Cervical carcinoma (CC) is one of the most common cancers and a leading cause of mortality in women worldwide. Epidemiologic and experimental studies have clearly confi rmed a causal role of high-risk Human Papillomavirus (HR-HPV) types in cervical carcinogenesis, which affect cellular processes by targeting and inactivating p53 and pRB host proteins. CC arises through a multi-step carcinogenesis process mainly induced by the HR-HPV E6 and E7 oncoproteins, that have the ability to deregulate several cellular processes such as apoptosis, cell cycle control, migration, immune evasion and induction of genetic instability, which, among others, promotes accumulation of mutationsand aneuploidy. The complex interactions between early HR-HPV genes affects important epigenetic mechanisms in host cell by means of direct targeting on histone methyltransferases (HMTs), modulating their enzymatic activities by increasing transcriptional activity on specifi c histone demethylases (KDM6 and KDM6B) thus leading to aberrant expression of cellular oncogenic and tumor suppressive miRNAs. It has been stated that HPV infection and E6/E7 expression are essential but not suffi cient for CC development; hence other genetic and epigenetic factors have to be involved in this complex disease. Recent evidence suggests an important level of interaction between E6/E7 viral proteins and cellular miRNAs and other noncoding RNAs. The aim of the current chapter is to review and analyze recent data pointing to describe the infl uence of the HPV life cycle on specifi c noncoding RNAs, leading to a mechanistic view of HPV-induced oncogenesis. Finally, we review the use of RNA interference (RNAi) as a therapeutical alternative, seeking to block E6 and E7 expression to restore p53 and pRb levels.