TY - JOUR
T1 - MicroRNAs in cervical cancer
T2 - Evidences for a miRNA profile deregulated by HPV and its impact on radio-resistance
AU - Pedroza-Torres, Abraham
AU - López-Urrutia, Eduardo
AU - García-Castillo, Verónica
AU - Jacobo-Herrera, Nadia
AU - Herrera, Luis A.
AU - Peralta-Zaragoza, Oscar
AU - López-Camarillo, César
AU - De Leon, David Cantú
AU - Fernández-Retana, Jorge
AU - Cerna-Cortés, Jorge F.
AU - Pérez-Plasencia, Carlos
PY - 2014/5
Y1 - 2014/5
N2 - Cervical carcinoma (CC) is one of the most common cancers and a leading cause of mortality in women worldwide. Epidemiologic and experimental data have clearly demonstrated a causal role of high-risk Human Papillomavirus (HR-HPV) types in CC initiation and progression, affecting the cellular processes by targeting and inactivating p53 and pRB host proteins. HR-HPV E5, E6 and E7 oncoproteins have the ability to deregulate several cellular processes, mostly apoptosis, cell cycle control, migration, immune evasion, and induction of genetic instability, which promote the accumulation of mutations and aneuploidy. In this scenario, genomic profiles have shown that aberrant expression of cellular oncogenic and tumor suppressive miRNAs have an important role in CC carcinogenesis. It has been stated that HPV infection and E6/E7 expression are essential but not sufficient to lead to CC development; hence other genetic and epigenetic factors have to be involved in this complex disease. Recent evidence suggests an important level of interaction among E6/E7 viral proteins and cellular miRNA, and other noncoding RNAs. The aim of the current review is to analyze recent data that mainly describe the interaction between HR-HPV established infections and specific cellular miRNAs; moreover, to understand how those interactions could affect radio-Therapeutic response in tumor cells.
AB - Cervical carcinoma (CC) is one of the most common cancers and a leading cause of mortality in women worldwide. Epidemiologic and experimental data have clearly demonstrated a causal role of high-risk Human Papillomavirus (HR-HPV) types in CC initiation and progression, affecting the cellular processes by targeting and inactivating p53 and pRB host proteins. HR-HPV E5, E6 and E7 oncoproteins have the ability to deregulate several cellular processes, mostly apoptosis, cell cycle control, migration, immune evasion, and induction of genetic instability, which promote the accumulation of mutations and aneuploidy. In this scenario, genomic profiles have shown that aberrant expression of cellular oncogenic and tumor suppressive miRNAs have an important role in CC carcinogenesis. It has been stated that HPV infection and E6/E7 expression are essential but not sufficient to lead to CC development; hence other genetic and epigenetic factors have to be involved in this complex disease. Recent evidence suggests an important level of interaction among E6/E7 viral proteins and cellular miRNA, and other noncoding RNAs. The aim of the current review is to analyze recent data that mainly describe the interaction between HR-HPV established infections and specific cellular miRNAs; moreover, to understand how those interactions could affect radio-Therapeutic response in tumor cells.
KW - Cervical cancer
KW - HPV
KW - MiRNAs
KW - Mirnome
KW - Radio-resistance
UR - http://www.scopus.com/inward/record.url?scp=84901449241&partnerID=8YFLogxK
U2 - 10.3390/molecules19056263
DO - 10.3390/molecules19056263
M3 - Artículo de revisión
C2 - 24840898
SN - 1420-3049
VL - 19
SP - 6263
EP - 6281
JO - Molecules
JF - Molecules
IS - 5
ER -