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Inhibition of the transcription factor AP-1 in cervical cancer

Includes bibliographical references (leaves 100-110).

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Bibliographic Details
Main Author: Maritz, Michelle Frances
Other Authors: Leaner, Virna D
Format: Thesis
Language:English
Published: Division of Medical Biochemistry 2014
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access_status_str Open Access
author Maritz, Michelle Frances
author2 Leaner, Virna D
author_browse Leaner, Virna D
Maritz, Michelle Frances
author_facet Leaner, Virna D
Maritz, Michelle Frances
author_sort Maritz, Michelle Frances
collection Thesis
description Includes bibliographical references (leaves 100-110).
format Thesis
id oai:open.uct.ac.za:11427/3138
institution University of Cape Town (South Africa)
language eng
last_indexed 2026-06-10T12:33:23.204Z
license_str Not specified — see source repository
provenance_str_mv Harvested via OAI-PMH from UCTD — University of Cape Town Open Access Repository
publishDate 2014
publishDateRange 2014
publishDateSort 2014
publisher Division of Medical Biochemistry
publisherStr Division of Medical Biochemistry
record_format dspace
source_str UCTD — University of Cape Town Open Access Repository
spelling oai:open.uct.ac.za:11427/3138 Inhibition of the transcription factor AP-1 in cervical cancer Maritz, Michelle Frances Leaner, Virna D Medical Biochemistry Includes bibliographical references (leaves 100-110). AP-I is a dimeric transcription factor comprised primarily of Jun and Fos family proteins, that regulates numerous genes involved in cell proliferation, differentiation and oncogenesis. The expression of AP-I is shown to play an important role in many human cancers and plays a key role in the regulation of the E6 and E7 oncoproteins of high-risk Human Papillomaviruses (HPV) that are etiologically associated with cervical cancer. The c-Jun and Jun B components of AP-I were shown to be expressed at higher levels in cervical cancer patients compared to nonnal patient tissue while Jun D levels were largely unchanged. To define the role of AP-I in cervical cancer, the effect of inhibiting AP-I actvity was determined using a dominantnegative deletion mutant T AM67. CaSki cervical cancer cells with a doxycycline inducible T AM67 demonstrated that inhibition of AP-I activity and expression resulted in an altered cell morphology, a significant decrease in cell proliferation and inhibition of colony formation. This was accompanied by a slower progression of T AM67 expressing cells through the cell cycle, with an accompanying increase in G21M phase. An increase in the expression of the cell cycle regulatory protein, p21 CIPI, was observed that appeared independent of p53 expression. siRNA directed at inhibiting individual AP-I components showed that Jun B was an important regulator of CaSki cell proliferation. These results suggest that AP-I is involved in the cell proliferation and tumourigenic phenotype of cervical cancer cells, such as CaSki cells, possibly via a direct repression of cell cycle regulator p21 CIP1 2014-07-28T14:55:40Z 2014-07-28T14:55:40Z 2007 Master Thesis Masters MSc http://hdl.handle.net/11427/3138 eng application/pdf Division of Medical Biochemistry Faculty of Health Sciences University of Cape Town
spellingShingle Medical Biochemistry
Maritz, Michelle Frances
Inhibition of the transcription factor AP-1 in cervical cancer
thesis_degree_str Master's
title Inhibition of the transcription factor AP-1 in cervical cancer
title_full Inhibition of the transcription factor AP-1 in cervical cancer
title_fullStr Inhibition of the transcription factor AP-1 in cervical cancer
title_full_unstemmed Inhibition of the transcription factor AP-1 in cervical cancer
title_short Inhibition of the transcription factor AP-1 in cervical cancer
title_sort inhibition of the transcription factor ap 1 in cervical cancer
topic Medical Biochemistry
url http://hdl.handle.net/11427/3138
work_keys_str_mv AT maritzmichellefrances inhibitionofthetranscriptionfactorap1incervicalcancer