEI SHI
dc.date.accessioned2011-11-08T18:00:34Z
dc.date.available2011-11-08T18:00:34Z
dc.date.issued2008-09-14
dc.identifier.citationONG PEI SHI (2008-09-14). Arsenic trioxide in ovarian cancer. ScholarBank@NUS Repository.
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/28135
dc.description.abstractArsenic trioxide (As2O3) has shown anti-tumour activity against a variety of solid tumours in vitro. However, the mechanisms responsible for its cytotoxicity against ovarian carcinoma remain elusive. In this thesis, the molecular determinants of its effects and factors mediating its chemoresistance in ovarian cancer cells were investigated. It was found that As2O3 treatment caused both apoptosis induction and caspase-independent cell death involving mitochondrial dysfunction. This was accompanied by endoplasmic reticulum stress induction and an increase in intracellular glutathione (GSH) level. The latter was in turn prevented by the concurrent use of GSH modulator, buthionine sulfoximine but not ascorbic acid. Gene expression analysis of arsenic-resistant OVCAR-3 (OVCAR-3/AsR) cells showed the involvement of multiple factors mediating its chemoresistance. Of particular interest, a genetic hub involving elevated interleukin 1A signalling was identified. This could consecutively modulate the expression of other genes, thus promoting and ensuing the continual growth and survival of OVCAR-3/AsR cells.
dc.language.isoen
dc.subjectArsenic Trioxide; Ovarian cancer; Mitochondrial dysfunction; Caspase-independent cell death; Endoplasmic reticulum stress; glutathione
dc.typeThesis
dc.contributor.departmentPHARMACY
dc.contributor.supervisorHO CHI LUI, PAUL
dc.contributor.supervisorCHAN SUI YUNG
dc.description.degreePh.D
dc.description.degreeconferredDOCTOR OF PHILOSOPHY
dc.identifier.isiutNOT_IN_WOS
Appears in Collections:Ph.D Theses (Open)

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