IDENTIFYING CELLULAR TARGETS OF HIGH-RISK HPV ONCOGENES E6 AND E7

Abstract

Human papillomavirus (HPV) is known to cause both benign warts and oncogenic lesions, and it is the high-risk HPV types that have been implicated in cervical cancer. HPV16 and HPV18 are the two most prevalent high-risk HPV strains, and HPV exerts its oncogenic activities primarily through E6 and E7. In this thesis, I sought to identify novel targets of E6 and E7. I explored the transcriptional targets of TIP60, a lysine acetyltransferase which has been shown to be proteasomally degraded by high-risk HPV E6. Additionally, I explored circRNA which are differentially regulated by E6/E7. Currently, treatment options for cervical cancer patients involve surgery, radiotherapy, or chemotherapy, all of which do not exploit the presence of the viral genome in cancer cells. The identification of novel targets of HPV would open another avenue of treatment– in either restoring tumor suppressor genes downregulated by HPV or by targeting upregulated oncogenes.