TY - JOUR
T1 - The Hallmarks of Cervical Cancer
T2 - Molecular Mechanisms Induced by Human Papillomavirus
AU - Rosendo-Chalma, Pedro
AU - Antonio-Véjar, Verónica
AU - Ortiz Tejedor, Jonnathan Gerardo
AU - Ortiz Segarra, Jose
AU - Vega Crespo, Bernardo
AU - Bigoni-Ordóñez, Gabriele Davide
N1 - Publisher Copyright:
© 2024 by the authors.
PY - 2024/2
Y1 - 2024/2
N2 - 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.
AB - 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.
KW - HPV
KW - integration
KW - metastasis
KW - methylation
KW - uterine cervical cancer
KW - viral load
KW - viral physical state
UR - https://www.scopus.com/pages/publications/85189096845
U2 - 10.3390/biology13020077
DO - 10.3390/biology13020077
M3 - Artículo de revisión
AN - SCOPUS:85189096845
SN - 2079-7737
VL - 13
JO - Biology
JF - Biology
IS - 2
M1 - 77
ER -
