The Hallmarks of Cervical Cancer: Molecular Mechanisms Induced by Human Papillomavirus
Pedro Rosendo-Chalma,
Verónica Antonio-Véjar,
Jonnathan Gerardo Ortiz Tejedor,
Jose Ortiz Segarra,
Bernardo Vega Crespo,
Gabriele Davide Bigoni-Ordóñez
Affiliations
Pedro Rosendo-Chalma
Laboratorio 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
Verónica Antonio-Véjar
Laboratorio de Biomedicina Molecular, Facultad de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Chilpancingo 39090, Guerrero, Mexico
Jonnathan Gerardo Ortiz Tejedor
Unidad Académica de Posgrado, Universidad Católica de Cuenca, Cuenca 010101, Ecuador
Jose Ortiz Segarra
Carrera de Medicina, Facultad de Ciencias Médicas, Universidad de Cuenca, Cuenca 010107, Ecuador
Bernardo Vega Crespo
Carrera de Medicina, Facultad de Ciencias Médicas, Universidad de Cuenca, Cuenca 010107, Ecuador
Gabriele Davide Bigoni-Ordóñez
Carrera de Laboratorio Clínico, Facultad de Ciencias Médicas, Universidad de Cuenca, Cuenca 010107, Ecuador
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.
