The high‐risk HPV E6 proteins modify the activity of the eIF4E protein via the MEK/ERK and AKT/PKB pathways

摘要

In this study, we show that high‐risk E6 oncogenes (HPV16, HPV‐18, and HPV52) regulate eIF4E activity through downstream targets of PI3K/AKT/mTORC1 and MEK/ERK pathways, increasing translation of cellular proteins regulated by CAP‐dependent mechanisms (CCND1 and ODC1). The pharmacological inhibition of eIF4E phosphorylation by Ribavirin highlights the utility of this approach for the treatment of cervical cancer.