Molecular mechanisms in progression of HPV-associated cervical carcinogenesis

Abstract

Cervical cancer is the fourth most frequent cancer in women worldwide and a major cause of mortality in developing countries. Persistent infection with high-risk human papillomavirus (HPV) is a necessary cause for the development of cervical cancer. In addition, genetic and epigenetic alterations in host cell genes are crucial for progression of cervical precancerous lesions to invasive cancer. Although much progress has been made in understanding the life cycle of HPV and it's role in the development of cervical cancer, there is still a critical need for accurate surveillance strategies and targeted therapeutic options to eradicate these cancers in patients. Given the widespread nature of HPV infection and the type specificity of currently available HPV vaccines, it is crucial that molecular details of the natural history of HPV infection as well as the biological activities of viral oncoproteins be elucidated. A better understanding of the mechanisms involved in oncogenesis can provide novel insights and opportunities for designing effective therapeutic approaches against HPV-associated malignancies. In this review, we briefly summarize epigenetic alterations and events that cause alterations in host genomes inducing cell cycle deregulation, aberrant proliferation and genomic instability contributing to tumorigenesis.