Worldwide cervical cancer is the second most common cause of cancer related death in women. Over the last three decades high-risk HPV has been conclusively established as the major etiological factor in cervical cancer and the expression of its two oncogenes, E6 and E7, are critical to the neoplastic progression. Integration of high-risk HPV and subsequent permanent expression of E6 and E7 are key events in the pathogenesis of cervical cancer. While E6 and E7 expression is necessary for the neoplastic progression of cervical cancer, their expression alone is not sufficient to induce tumourigenesis. However it is believed that the expression of these viral oncogenes produces an environment in which other pro-oncogenic alterations occur at an increased rate. The purpose of this study was to further substantiate this view, and to investigate novel pathways involved in the pathogenesis of cervical cancer, this study aimed to examine the effect of suppressing the expression of endogenously expressed viral oncogenes. To achieve this goal, two independent approaches were pursued; firstly, the RNA of the E6/E7 oncogenes was targeted using siRNA, secondly, the protein product of the E7 oncogenes was targeted using the NSAID, Sulindac. The final objective was to establish the downstream effects of these silencing events. TARA (Trinity’s Access to Research Archive) has a robust takedown policy. Please contact us if you have any concerns: rssadmin@tcd.ie