Abstract
#Epidemiological studies have found that cervical cancer is closely
related to human #papilloma virus (HPV) infection, probably due to
genetic damage of cells and integration of high-risk HPV- DNA [1].
Studies have shown that PI3K/Akt signal is over-activated in various
human squamous cell carcinomas associated with HPV infection. This
conclusion has been further confirmed in cervical cancer. Abnormal
activation of this pathway and HPV-encoded E-series #carcinogens have
been reported to play a synergistic role in promoting malignant
transformation of cervical cells [2]. transfected cervical cancer cells
with E5 gene and found that E5 protein could up-regulate the expression
of vascular #endothelial growth factor by activating PI3K/Akt signal [3].
Transfected cervical cancer HeLa cells with lentiviral vector carrying
siRNA of HPV18-E6 gene. It was found that inhibition of E6 protein
expression could significantly down-regulate Akt expression at mRNA and
protein levels, effectively inhibiting the growth of HeLa cells [4].It was also found that over-activation of mTOR could inactivate the
#phosphorylation of 4EBPl, the downstream target of mTOR, up-regulate the
level of E7 mRNA cap-dependent translation and maintain the high
expression of E7 protein. In turn, E7 protein could increase the level
of Akt phosphorylation and maintain the survival of tumor cells by
inhibiting Bax, the precursor of #apoptosis (Figure 1).
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