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Published on: March 11, 2014
The Hallmarks of Cervical Cancer: Molecular Mechanisms Induced by Human Papillomavirus
Pedro Rosendo-Chalma1,2, Verónica Antonio-Véjar3, Jonnathan Gerardo Ortiz Tejedor2,4
1Laboratorio de Virus y Cáncer, Unidad de Investigación Biomédica en Cáncer of Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México (IIB-UNAM), Mexico City 14080, Mexico.
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.
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