The Hallmarks of Cervical Cancer: Molecular Mechanisms Induced by Human Papillomavirus

Simple Summary The role of human papillomavirus (HPV) in cervical carcinogenesis is widely documented; however, with an increasing number of scientific publications on the molecular and cellular mechanisms activated by the virus and, specifically, by high-risk HPVs (HR-HPVs) that are involved in the development of uterine cervical cancer (CaCU) and its precursor lesions, we consider it is important to present a review of scientific articles that address ten of the mechanisms associated with at least seven of the fourteen hallmarks of cancer recently proposed. Understanding the mechanisms activated by HR-HPVs in the context of the distinctive physiological capabilities of cancer will allow the identification of clinically relevant biomarkers to improve the diagnosis and treatment of CaCU.Abstract Human papillomaviruses (HPVs) and, specifically, high-risk HPVs (HR-HPVs) are identified as necessary factors in the development of cancer of the lower genital tract, with CaCU standing out as the most prevalent tumor. This review summarizes ten mechanisms activated by HR-HPVs during cervical carcinogenesis, which are broadly associated with at least seven of the fourteen distinctive physiological capacities of cancer in the newly established model by Hanahan in 2022. These mechanisms involve infection by human papillomavirus, cellular tropism, genetic predisposition to uterine cervical cancer (CaCU), viral load, viral physical state, regulation of epigenetic mechanisms, loss of function of the E2 protein, deregulated expression of E6/E7 oncogenes, regulation of host cell protein function, and acquisition of the mesenchymal phenotype.