The silencing of HPV16 Oncogenes using E6siRNAs

Abstract

Cervical cancer is the fourth most common cancer worldwide and remains a rising cause of cancer deaths amongst women worldwide, particularly in low to mid-income countries. High risk HPV is the main etiological factor in cervical carcinogenesis. The overexpression of high risk HPV E6 and E7 due to viral genome integration and loss of high risk E2 is the key factor in this disease progression. These oncogenes subvert cellular tumour suppressor genes (p53 and unphosphorylated pRB) and create a neoplastic environment that facilitates increased cellular alterations that promote malignancy.